Background: Coronavirus disease (COVID-19) induces inflammation, coagulopathy following platelet and monocyte activation, and fibrinolysis, resulting in elevated D-dimer levels.Activated platelets and monocytes produce microvesicles (MVs). We analyzed the differences in platelet and monocyte MV counts in mild, moderate, and severe COVID-19, as well as their correlation with D-dimer levels. Methods: In this cross-sectional study, blood specimens were collected from 90 COVID-19 patients and analyzed for D-dimers using SYSMEX CS-2500. Platelet MVs (PMVs; PMVCD42b+ and PMVCD41a+ ), monocyte MVs (MMVs; MMVCD14+ ), and phosphatidylserinebinding annexin V (PS, AnnV+ ) were analyzed using a BD FACSCalibur instrument. Results: PMV and MMV counts were significantly increased in COVID-19 patients. AnnV+ PMVCD42b+ and AnnV+ PMVCD41a+ cell counts were higher in patients with severe COVID-19 than in those with moderate clinical symptoms. The median (range) of AnnV+ PMVCD42b+ (MV/µL) in mild, moderate, and severe COVID-19 was 1,118.3 (328.1–1,910.5), 937.4 (311.4–2,909.5), and 1,298.8 (458.2–9,703.5), respectively (P = 0.009). The median (range) for AnnV+ PMVCD41a+ (MV/µL) in mild, moderate, and severe disease was 885.5 (346.3–1,682.7), 663.5 (233.8–2,081.5), and 1,146.3 (333.3–10,296.6), respectively (P = 0.007). D-dimer levels (ng/mL) weak correlated with AnnV+ PMVCD41a+(P = 0.047, r = 0.258). Conclusions PMV PMVCD42b+ and PMVCD41a+ counts were significantly increased in patients with severe clinical symptoms, and PMVCD41a+ counts correlated with D-dimer levels. Therefore, MV counts can be used as a potential biomarker of COVID-19 severity.

Background: Coronavirus disease (COVID-19) induces inflammation, coagulopathy following platelet and monocyte activation, and fibrinolysis, resulting in elevated D-dimer levels.Activated platelets and monocytes produce microvesicles (MVs). We analyzed the differences in platelet and monocyte MV counts in mild, moderate, and severe COVID-19, as well as their correlation with D-dimer levels. Methods: In this cross-sectional study, blood specimens were collected from 90 COVID-19 patients and analyzed for D-dimers using SYSMEX CS-2500. Platelet MVs (PMVs; PMVCD42b+ and PMVCD41a+ ), monocyte MVs (MMVs; MMVCD14+ ), and phosphatidylserinebinding annexin V (PS, AnnV+ ) were analyzed using a BD FACSCalibur instrument. Results: PMV and MMV counts were significantly increased in COVID-19 patients. AnnV+ PMVCD42b+ and AnnV+ PMVCD41a+ cell counts were higher in patients with severe COVID-19 than in those with moderate clinical symptoms. The median (range) of AnnV+ PMVCD42b+ (MV/µL) in mild, moderate, and severe COVID-19 was 1,118.3 (328.1–1,910.5), 937.4 (311.4–2,909.5), and 1,298.8 (458.2–9,703.5), respectively (P = 0.009). The median (range) for AnnV+ PMVCD41a+ (MV/µL) in mild, moderate, and severe disease was 885.5 (346.3–1,682.7), 663.5 (233.8–2,081.5), and 1,146.3 (333.3–10,296.6), respectively (P = 0.007). D-dimer levels (ng/mL) weak correlated with AnnV+ PMVCD41a+(P = 0.047, r = 0.258). Conclusions PMV PMVCD42b+ and PMVCD41a+ counts were significantly increased in patients with severe clinical symptoms, and PMVCD41a+ counts correlated with D-dimer levels. Therefore, MV counts can be used as a potential biomarker of COVID-19 severity.

Background: Coronavirus disease (COVID-19) induces inflammation, coagulopathy following platelet and monocyte activation, and fibrinolysis, resulting in elevated D-dimer levels.Activated platelets and monocytes produce microvesicles (MVs). We analyzed the differences in platelet and monocyte MV counts in mild, moderate, and severe COVID-19, as well as their correlation with D-dimer levels. Methods: In this cross-sectional study, blood specimens were collected from 90 COVID-19 patients and analyzed for D-dimers using SYSMEX CS-2500. Platelet MVs (PMVs; PMVCD42b+ and PMVCD41a+ ), monocyte MVs (MMVs; MMVCD14+ ), and phosphatidylserinebinding annexin V (PS, AnnV+ ) were analyzed using a BD FACSCalibur instrument. Results: PMV and MMV counts were significantly increased in COVID-19 patients. AnnV+ PMVCD42b+ and AnnV+ PMVCD41a+ cell counts were higher in patients with severe COVID-19 than in those with moderate clinical symptoms. The median (range) of AnnV+ PMVCD42b+ (MV/µL) in mild, moderate, and severe COVID-19 was 1,118.3 (328.1–1,910.5), 937.4 (311.4–2,909.5), and 1,298.8 (458.2–9,703.5), respectively (P = 0.009). The median (range) for AnnV+ PMVCD41a+ (MV/µL) in mild, moderate, and severe disease was 885.5 (346.3–1,682.7), 663.5 (233.8–2,081.5), and 1,146.3 (333.3–10,296.6), respectively (P = 0.007). D-dimer levels (ng/mL) weak correlated with AnnV+ PMVCD41a+(P = 0.047, r = 0.258). Conclusions PMV PMVCD42b+ and PMVCD41a+ counts were significantly increased in patients with severe clinical symptoms, and PMVCD41a+ counts correlated with D-dimer levels. Therefore, MV counts can be used as a potential biomarker of COVID-19 severity.

Background: Coronavirus disease (COVID-19) induces inflammation, coagulopathy following platelet and monocyte activation, and fibrinolysis, resulting in elevated D-dimer levels.Activated platelets and monocytes produce microvesicles (MVs). We analyzed the differences in platelet and monocyte MV counts in mild, moderate, and severe COVID-19, as well as their correlation with D-dimer levels. Methods: In this cross-sectional study, blood specimens were collected from 90 COVID-19 patients and analyzed for D-dimers using SYSMEX CS-2500. Platelet MVs (PMVs; PMVCD42b+ and PMVCD41a+ ), monocyte MVs (MMVs; MMVCD14+ ), and phosphatidylserinebinding annexin V (PS, AnnV+ ) were analyzed using a BD FACSCalibur instrument. Results: PMV and MMV counts were significantly increased in COVID-19 patients. AnnV+ PMVCD42b+ and AnnV+ PMVCD41a+ cell counts were higher in patients with severe COVID-19 than in those with moderate clinical symptoms. The median (range) of AnnV+ PMVCD42b+ (MV/µL) in mild, moderate, and severe COVID-19 was 1,118.3 (328.1–1,910.5), 937.4 (311.4–2,909.5), and 1,298.8 (458.2–9,703.5), respectively (P = 0.009). The median (range) for AnnV+ PMVCD41a+ (MV/µL) in mild, moderate, and severe disease was 885.5 (346.3–1,682.7), 663.5 (233.8–2,081.5), and 1,146.3 (333.3–10,296.6), respectively (P = 0.007). D-dimer levels (ng/mL) weak correlated with AnnV+ PMVCD41a+(P = 0.047, r = 0.258). Conclusions PMV PMVCD42b+ and PMVCD41a+ counts were significantly increased in patients with severe clinical symptoms, and PMVCD41a+ counts correlated with D-dimer levels. Therefore, MV counts can be used as a potential biomarker of COVID-19 severity.

Gene manipulation tools have transformed biomedical research and improved the possibilities of their uses for therapeutic purposes. These tools have aided effective genomic modification in many organisms and have been successfully applied in biomedical engineering, biotechnology and biomedicine. They also shown a potential for therapeutic applications to alleviate genetic and non-genetic diseases. Small interfering RNA (siRNA) and clustered regularly inter-spaced short-palindromic repeat/associated-protein system (CRISPR/Cas) are two of the tools applied in genetic manipulation. This review aims to evaluate the molecular influence of siRNA and CRISPR/Cas as novel tools for genetic manipulations. This review discusses the molecular mechanism of siRNA and CRISPR/Cas, and the advantages and disadvantages of siRNA and CRISPR/Cas. This review also presents comparison between siRNA and CRISPR/Cas as potential tools for gene therapy. siRNA therapeutic applications occur through protein knockout without causing damage to cells. siRNA knocks down gene expression at the mRNA level, whereas CRISPR/Cas knocks out gene permanently at the DNA level. Inconclusion, gene manipulation tools have potential for applications that improve therapeutic strategies and plant-derived products, but ethical standards must be established before the clinical application of gene editing.

Introduction: Coagulopathy associated with Coronavirus disease 2019 (COVID-19) may cause life-threatening complications, especially in severe or critically ill COVID-19 patients. Thromboelastography (TEG) is an effective, dynamic, and reliable test to assess the complete coagulation process. This study aimed to determine the association between selected TEG parameters and survival in COVID-19 patients. Methods: This study was a retrospective observational study using data from medical records of COVID-19 patients who were hospitalized in Dr. Soetomo Hospital, Surabaya, Indonesia. There were 94 COVID-19 patients consisting of 76 survivors and 18 non-survivors. The association between TEG results and certain TEG parameters with survival status was considered significant if the p-value ≤ 0.05. Results: Increased coagulation activity had a significant association with the survival status of COVID-19 patients (p=0.04). There were no significant differences in all TEG parameters between COVID-19 patients who survived and those who did not survive (p > 0.05). Based on the TEG analysis tree, the most TEG results found were secondary fibrinolysis (21.3%) and fibrinolytic shutdown (24.5%). No significant association was found between the coagulability and fibrinolysis abnormality with the survival status in COVID-19 patients (p > 0.05). Conclusion: There was no significant difference in TEG results between COVID-19 survivors and non-survivors. However, based on the TEG result, an increase in coagulation activity is associated with a lower survival rate. Further study with detailed timing of TEG examination, disease severity and comorbidities stratification in COVID-19 patients may be needed.

Emanuel syndrome, also referred to as supernumerary der(22) or t(11;22) syndrome, is a rare genomic syndrome. Patients are normally presented with multiple congenital anomalies and severe developmental disabilities. Affected newborns usually carry a derivative chromosome 22 inherited from either parent, which stems from a balanced translocation between chromosomes 11 and 22. Unfortunately, identification of Emanuel syndrome carriers is difficult as balanced translocations do not typically present symptoms. We identified two patients diagnosed as Emanuel syndrome with identical chromosomal aberration: 47,XX,+der(22)t(11;22)(q24;q12.1)mat karyotype but presenting variable phenotypic features. Emanuel syndrome patients present variable phenotypes and karyotypes have also been inconsistent albeit the existence of a derivative chromosome 22. Our data suggests that there may exist accompanying genetic aberrations which influence the outcome of Emanuel syndrome phenotypes but it should be cautioned that more patient observations, diagnostic data and research is required before conclusions can be drawn on definitive karyotypic-phenotypic correlations.

Introduction: Rac1 and STIM1 genes are emerging therapeutic targets for cancers. However, their roles in acute myeloid leukaemia (AML) are not well understood. The goal of this study was to evaluate the effects of dose and time on Rac1 and STIM1 knockdown in the AML cell line model (THP-1 cells). Methods: THP-1 cells were transfected with siRac1 at doses of 50, 100, and 200 nM or dsiSTIM1 at doses of 2, 5, and 10 nM. Expression level of Rac1 and STIM1 then were assessed at time points between 12 and 72 h post-transfection using real-time reverse transcription polymerase chain reaction. Results: Compared to the control, 87% Rac1 knockdown was attained with 50 nM siRac1 at 24 h post-transfection, and 70% STIM1 knockdown was achieved with 10 nM dsiSTIM1 at 48 h post-transfection. Conclusion: These results show that effective knockdown of Rac1 and STIM1 is possible, and therapy that includes Rac1 and STIM1 inhibitors eventually could provide a new and highly effective strategy for AML treatment.