المؤلفون: Zeidan, Nancy M. S., Lateef, Hanan M. Abd El, Selim, Dalia M., Razek, Suzan A., Abd-Elrehim, Ghada A. B., Nashat, Mohamed, ElGyar, Noha, Waked, Nevin M., Soliman, Attia A., Elhewala, Ahmed A., Shehab, Mohamed M. M., Ibraheem, Ahmed A. A., Shehata, Hassan, Yousif, Yousif M., Akeel, Nagwa E., Hashem, Mustafa I. A., Ahmed, Amani A., Emam, Ahmed A., Abdelmohsen, Mohamed M., Ahmed, Mohamed F., Saleh, Ahmed S. E., Eltrawy, Heba H., Shahin, Gehan H., Nabil, Rehab M., Hosny, Thoraya A., Abdelhamed, Mohamed R., Afify, Mona R., Alharbi, Mohanned T., Nagshabandi, Mohammed K., Tarabulsi, Muyassar K., Osman, Sherif F., Abd-Elrazek, Amal S. M., Rashad, Manal M., El-Gaaly, Sonya A. A., Gad, Said A. B., Mohamed, Mohamed Y., Abdelkhalek, Khalil, Yousef, Aly A.

المصدر: Pediatric Research ; volume 93, issue 5, page 1383-1390 ; ISSN 0031-3998 1530-0447

مصطلحات موضوعية: Pediatrics, Perinatology and Child Health

الوصف: Background Given the sparse data on vitamin D status in pediatric COVID-19, we investigated whether vitamin D deficiency could be a risk factor for susceptibility to COVID-19 in Egyptian children and adolescents. We also investigated whether vitamin D receptor (VDR) FokI polymorphism could be a genetic marker for COVID-19 susceptibility. Methods One hundred and eighty patients diagnosed to have COVID‐19 and 200 matched control children and adolescents were recruited. Patients were laboratory confirmed as SARS-CoV-2 positive by real-time RT-PCR. All participants were genotyped for VDR Fok1 polymorphism by RT-PCR. Vitamin D status was defined as sufficient for serum 25(OH) D at least 30 ng/mL, insufficient at 21–29 ng/mL, deficient at <20 ng/mL. Results Ninety-four patients (52%) had low vitamin D levels with 74 (41%) being deficient and 20 (11%) had vitamin D insufficiency. Vitamin D deficiency was associated with 2.6-fold increased risk for COVID-19 (OR = 2.6; [95% CI 1.96–4.9]; P = 0.002. The FokI FF genotype was significantly more represented in patients compared to control group (OR = 4.05; [95% CI: 1.95–8.55]; P < 0.001). Conclusions Vitamin D deficiency and VDR Fok I polymorphism may constitute independent risk factors for susceptibility to COVID-19 in Egyptian children and adolescents. Impact Vitamin D deficiency could be a modifiable risk factor for COVID-19 in children and adolescents because of its immune-modulatory action. To our knowledge, ours is the first such study to investigate the VDR Fok I polymorphism in Caucasian children and adolescents with COVID-19. Vitamin D deficiency and the VDR Fok I polymorphism may constitute independent risk factors for susceptibility to COVID-19 in Egyptian children and adolescents. Clinical trials should be urgently conducted to test for causality and to evaluate the efficacy of vitamin D supplementation for prophylaxis and treatment of COVID-19 taking into account the VDR polymorphisms.

الإتاحة: https://doi.org/10.1038/s41390-022-02275-6Test
https://www.nature.com/articles/s41390-022-02275-6.pdfTest
https://www.nature.com/articles/s41390-022-02275-6Test

المؤلفون: Yousef,Aly A, Mohamed,Faisal Y, Boraey,Naglaa F, Akeel,Nagwa E, Soliman,Attia A, Waked,Nevin M, Hashem,Mustafa IA, Shehata,Hassan, Fahmy,Dalia S, Ismael,Ali, Ibrahim,Lamya M, Ibrahim,Mohamed AM, Salem,Hanan F, Yousry,Sherif M, Osman,Sherif F, Fouad,Rania A, Enan,Eman T, Attia,Mohammed A, Afify,Mona R, Zeidan,Nancy MS, Nashat,Mohamed

مصطلحات موضوعية: Journal of Inflammation Research

الوصف: Yousef AA, Mohamed FY, Boraey NF, et al. J Inflamm Res. 2020;13:1103— 1111. The authors have advised the affiliation list on page 1103is incorrect. The correct author list and affiliations are asfollows: Aly A Yousef, 1 Faisal Y Mohamed, 2 Naglaa F Boraey, 3Nagwa E Akeel, 4 Attia A Soliman, 4 Nevin M Waked, 5Mustafa IA Hashem, 4 Hassan Shehata, 4 Dalia S Fahmy, 6Ali Ismael, 7 Lamya M Ibrahim, 8 Mohamed AM Ibrahim, 9Hanan F Salem, 10 Sherif M Yousry, 11 Sherif F Osman, 12Rania A Fouad, 13,14 Eman T Enan, 15 MohammedA Attia, 16,17 Mona R Afify, 18 Nancy MS Zeidan, 19Mohamed Nashat 20 Read the original article

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العلاقة: https://www.dovepress.com/corrigendum-association-of-plasminogen-activator-inhibitor-1-pai-1-4g5-peer-reviewed-fulltext-article-JIRTest

الإتاحة: https://doi.org/10.2147/JIR.S302580Test
https://www.dovepress.com/corrigendum-association-of-plasminogen-activator-inhibitor-1-pai-1-4g5-peer-reviewed-fulltext-article-JIRTest

المؤلفون: Yousef, Aly A, Mohamed, Faisal Y, Boraey, Naglaa F, Akeel, Nagwa E, Soliman, Attia A, Waked, Nevin M, Hashem, Mustafa IA, Shehata, Hassan, Fahmy, Dalia S, Ismael, Ali, Ibrahim, Lamya M, Ibrahim, Mohamed AM, Salem, Hanan F, Yousry, Sherif M, Osman, Sherif F, Fouad, Rania A, Enan, Eman T, Attia, Mohammed A, Afify, Mona R, Zeidan, Nancy MS, Nashat, Mohamed

المصدر: Journal of Inflammation Research ; volume Volume 14, page 265-266 ; ISSN 1178-7031

الإتاحة: https://doi.org/10.2147/jir.s302580Test
https://www.dovepress.com/getfile.php?fileID=66221Test

المؤلفون: Yousef,Aly A, Mohamed,Faisal Y, Boraey,Naglaa F, Akeel,Nagwa E, Soliman,Attia A, Waked,Nevin M, Hashem,Mustafa IA, Shehata,Hassan, Fahmy,Dalia S, Ismael,Ali, Ibrahim,Lamya M, Ibrahim,Mohamed AM, Salem,Hanan F, Yousry,Sherif M, Osman,Sherif F, Fouad,Rania A, Enan,Eman T, Attia,Mohammed A, Afify,Mona R, Zeidan,Nancy MS, Nashat,Mohamed

مصطلحات موضوعية: Journal of Inflammation Research

الوصف: Aly A Yousef, 1 Faisal Y Mohamed, 2 Naglaa F Boraey, 3 Nagwa E Akeel, 4 Attia A Soliman, 4 Nevin M Waked, 5 Mustafa IA Hashem, 4 Hassan Shehata, 4 Dalia S Fahmy, 6 Ali Ismael, 7 Lamya M Ibrahim, 8 Mohamed AM Ibrahim, 9 Hanan F Salem, 10 Sherif M Yousry, 11 Sherif F Osman, 12 Rania A Fouad, 13, 14 Eman T Enan, 15, 16 Mohammed A Attia, 17, 18 Mona R Afify, 19 Nancy MS Zeidan, 20 Mohamed Nashat 21 1Department of Pediatrics, Faculty of Medicine, Helwan University, Helwan, Egypt; 2Department of Pediatrics, Faculty of Medicine, Ain-Shams University, Cairo, Egypt; 3Department of Pediatrics, Faculty of Medicine, Sohag University, Sohag, Egypt; 4Department of Pediatrics, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 5Department of Pediatrics, Faculty of Medicine, October 6 University, October 6, Egypt; 6Department of Rheumatology, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 7Department of Internal Medicine, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 8Department of Clinical Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt; 9Department of Clinical Pathology, Faculty of Medicine, Sohag University, Sohag, Egypt; 10Department of Anesthesia, Faculty of Medicine, Banha University, Banha, Egypt; 11Department of Clinical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt; 12Department of Radiology, Texas Tech University Health Sciences Center, El Paso, TX, USA; 13Department of Medical Biochemistry, College of Medicine, El-Mareefa University, Riyadh, Kingdom of Saudi Arabia; 14Department of Medical Biochemistry, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 15Department of Pathology, College of Medicine, El-Mareefa University, Riyadh, Kingdom of Saudi Arabia; 16Department of Pathology, Faculty of Medicine, Mansoura University, Mansoura, 35516, Egypt; 17Department of Clinical Pharmacology, College of Medicine, El-Mareefa University, Riyadh, Kingdom of Saudi Arabia; 18Department of Clinical Pharmacology, Faculty of Medicine, Mansoura University, ...

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العلاقة: https://www.dovepress.com/association-of-plasminogen-activator-inhibitor-1-pai-1-4g5g-polymorphi-peer-reviewed-fulltext-article-JIRTest

الإتاحة: https://doi.org/10.2147/JIR.S277373Test
https://www.dovepress.com/association-of-plasminogen-activator-inhibitor-1-pai-1-4g5g-polymorphi-peer-reviewed-fulltext-article-JIRTest

المؤلفون: Yousef, Aly A, Mohamed, Faisal Y, Boraey, Naglaa F, Akeel, Nagwa E, Soliman, Attia A, Waked, Nevin M, Hashem, Mustafa IA, Shehata, Hassan, Fahmy, Dalia S, Ismael, Ali, Ibrahim, Lamya M, Ibrahim, Mohamed AM, Salem, Hanan F, Yousry, Sherif M, Osman, Sherif F, Fouad, Rania A, Enan, Eman T, Attia, Mohammed A, Afify, Mona R, Zeidan, Nancy MS, Nashat, Mohamed

المصدر: Journal of Inflammation Research ; volume Volume 13, page 1103-1111 ; ISSN 1178-7031

الإتاحة: https://doi.org/10.2147/jir.s277373Test
https://www.dovepress.com/getfile.php?fileID=64719Test

المؤلفون: Zeidan, Nancy M. S., Lateef, Hanan M. Abd El, Selim, Dalia M., Razek, Suzan A., Abd-Elrehim, Ghada A. B., Nashat, Mohamed, ElGyar, Noha, Waked, Nevin M., Soliman, Attia A., Elhewala, Ahmed A., Shehab, Mohamed M. M., Ibraheem, Ahmed A. A., Shehata, Hassan, Yousif, Yousif M., Akeel, Nagwa E., Hashem, Mustafa I. A., Ahmed, Amani A., Emam, Ahmed A., Abdelmohsen, Mohamed M., Ahmed, Mohamed F.

المصدر: Pediatric Research; Apr2023, Vol. 93 Issue 5, p1383-1390, 8p

المؤلفون: Elkoumi, Mohamed A., Abdellatif, Sawsan H., Mohamed, Faisal Y., Sherif, Ahmed H., Elashkar, Shaimaa S. A., Saleh, Rabab M., Boraey, Naglaa F., Abdelaal, NourEldin M., Akeel, Nagwa E., Elhewala, Ahmed A., Mosbah, Amira A., Zakaria, Mervat T., Soliman, Mohammed M., Salah, Ahmed, Sedky, Yasser M., Sobieh, Alaa A., Mashali, Mohamed H., Waked, Nevin M., Elshreif, Anas M., Hafez, Sahbaa F., Hashem, Mustafa I. A., Shehab, Mohamed M., Soliman, Attia A., Emam, Ahmed A., Ahmed, Abdelrahman A. A., Fahim, Mohamed S., Elshehawy, Naglaa A., Abdel‐Aziz, Marwa M., Abdou, Adel M., El‐Shehawy, Ahmed A., Youssef, Manal A. A., Fahmy, Dalia S., Malek, Mai M., Osman, Sherif F., Ibrahim, Mohamed A. M., Alanwar, Mohamed I., Zeidan, Nancy M. S.

المصدر: Pediatric Pulmonology ; volume 55, issue 5, page 1175-1183 ; ISSN 8755-6863 1099-0496

الوصف: Background Pneumonia is the foremost cause of child death worldwide. M‐ficolin is encoded by the FCN1 gene and represents a novel link between innate and adaptive immunity. Objectives To investigate the FCN1 −144 C/A (rs10117466) polymorphism as a potential marker for pneumonia severity and adverse outcome namely complications or mortality in the under‐five Egyptian children. Methods This was a prospective multicenter study that included 620 children hospitalized with World Health Organization‐defined severe pneumonia and 620 matched healthy control children. Polymorphism rs10117466 of the FCN1 gene promoter was analyzed by PCR‐SSP , while serum M‐ficolin levels were assessed by ELISA . Results The FCN1 A/A genotype and A allele at the −144 position were more frequently observed in patients compared to the control children (43.4% vs 27.6%; odds ratio [OR]: 1.62; [95% confidence interval {CI}: 1.18‐2.2]; for the A/A genotype) and (60.8% vs 52.5%; OR: 1.4; [95% CI: 1.19‐1.65]; for the A allele); P < .01. The FCN1 −144 A/A homozygous patients had significantly higher serum M‐ficolin concentrations (mean: 1844 ± 396 ng/mL) compared with those carrying the C/C or C/A genotype (mean: 857 ± 278 and 1073 ± 323 ng/mL, respectively; P = .002). FCN1 −144 A/A genotype was an independent risk factor for adverse outcomes in children with severe pneumonia (adjusted OR = 4.85, [95% CI: 2.96‐10.25]; P = .01). Conclusion The FCN1 A/A genotype at the −144 position was associated with high M‐ficolin serum levels and possibly contributes to enhanced inflammatory response resulting in the adverse outcome of pneumonia in the under‐five Egyptian children.

الإتاحة: https://doi.org/10.1002/ppul.24719Test

المؤلفون: Elkoumi, Mohamed A, Allah, Mayy AN, Mohamed, Faisal Y, Boraey, Naglaa F, Abdellatif, Sawsan H, Shehab, Mohamed MM, Sherif, Ahmed H, Akeel, Nagwa E, Saleh, Rabab M, Elshreif, Anas M, Abdelrahman, Hind M, Soliman, Attia A, Emam, Ahmed A, Youssef, Manal AA, Fahmy, Dalia S, Sallam, Mohammad M, Nawara, Abdalla M, Elgohary, Elsayed A, Ismael, Ali, El-Kaffas, Sameh MH, Sobeih, Alaa A, Ibrahim, Lamya M, Ibrahim, Mohamed AM, Abdou, Adel M, Yousry, Sherif M, Osman, Sherif F, El-Deeb, Fatma M, Elhewala, Ahmed A, Hafez, Sahbaa FM, Waked, Nevin M, Elbasyouni, Hany AA, Fouad, Rania A, Zeidan, Nancy MS, Nashat, Mohamed, Farghaly, Mohsen AA

المصدر: Lupus ; volume 29, issue 7, page 767-775 ; ISSN 0961-2033 1477-0962

مصطلحات موضوعية: Rheumatology

الوصف: Background Recently, the interleukin-17A ( IL-17A) gene has emerged as a potential candidate gene for autoimmune disorders, including systemic lupus erythematosus (SLE). Objectives This study aimed to investigate whether IL-17A polymorphisms at rs2275913 G/A, rs8193036 C/T and rs3748067 C/T could be susceptibility markers for juvenile-onset SLE (JSLE) and lupus nephritis (LN) in Egyptian children and adolescents. Methods In this multi-centre study, we genotyped 320 patients diagnosed with JSLE and 320 matched control children for three IL-17A polymorphisms at rs2275913 G/A, rs8193036 C/T and rs3748067 C/T using TaqMan probe-based real-time polymerase chain reaction. Meanwhile, IL-17A serum levels were assessed using ELISA. Results The IL-17 rs2275913 A/A genotype and A allele were more represented in JSLE patients compared to the control group (21% vs. 7%, odds ratio (OR) = 3.8, 95% confidence interval (CI) 1.78–5.5, p = 0.001, pBonf = 0.003 for the A/A genotype; 37% vs. 29%, OR = 1.4, 95% CI 1.11–1.8, p = 0.003, pBonf = 0.009 for the A allele. No significant difference was found for IL-17 rs8193036 and rs3748067 single nucleotide polymorphisms (SNPs) in genotype distribution or allele frequencies ( p>0.05). Patients carrying the IL-17 rs2275913 A/A genotype and A allele were more likely to develop LN (OR = 5.64, 95% CI 2.39–13.77, pBonf = 0.001 for the A/A genotype; OR = 2.73, 95% CI 1.84–4.07, pBonf = 0.02 for the A allele). Conclusion The IL-17 rs2275913 A allele and A/A genotype were associated with high IL-17 serum levels and may contribute to susceptibility to JSLE and the development of LN in Egyptian children and adolescents. However, no significant association was evident between the studied IL-17A SNPs and other clinical phenotypes, disease activity scores or laboratory profile of JSLE.

الإتاحة: https://doi.org/10.1177/0961203320922305Test