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Article ; Online: Investigation of homocysteine, D-dimer and platelet count levels as potential predictors of thrombosis risk in COVID-19 patients.

Eslamifar, Zahra / Behzadifard, Mahin / Zare, Ehsan

2024

Abstract: Thrombosis plays an important role in induction of Coronavirus disease 19 (COVID-19) complications including heart attack and stroke. Reliable biomarkers are needed to predict thrombosis risk for better management and improve patient outcomes. This study ...

Abstract	Thrombosis plays an important role in induction of Coronavirus disease 19 (COVID-19) complications including heart attack and stroke. Reliable biomarkers are needed to predict thrombosis risk for better management and improve patient outcomes. This study aimed to investigate the relationship between homocysteine, a thrombosis-related biomarker, and other thrombosis-related parameters, such as D-dimer and platelet count with disease outcome in COVID-19 patients. This case-control study including 50 intensive care unit hospitalized patients with Covid-19 with a positive RT-PCR test for SARS-CoV-2 infection and 50 healthy individuals as a control group was conducted. Both groups were matched for age and body mass index (BMI) and had no history of underlying diseases such as cardiovascular, liver, kidney or smoking. Blood samples were collected from both groups to measure serum homocysteine, platelet count and D-dimer levels. Data were analyzed using GraphPad Prism version 8.3 software. The study found no statistically significant difference in homocysteine levels between COVID-19 patients and the control group. However, D-dimer levels were significantly higher in the patient group. Platelet count analysis revealed a significant difference between patients who died and those who were discharged from the hospital (P < 0.05). Despite previous studies suggesting a link between homocysteine and thrombosis, this study found no significant difference in homocysteine levels between COVID-19 patients and the control group. The significantly elevated D-dimer levels in the death group patient suggest that D-dimer and thrombocytopenia may be more reliable predictors of thrombosis and worse outcome in COVID-19 patients without underlying diseases.
Language	English
Publishing date	2024-03-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-024-04967-5
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Article: NETosis and SARS-COV-2 infection related thrombosis: a narrative review.

Behzadifard, Mahin / Soleimani, Masoud

Thrombosis journal

2022 Volume 20, Issue 1, Page(s) 13

Abstract: Background: Coronavirus disease 2019 (COVID-19) infection is related to immune hyperactivity, the release of inflammatory cytokines, and immunothrombosis. Among the underlying mechanisms in COVID-19 thrombosis, neutrophil extracellular traps (NETs) ... ...

Abstract	Background: Coronavirus disease 2019 (COVID-19) infection is related to immune hyperactivity, the release of inflammatory cytokines, and immunothrombosis. Among the underlying mechanisms in COVID-19 thrombosis, neutrophil extracellular traps (NETs) formation, NETosis, may have a significant role. COVID-19 thrombi obtained from extracorporeal membrane oxygenation contained an accumulation of neutrophils and in a higher amount of NETs when compared with non-COVID-19 thrombi specimens. Main body: During sepsis and inflammatory status, NETs released from neutrophils and histones and nucleosomes extruded into the extracellular space and take part in the host innate immunity defense, inflammation, and thrombosis. Excessive NETosis is related to clinical progression and respiratory failure in infections and sepsis. NETosis act as a scaffold for thrombus formation, and new associative data support the relation between deregulated immune responses with thrombus formation and organ failure. NETosis is reported in COVID-19 patients. In COVID-19 infection, overproduction of tissue factor (TF) by neutrophils has a role in immunothrombosis. Additionally, NETs can trap TF pathway inhibitor (TFPI) as the only endogenous protein that effectively inhibits the activity of the significant proteases- complexes, TF-FVIIa and prothrombinase. Conclusion: Because of NETosis can induce intrinsic and extrinsic coagulation cascade activation through the production of TF, activation of FXII, and inhibition of TFPI and fibrinolysis and induce immunothrombosis, targeting NETosis may diminish thrombus formation related to NETs in COVID-19 patients.
Language	English
Publishing date	2022-03-30
Publishing country	England
Document type	Letter
ZDB-ID	2118392-2
ISSN	1477-9560
ISSN	1477-9560
DOI	10.1186/s12959-022-00375-1
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Article: Severe hemolysis with negative direct antiglobulin test: A case report.

Behzadifard, Mahin / Arianezhad, Ali / Bandehzadeh, Ali / Gholampour, Mohammadali

Annals of medicine and surgery (2012)

2022 Volume 81, Page(s) 104444

Abstract: A 49-year-old woman with type 2 diabetes mellitus (T2DM) presented to the emergency department. Her examination showed marked pallor, exhaustion, lethargy, yellowish eyes, anorexia, nausea and vomiting. Hematuria; negative standard direct antiglobulin ... ...

Abstract	A 49-year-old woman with type 2 diabetes mellitus (T2DM) presented to the emergency department. Her examination showed marked pallor, exhaustion, lethargy, yellowish eyes, anorexia, nausea and vomiting. Hematuria; negative standard direct antiglobulin test (DAT); normal glucose 6 phosphate dehydrogenase (G6PD); hemoglobin (Hb), 4.8 g/dl; Mean cell volume (MCV), 91fl; platelet count, 233 × 10
Language	English
Publishing date	2022-08-18
Publishing country	England
Document type	Case Reports
ZDB-ID	2745440-X
ISSN	2049-0801
ISSN	2049-0801
DOI	10.1016/j.amsu.2022.104444
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Article: Coagulation abnormalities in SARS-CoV-2 infection: overexpression tissue factor.

Eslamifar, Zahra / Behzadifard, Mahin / Soleimani, Masoud / Behzadifard, Saba

Thrombosis journal

2020 Volume 18, Issue 1, Page(s) 38

Abstract: Among the pathways and mediators that may be dysregulated in COVID-19 infection, there are proinflammatory cytokines, lymphocyte apoptosis, and the coagulation cascade. Venous and arterial thromboembolisms also are frequent in COVID-19 patients with the ... ...

Abstract	Among the pathways and mediators that may be dysregulated in COVID-19 infection, there are proinflammatory cytokines, lymphocyte apoptosis, and the coagulation cascade. Venous and arterial thromboembolisms also are frequent in COVID-19 patients with the increased risk of some life-threatening complications such as pulmonary embolism, myocardial infarction, and ischemic stroke. In this regard, overproduction of proinflammatory cytokines such as IL-6, IL-1β, and TNF-α induce cytokine storms, increase the risk of clot formation, platelet activation, and multiorgan failure that may eventually lead to death among these patients. Surface S protein of SARS-CoV-2 binds to its target transmembrane receptor, named as angiotensin converting enzyme 2 (ACE2(, on various cells such as lymphocyte, alveolar cells, monocytes/macrophages, and platelets. Notably, the activation of the coagulation cascade occurs through tissue factor (TF)/FVIIa-initiated hemostasis. Accordingly, TF plays the major role in the activation of coagulation system during viral infection. In viral infections, the related coagulopathy multiple factors such as inflammatory cytokines and viral specific TLRs are involved, which consequently induce TF expression aberrantly. SARS-COV-2 may directly infect monocytes/ macrophages. In addition, TF expression/release from these cells may play a critical role in the development of COVID-19 coagulopathy. In this regard, the use of TF- VIIa complex inhibitor may reduce the cytokine storm and mortality among COVID-19 patients.
Language	English
Publishing date	2020-12-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2118392-2
ISSN	1477-9560
ISSN	1477-9560
DOI	10.1186/s12959-020-00250-x
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Article ; Online: Eotaxin-1 (CCL11) in neuroinflammatory disorders and possible role in COVID-19 neurologic complications.

Nazarinia, Donya / Behzadifard, Mahin / Gholampour, Javad / Karimi, Roqaye / Gholampour, Mohammadali

Acta neurologica Belgica

2022 Volume 122, Issue 4, Page(s) 865–869

Abstract: The related neurologic complications of SARS-CoV-2 infection in COVID-19 patients and survivors comprise symptoms including depression, anxiety, muscle pain, dizziness, headaches, fatigue, and anosmia/hyposmia that may continue for months. Recent studies ...

Abstract	The related neurologic complications of SARS-CoV-2 infection in COVID-19 patients and survivors comprise symptoms including depression, anxiety, muscle pain, dizziness, headaches, fatigue, and anosmia/hyposmia that may continue for months. Recent studies have been demonstrated that chemokines have brain-specific attraction and effects such as chemotaxis, cell adhesion, modulation of neuroendocrine functions, and neuroinflammation. CCL11 is a member of the eotaxin family that is chemotactic agents for eosinophils and participate in innate immunity. Eotaxins may exert physiological and pathological functions in the central nerve system, and CCL11 may induce neuronal cytotoxicity effects by inducing the production of reactive oxygen species (ROS) in microglia cells. Plasma levels of CCL11 elevated in neuroinflammation and neurodegenerative disorders. COVID-19 patients display elevations in CCL11 levels. As CCL11 plays roles in physiosomatic and neuroinflammation, analyzing the level of this chemokine in COVID-19 patients during hospitalization and to predicting post-COVID-19-related neurologic complications may be worthwhile. Moreover, using chemokine modulators may be helpful in lessening the neurologic complications in such patients.
MeSH term(s)	COVID-19/complications ; COVID-19/metabolism ; Chemokine CCL11/metabolism ; Humans ; Neuroinflammatory Diseases/metabolism ; Neuroinflammatory Diseases/virology ; SARS-CoV-2
Chemical Substances	CCL11 protein, human ; Chemokine CCL11
Language	English
Publishing date	2022-06-12
Publishing country	Italy
Document type	Journal Article ; Review
ZDB-ID	127315-2
ISSN	2240-2993 ; 0300-9009
ISSN (online)	2240-2993
ISSN	0300-9009
DOI	10.1007/s13760-022-01984-3
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Article ; Online: Ameliorative Effects of Gallic Acid on Cisplatin-Induced Nephrotoxicity in Rat Variations of Biochemistry, Histopathology, and Gene Expression.

Eslamifar, Zahra / Moridnia, Abbas / Sabbagh, Susan / Ghaffaripour, Reza / Jafaripour, Leila / Behzadifard, Mahin

BioMed research international

2021 Volume 2021, Page(s) 2195238

Abstract: Background: Cisplatin is a powerful chemotherapeutic drug mainly used in the treatment of solid tumors. Aggregation of the drug in renal proximal tubule cells causes nephrotoxicity and renal failure. Investigations showed nephrotoxicity as Cisplatin's ... ...

Abstract	Background: Cisplatin is a powerful chemotherapeutic drug mainly used in the treatment of solid tumors. Aggregation of the drug in renal proximal tubule cells causes nephrotoxicity and renal failure. Investigations showed nephrotoxicity as Cisplatin's dose-limiting side effect. One of the Cisplatin toxicity mechanisms is generation of reactive oxygen species, which leads to oxidative stress and renal damage. The purpose of this study was evaluation of the modulating effects of Gallic acid on Cisplatin-induced variations including Caspase-3 and Clusterin expression and histopathological and biochemical parameters in adult male Wistar rats. Method: Rats were kept under standard condition of temperature, light, and humidity. The animals were divided into 4 groups: GpI: control group (received distilled water for 10 days); GpII: Gallic acid (alone) (50 mg/kg bw, once a day for 10 days); GpIII: Cisplatin (alone), single dose (6 mg/kg bw, I.P. on 5th day of study); GpIV: Gallic acid (50 mg/kg bw, once a day for 10 days) and also injected with single dose of Cisplatin (6 mg/kg bw, I.P., on 5th day of study). After 10 days, all rats were anaesthetized and plasma collected to estimate urea, creatinine, and uric acid. The right kidneys were removed for the study of gene expression and biochemical parameters. The left kidneys were used for histopathological studies. Results: The Cisplatin-induced nephrotoxicity was evident from the elevated levels of creatinine, urea, uric acid, and renal tissue MDA and also decreased levels of SOD, CAT, GPX, and GSH in renal tissue. Administration of Gallic acid significantly modulated nephrotoxicity markers, gene expression variations, and histopathological damage. Conclusion: Outcomes of the present investigation suggest that Gallic acid provides protection against CP-induced nephrotoxicity, but for application in people, further studies are needed.
MeSH term(s)	Animals ; Biomarkers/blood ; Caspase 3/analysis ; Caspase 3/genetics ; Cisplatin/pharmacology ; Cisplatin/toxicity ; Clusterin/analysis ; Clusterin/genetics ; Gallic Acid/pharmacology ; Gene Expression/drug effects ; Kidney/drug effects ; Kidney/pathology ; Male ; Oxidative Stress/drug effects ; Rats ; Rats, Wistar ; Reactive Oxygen Species/metabolism ; Renal Insufficiency/drug therapy
Chemical Substances	Biomarkers ; Clu protein, rat ; Clusterin ; Reactive Oxygen Species ; Gallic Acid (632XD903SP) ; Casp3 protein, rat (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2021-10-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2021/2195238
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Article ; Online: Neuroprotective Effects of Conditioned Medium of Mesenchymal Stem Cells (MSC-CM) as a Therapy for Ischemic Stroke Recovery: A Systematic Review.

Behzadifard, Mahin / Aboutaleb, Nahid / Dolatshahi, Mojtaba / Khorramizadeh, Maryam / Mirshekari Jahangiri, Hamzeh / Kord, Zeynab / Nazarinia, Donya

Neurochemical research

2022 Volume 48, Issue 5, Page(s) 1280–1292

Abstract: It has been reported that the therapeutic potential of stem cells is mainly mediated by their paracrine factors. In order to identify the effects of conditioned medium of mesenchymal stem cells (MSC-CM) against stroke, a systematic review was conducted. ... ...

Abstract	It has been reported that the therapeutic potential of stem cells is mainly mediated by their paracrine factors. In order to identify the effects of conditioned medium of mesenchymal stem cells (MSC-CM) against stroke, a systematic review was conducted. We searched PubMed, Scopus, and ISI Web of Science databases for all available articles relevant to the effects of MSC-CM against the middle cerebral artery occlusion (MCAO) model of ischemic stroke until August 2022. The quality of the included studies was evaluated using The STAIR scale. During the systematic search, a total of 356 published articles were found. A total of 15 datasets were included following screening for eligibility. The type of cerebral ischemia was the MCAO model and CM was obtained from MSCs. The results showed that the therapeutic time window can be considered a crucial factor when researchers use MSC-CM for stroke therapy. In addition, MSC-CM therapy contributes to functional recovery and reduces infarct volume after stroke by targeting different cellular signaling pathways. Our findings showed that MSC-CM therapy has the ability to improve functional recovery and attenuate brain infarct volume after ischemic stroke in preclinical studies. We hope our study accelerates needed progress towards clinical trials.
MeSH term(s)	Humans ; Animals ; Ischemic Stroke/metabolism ; Neuroprotective Agents/pharmacology ; Culture Media, Conditioned/pharmacology ; Culture Media, Conditioned/metabolism ; Stroke/metabolism ; Infarction, Middle Cerebral Artery/metabolism ; Mesenchymal Stem Cells/metabolism ; Mesenchymal Stem Cell Transplantation/methods ; Disease Models, Animal
Chemical Substances	Neuroprotective Agents ; Culture Media, Conditioned
Language	English
Publishing date	2022-12-30
Publishing country	United States
Document type	Systematic Review ; Journal Article ; Review
ZDB-ID	199335-5
ISSN	1573-6903 ; 0364-3190
ISSN (online)	1573-6903
ISSN	0364-3190
DOI	10.1007/s11064-022-03848-x
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Article ; Online: Ameliorative Effects of Gallic Acid on Cisplatin-Induced Nephrotoxicity in Rat Variations of Biochemistry, Histopathology, and Gene Expression

Zahra Eslamifar / Abbas Moridnia / Susan Sabbagh / Reza Ghaffaripour / Leila Jafaripour / Mahin Behzadifard

BioMed Research International, Vol

2021 Volume 2021

Abstract: Background. Cisplatin is a powerful chemotherapeutic drug mainly used in the treatment of solid tumors. Aggregation of the drug in renal proximal tubule cells causes nephrotoxicity and renal failure. Investigations showed nephrotoxicity as Cisplatin’s ... ...

Abstract	Background. Cisplatin is a powerful chemotherapeutic drug mainly used in the treatment of solid tumors. Aggregation of the drug in renal proximal tubule cells causes nephrotoxicity and renal failure. Investigations showed nephrotoxicity as Cisplatin’s dose-limiting side effect. One of the Cisplatin toxicity mechanisms is generation of reactive oxygen species, which leads to oxidative stress and renal damage. The purpose of this study was evaluation of the modulating effects of Gallic acid on Cisplatin-induced variations including Caspase-3 and Clusterin expression and histopathological and biochemical parameters in adult male Wistar rats. Method. Rats were kept under standard condition of temperature, light, and humidity. The animals were divided into 4 groups: GpI: control group (received distilled water for 10 days); GpII: Gallic acid (alone) (50 mg/kg bw, once a day for 10 days); GpIII: Cisplatin (alone), single dose (6 mg/kg bw, I.P. on 5th day of study); GpIV: Gallic acid (50 mg/kg bw, once a day for 10 days) and also injected with single dose of Cisplatin (6 mg/kg bw, I.P., on 5th day of study). After 10 days, all rats were anaesthetized and plasma collected to estimate urea, creatinine, and uric acid. The right kidneys were removed for the study of gene expression and biochemical parameters. The left kidneys were used for histopathological studies. Results. The Cisplatin-induced nephrotoxicity was evident from the elevated levels of creatinine, urea, uric acid, and renal tissue MDA and also decreased levels of SOD, CAT, GPX, and GSH in renal tissue. Administration of Gallic acid significantly modulated nephrotoxicity markers, gene expression variations, and histopathological damage. Conclusion. Outcomes of the present investigation suggest that Gallic acid provides protection against CP-induced nephrotoxicity, but for application in people, further studies are needed.
Keywords	Medicine ; R
Subject code	630
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Detection of N-RAS gene mutations in codons 12,13 and 61 in patients with pediatric acute lymphoblastic leukemia

Mahin Behzadifard / Yosof Mortazavi / Sadegh Rezapour / Ali akbar Pourfatholah / Saeed Kavyani / Mansoure Haghighi / Samane Behzadifard

Yafteh, Vol 13, Iss 3, Pp 9-

2011 Volume 15

Abstract: Background: Acute leukemia is the prevalent malignancy in pediatrics. One of the most important causing factors of acute lymphoblastic leukemia is mutations of proto oncogenes and their chang in to oncogenes. Activation of N-RAS proto-oncogene due to ... ...

Abstract	Background: Acute leukemia is the prevalent malignancy in pediatrics. One of the most important causing factors of acute lymphoblastic leukemia is mutations of proto oncogenes and their chang in to oncogenes. Activation of N-RAS proto-oncogene due to point mutations plays a major role in ALL malignancy. Since there was no report on the frequency of N-RAS gene mutation in Iranian pediatric ALL patients, therefore we decided to determine its frequency and compare the results with age, sex and type of ALL. Materials and Methods: In this study, 60 pediatric ALL patients from Tehran Mahak hospital were screened for the mutations of N-RAS gene at codons 12 ,13 1nd 61.DNA was extracted from peripheral blood samples before the start of chemotherapy. The above mentioned codons were amplified by PCR and analyzed by restriction endonuclease enzymes. Results: We could detect mutations in 7 cases of 60(11.7%) patients. Most of the mutations were detected in males with an age less than 5 years old. The frequency of mutations for codons 12, 13 and 61 were 8.3%,3.3% and 1.7% respectively. Most of the mutations (71.4%) were found in c-ALL subtype. Conclusion: We detected mutations in 11.7% of our ALL patients. In general , frequency of the mutations that we found was in agreement with the results of other studies. However , to do study with more patients and wider range of age using a combination of PCR-RFLP and direct gene sequencing is highly recommended.
Keywords	All ; N-RAS gene ; PCR-RELP ; Proto-oncogene ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	610 ; 616
Language	Persian
Publishing date	2011-12-01T00:00:00Z
Publisher	Lorestan University of Medical Science
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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