Introduction Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also referred to as COVID-19, was declared a pandemic by the World Health Organization in March 2020. The manifestations of COVID-19 are widely variable and range from asymptomatic infection to multi-organ failure and death. Like other viral illnesses, acute myocarditis has been reported to be associated with COVID-19 infection. However, guidelines for the diagnosis of COVID-19 myocarditis have not been established. Methods Using a combination of search terms in the PubMed/Medline, Ovid Medline and the Cochrane Library databases and manual searches on Google Scholar and the bibliographies of articles identified, we reviewed all cases reported in the English language citing myocarditis associated with COVID-19 infection. Results Fourteen records comprising a total of fourteen cases that report myocarditis/myopericarditis secondary to COVID-19 infection were identified. There was a male predominance (58%), with the median age of the cases described being 50.4 years. The majority of patients did not have a previously identified comorbid condition (50%), but of those with a past medical history, hypertension was most prevalent (33%). Electrocardiogram findings were variable, and troponin was elevated in 91% of cases. Echocardiography was performed in 83% of cases reduced function was identified in 60%. Endotracheal intubation was performed in the majority of cases. Glucocorticoids were most commonly used in treatment of myocarditis (58%). Majority of patients survived to discharge (81%) and 85% of those that received steroids survived to discharge. Conclusion Guidelines for diagnosis and management of COVID-19 myocarditis have not been established and our knowledge on management is rapidly changing. The use of glucocorticoids and other agents including IL-6 inhibitors, IVIG and colchicine in COVID-19 myocarditis is debatable. In our review, there appears to be favorable outcomes related to myocarditis treated with steroid therapy. However, until larger scale studies are conducted, treatment approaches have to be made on an individualized case-by-case basis.

A response in writing: A low‐cost bioactive paper device is designed to perform ABO and RhD blood typing tests, and the paper reports the results in writing. This idea was inspired by the vision of the British author, J. K. Rowling, through her novel “Harry Potter and the Chamber of Secrets” in which a piece of paper could be interrogated for information and unambiguous answers were received from the paper in writing.

We developed and validated a new paper-based assay for the detection of human blood type. Our method involves spotting a 3 μL blood sample on a paper surface where grouping antibodies have already been introduced. A thin film chromatograph tank was used to chromatographically elute the blood spot with 0.9% NaCl buffer for 10 min by capillary absorption. Agglutinated red blood cells (RBCs) were fixed on the paper substrate, resulting in a high optical density of the spot, with no visual trace in the buffer wicking path. Conversely, nonagglutinated RBCs could easily be eluted by the buffer and had low optical density of the spot and clearly visible trace of RBCs in the buffer wicking path. Different paper substrates had comparable ability to fix agglutinated blood, while a more porous substrate like Kleenex paper had enhanced ability to elute nonagglutinated blood. Using optimized conditions, a rapid assay for detection of blood groups was developed by spotting blood to antibodies absorbed to paper and eluted with 200 μL of 0.9% NaCl buffer directly by pipetting. RBCs fixation on paper accurately detected blood groups (ABO and RhD) using ascending buffer for 10 min or using a rapid elution step in 100/100 blood samples including 4 weak AB and 4 weak RhD samples. The assay has excellent reproducibility where the same blood group was obtained in 26 samples assessed in 2 different days. Agglutinated blood fixation on porous paper substrate provides a new, simple, and sensitive assay for rapid detection of blood group for point-of-care applications.

Ligand-induced ectodomain shedding of glycoprotein VI (GPVI) is a metalloproteinase-dependent event. We examined whether shear force, in the absence of GPVI ligand, was sufficient to induce shedding of GPVI. Human-citrated platelet-rich plasma or washed platelets were subjected to increasing shear rates in a cone-plate viscometer, and levels of intact and cleaved GPVI were examined by Western blot and ELISA. Pathophysiologic shear rates (3000-10 000 seconds ؊1 ) induced platelet aggregation and metalloproteinase-dependent appearance of soluble GPVI ectodomain, and GPVI platelet remnant. Shedding of GPVI continued after transient exposure to shear. Blockade of ␣ IIb ␤ 3 , GPIb␣, or intracellular signaling inhibited shear-induced platelet aggregation but minimally affected shearinduced shedding of GPVI. Shearinduced GPVI shedding also occurred in platelet-rich plasma or washed platelets isolated from a von Willebrand disease type 3 patient with no detectable VWF, implying that shear-induced activation of platelet metalloproteinases can occur in the absence of GPVI and GPIb␣ ligands. Significantly elevated levels of sGPVI were observed in 10 patients with stable angina pectoris, with well-defined single vessel coronary artery disease and mean intracoronary shear estimates at 2935 seconds ؊1 (peak shear, 19 224 seconds ؊1 ). Loss of GPVI in platelets exposed to shear has potential implications for the stability of a forming thrombus at arterial shear rates. IntroductionPlatelet activation and accumulation at sites of vascular injury play a critical role in thrombus formation. This complex process is mainly initiated by 3 different but overlapping pathways: (1) exposure of subendothelial matrix proteins, including collagen and VWF, which activate the platelet adhesion-signaling receptors glycoprotein VI (GPVI) and GPIb␣ of the GPIb-IX-V complex, respectively; (2) exposure of tissue factor, which activates the coagulation cascade resulting in formation of active thrombin facilitating fibrin deposition as well as enhancing platelet activation; and (3) disturbed blood flow because of narrowing of the vascular lumen, which modulates the adhesive function of platelets and accelerates platelet activation and thrombus growth. 1 Indeed, changes in blood flow rates and hydrodynamic force are now recognized to play a more critical role in thrombus formation, especially at sites of vascular occlusion, as indicated by the ability of elevated (pathologic) shear stress to induce stable platelet aggregate formation without the requirement for platelet activation and adhesion 2 or for soluble agonists. 3 Human platelets normally circulate in a resting state and are exposed to shear rates within a physiologic range (ϳ 20-2000 seconds Ϫ1 ). Platelets may encounter shear rates beyond 10 000 seconds Ϫ1 under pathologic conditions, for example, in a stenosed atherosclerotic artery, and become activated and begin to aggregate. [3][4][5] Shear-dependent platelet activation is initiated by binding of plasma VWF to platelets primarily throu...