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aiman S Alabsi,7 Saeed M Kabrah,1 Haneen O Alhaj,8 Musaed M Alshahrani,9 Nora Y Hakami101Department of Clinical Laboratory Sciences, Faculty of Applied Medical Sciences, Umm Al-Qura University, Makkah, Saudi Arabia; 2Department of Laboratory and Blood Bank, Prince Mohammed Bin Nasser Hospital, Ministry of Health, Jazan, Saudi Arabia; 3Department of Laboratory and Blood Bank, King Faisal Medical City for Southern Regions, Ministry of Health, Abha, Saudi Arabia; 4Armed Forces Hospital in Jazan, Ministry of Defence, Jazan, Saudi Arabia; 5General Medical Committee, tDirectorate General of Health Affairs, Jazan, Saudi Arabia; 6Department of Pharmacy, Ahad Al Masarihah General Hospital, Ministry of Health, Jazan, Saudi Arabia; 7King Abdulaziz Medical City, Jeddah, Saudi Arabia; 8Kholoud Laboratory for Medical Analysis, Makkah, Saudi Arabia; 9Blood Bank Laboratory, Prince Sultan Military Medical City, Saudi Arabia; 10Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia Correspondence: Amr J Halawani, Department of Clinical Laboratory Sciences, Faculty of Applied Medical Sciences Umm Al-Qura University, Makkah, Saudi Arabia, Email [email protected] Purpose: Jazan Province in Saudi Arabia is notable for its high prevalence of inherited hemoglobinopathies, including sickle cell disease and thalassemia, necessitating frequent blood transfusions for affected individuals. To mitigate risks such as RBC alloimmunization and hemolytic transfusion reactions, ensuring blood compatibility is crucial. The Kell (KEL) blood group system, pivotal alongside the ABO and RH systems, encompasses multiple antigens implicated in these complications. This study aimed to investigate the frequencies of KEL blood group antigens (K, k, Kpa, and Kpb) and determine KEL phenotypes (K/k and Kpa/Kpb) among Saudi blood donors living in Jazan Province. Methods: A total of 138 anonymous healthy Saudi blood donors from Prince Mohammed bin Nasser Hospital in Jazan Province, Saudi Arabia, were enrolled in this study. Anticoagulated blood was analyzed using the gel card technique to assess K, k, Kpa, and Kpb antigens. Results: The prevalence of KEL antigens was as follows: K (n = 9, 6.52%), k (n = 137, 99.28%), Kpa (n = 1, 0.72%), and Kpb (n = 138, 100%). KEL phenotypes observed were K+k+ (n = 8, 5.80%), K+k− (n = 1 0.72%), K−k+ (n = 129, 93.48%), Kp(a+b+) (n = 1, 0.72%), and Kp(a−b+) (n = 137, 99.28%). Conclusion: This study provides insights into the prevalence of KEL blood group antigens and phenotypes in Jazan Province, Saudi Arabia. These findings may contribute to the establishment of a national blood group database and guide transfusion practices to ensure compatibility and minimize alloimmunization risks. [ABSTRACT FROM AUTHOR]

aiman M Bayuomi,3 Talal Qadah11Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia; 2Hematology Department, King Salman Bin Abdulaziz Medical City, Medinah, Saudi Arabia; 3Blood Transfusion Services Unit, King Abdulaziz University Hospital, Jeddah, Saudi Arabia; 4Clinical Chemistry Laboratory, King Abdulaziz University Hospital, Jeddah, Saudi Arabia Correspondence: Nora Y Hakami, Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia, Email [email protected] Background: Platelets are a commonly used blood component to prevent or treat bleeding in patients with thrombocytopenia or platelet dysfunction. They are stored at room temperature (22– 24°C) for five days unless specific measures are taken to extend the shelf life to seven days or more. After five days, this study evaluated platelet units' biochemical changes and bacterial growth. Study Design and Methods: Platelet concentrate was collected from 30 random donors: 8 females and 22 males. The collected samples were then placed on an agitator at room temperature and tested for their pH, protein content, and glucose levels using Roche Combur 100 Test® Strips. The Haemonetics eBDS™ System was used for bacterial detection. The measurements were taken on day five as the control and then repeated on days 7, 9, and 11 to observe any changes. On days 5 and 7, all parameters remained unchanged. However, glucose levels significantly changed (p=< 0.0001) on days 9 and 11. Regarding pH, a significant change was observed on day 9 (p=0.033) and day 11 (p=0.0002). Results: There were no significant changes in all parameters on days 5 and 7. However, glucose was substantially changed (p=< 0.0001) on days 9 and 11. For pH, there was a significant change in pH on day 9 (p=0.033) and day 11 (p=0.0002). Discussions: Our study found that platelet concentrate extension is possible for up to seven days. However, further studies are needed to evaluate platelet function during expiry time and to assess the stability of platelet morphology and function. [ABSTRACT FROM AUTHOR]

Histone deacetylase ( HDAC) inhibitors are known to suppress abnormal development of blood vessels. Angiogenic activity in endothelial cells depends upon NADPH oxidase 4 (Nox4)-dependent redox signalling. We set out to study whether the HDAC inhibitor trichostatin A ( TSA) affects Nox4 expression and angiogenesis. Nox4 expression was measured by real time PCR and Western blot analysis in endothelial cells. Hydrogen peroxide (H2O2) was measured by amplex® red assay in endothelial cells. Nox4 was knocked down by Nox4 sh RNA. In vitro angiogenic activities such migration and tubulogenesis were assessed using wound healing and Matrigel assays, respectively. In vivo angiogenic activity was assessed using subcutaneous sponge assay in C57Bl/6 and Nox4-deficient mice. Trichostatin A reduced Nox4 expression in a time- and concentration-dependent manner. Both TSA and Nox4 silencing decreased Nox4 protein and H2O2. Mechanistically, TSA reduced expression of Nox4 via ubiquitination of p300- histone acetyltransferase (p300- HAT). Thus, blocking of the ubiquitination pathway using an inhibitor of ubiquitin-activating enzyme E1 ( PYR-41) prevented TSA inhibition of Nox4 expression. Trichostatin A also reduced migration and tube formation, and these effects were not observed in Nox4-deficient endothelial cells. Finally, transforming growth factor beta1 ( TGFβ1) enhanced angiogenesis in sponge model in C57 BL/6 mice. This response to TGFβ1 was substantially reduced in Nox4-deficient mice. Similarly intraperitoneal infusion of TSA (1 mg/kg) also suppressed TGFβ1-induced angiogenesis in C57 BL/6 mice. Trichostatin A reduces Nox4 expression and angiogenesis via inhibition of the p300- HAT-dependent pathway. This mechanism might be exploited to prevent aberrant angiogenesis in diabetic retinopathy, complicated vascular tumours and malformations. [ABSTRACT FROM AUTHOR]

Recent studies have indicated that microRNA and VEGF are considered to be genetic modifiers and are associated with elevated levels of fetal haemoglobin HbF, and thus they reduce the clinical impact of sickle haemoglobin (HbS) patients. This cross-sectional study was performed on clinical confirmed subjects of SCD cases. miR-423-rs6505162 C>T and VEGF-2578 C>A genotyping was conducted by ARMS-PCR in SCD and healthy controls. A strong clinical significance was reported while comparing the association of miR-423 C>T genotypes between SCD patients and controls ( p = 0.031). The microRNA-423 AA genotype was associated with an increased severity of SCD in codominant model with odd ratio (OR = 2.36, 95% CI, (1.15-4.84), p = 0.018) and similarly a significant association was observed in recessive inheritance model for microRNA-423 AA vs (CC+CA) genotypes (OR = 2.19, 95% CI, (1.32-3.62), p < 0.002). The A allele was associated with SCD severity (OR = 1.57, 95% CI, (1.13-2.19), p < 0.007). The distribution of VEGF-2578 C>A genotypes between SCD patients and healthy controls was significant ( p < 0.013). Our results indicated that in the codominant model, the VEGF-2578-CA genotype was strongly associated with increased SCD severity with OR = 2.56, 95% CI, (1.36-4.82), p < 0.003. The higher expression of HbA1 (65.9%), HbA2 (4.40%), was reported in SCD patients carrying miR-423-AA genotype than miR-423 CA genotype in SCD patients carrying miR-423 CA genotype HbA1 (59.98%), HbA2 (3.74%) whereas SCD patients carrying miR-423 CA genotype has higher expression of HbF (0.98%) and HbS (38.1%) than in the patients carrying AA genotype HbF (0.60%), HbS (36.1%). ARMS-PCR has been proven to be rapid, inexpensive and is highly applicable to gene mutation screening in laboratories and clinical practices. This research highlights the significance of elucidating genetic determinants that play roles in the amelioration of the HbF levels that is used as an indicator of severity of clinical complications of the monogenic disease. Further well-designed studies with larger sample sizes are necessary to confirm our findings.