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  1. Apr 2020
    1. Abdulla, A., Wang, B., Qian, F., Kee, T., Blasiak, A., Ong, Y. H., Hooi, L., Parekh, F., Soriano, R., Olinger, G. G., Keppo, J., Hardesty, C. L., Chow, E. K., Ho, D., & Ding, X. (n.d.). Project IDentif.AI: Harnessing Artificial Intelligence to Rapidly Optimize Combination Therapy Development for Infectious Disease Intervention. Advanced Therapeutics, n/a(n/a), 2000034. https://doi.org/10.1002/adtp.202000034

    1. Peto, J., Alwan, N. A., Godfrey, K. M., Burgess, R. A., Hunter, D. J., Riboli, E., Romer, P., Buchan, I., Colbourn, T., Costelloe, C., Smith, G. D., Elliott, P., Ezzati, M., Gilbert, R., Gilthorpe, M. S., Foy, R., Houlston, R., Inskip, H., Lawlor, D. A., … Yao, G. L. (2020). Universal weekly testing as the UK COVID-19 lockdown exit strategy. The Lancet, 0(0). https://doi.org/10.1016/S0140-6736(20)30936-3

    1. Sure. So I do want to start by just reminding listeners that talking about trauma, learning about trauma, can bring up some feelings, which is a very normal reaction to that. So I just want to remind people, if you notice that, that it’s okay to take a rain check on listening and engaging in this conversation. I also do recommend that even if you feel okay to engage with a discussion about trauma that it’s recommended that you do so in small doses, especially during these very challenging times.

      This is a lovely way to introduce this topic.

    1. Spontaneity is the big thing you'll miss

      Forget the calendar invite. Just jump into a conversation. That’s the idea powering a fresh batch of social startups poised to take advantage of our cleared schedules amidst quarantine. But they could also change the way we work and socialize long after COVID-19 by bringing the free-flowing, ad-hoc communication of parties and open office plans online. While “Live” has become synonymous with performative streaming, these new apps instead spread the limelight across several users as well as the task, game, or discussion at hand.

    1. Based on all of these approaches, it seems like a reasonable lower bound is that cases are at least 10x underreported, likely more than 20x underreported (according to several researchers), and potentially as much as 100x underreported.It seems reasonable, then, to assume that it’s not 1 out of every 10 people with COVID-19 who will need hospitalization -but rather 1 out of every 100 -500.Similarly, rather than 1 -4%, it seems likely that true CFR for COVID-19 will be well under half a percent, and potentially well under 0.1%for most of the population.
  2. onlinelibrary.wiley.com onlinelibrary.wiley.com
    1. ompared with patients without cardiac injury, patients with cardiac injury presented with more severe acute illness, manifested by abnormal laboratory and radiographic findings, such as higher levels of C-reactive protein, NT-proBNP, and creatinine levels; more multiple mottling and ground-glass opacity; and a greater proportion requiring noninvasive or invasive ventilation.
    2. After adjusting for age, preexisting cardiovascular diseases (hypertension, coronary heart disease, and chronic heart failure), cerebrovascular diseases, diabetes mellitus, chronic obstructive pulmonary disease, renal failure, cancer, ARDS, creatinine levels greater than 133 μmol/L, and NT-proBNP levels greater than 900 pg/mL, the multivariable adjusted Cox proportional hazard regression model showed a significantly higher risk of death in patients with cardiac injury than in those without cardiac injury, either during time from symptom onset (hazard ratio [HR], 4.26 [95% CI, 1.92-9.49]) or time from admission to study end point (HR, 3.41 [95% CI, 1.62-7.16]) (Table 3).
    3. Of patients with cardiac injury, only 22 (26.8%) underwent examination of electrocardiogram (ECG) after admission, and 14 of 22 ECGs (63.6%) were performed during the periods of elevation of cardiac biomarkers. All 14 ECGs were abnormal, with findings compatible with myocardial ischemia, such T-wave depression and inversion, ST-segment depression, and Q waves. The ECG changes in 3 patients with representative cardiac injury are shown in eFigure 2 in the
    4. The laboratory and radiologic findings are shown in Table 1. In the overall study population of 416 patients, median (IQR) levels of C-reactive protein (4.5 [1.4-8.5] mg/dL; to convert to milligrams per liter, multiply by 10) and procalcitonin (0.07 [0.04-0.15] ng/L) were elevated, while the median values of other laboratory indicators were within the normal range, such as counts of leukocytes, lymphocytes, platelets, erythrocytes; hemoglobin level; cardiac indicators
    5. In the present study, we also found that markers of inflammatory response, such as C-reactive protein, procalcitonin, and leukocytes, were significantly increased among patients who suffered from cardiac injury. The activation or enhanced release of these inflammatory cytokines can lead to apoptosis or necrosis of myocardial cells.
    6. In terms of laboratory findings, patients with cardiac injury compared with patients without cardiac injury showed higher median leukocyte count (median [IQR], 9400 [6900-13 800] cells/μL vs 5500 [4200-7400] cells/μL), and levels of C-reactive protein (median [IQR], 10.2 [6.4-17.0] mg/dL vs 3.7 [1.0-7.3] mg/dL), procalcitonin (median [IQR], 0.27 [0.10-1.22] ng/mL vs 0.06 [0.03-0.10] ng/mL), CK-MB (median [IQR], 3.2 [1.8-6.2] ng/mL vs 0.9 [0.6-1.3] ng/mL), myohemoglobin (median [IQR], 128 [68-305] μg/L vs 39 [27-65] μg/L), hs-TNI (median [IQR], 0.19 [0.08-1.12] μg/L vs <0.006 [<0.006-0.009] μg/L), N-terminal pro-B-type natriuretic peptide (NT-proBNP) (median [IQR], 1689 [698-3327] pg/mL vs 139 [51-335] pg/mL),
    1. 100 nM MLN-4760did not interfere with immunoprecipitation of ACE2 by S1-Ig,nor did this inhibitor interfere with S-protein-mediated infec-tion (Figure 4B and C)

      hACE2 inhibitorm MLN-4760, does not interfere with immunoprecipitation of ACE2 by S1-Ig, nor did this inhibitor interfere with S-protein-mediated infection. So ACE2 inhibtor should not be a good way to interfere SARS infection

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    1. There were numerous differences in laboratory findings between patients admitted to the ICU and those not admitted to the ICU (Table 2), including higher white blood cell and neutrophil counts, as well as higher levels of D-dimer, creatine kinase, and creatine.
    1. Plasma TnT levels demonstrated a high and significantly positive linear correlation with plasma high-sensitivity C-reactive protein levels (β = 0.530, P < .001) and N-terminal pro–brain natriuretic peptide (NT-proBNP) levels (β = 0.613, P < .001). Plasma TnT and NT-proBNP levels during hospitalization (median [interquartile range (IQR)], 0.307 [0.094-0.600]; 1902.00 [728.35-8100.00]) and impending death (median [IQR], 0.141 [0.058-0.860]; 5375 [1179.50-25695.25]) increased significantly compared with admission values (median [IQR], 0.0355 [0.015-0.102]; 796.90 [401.93-1742.25]) in patients who died (P = .001; P < .001), while no significant dynamic changes of TnT (median [IQR], 0.010 [0.007-0.019]; 0.013 [0.007-0.022]; 0.011 [0.007-0.016]) and NT-proBNP (median [IQR], 352.20 [174.70-636.70]; 433.80 [155.80-1272.60]; 145.40 [63.4-526.50]) was observed in survivors
  3. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    1. No study has described the incidence of ST-segment elevation myocardial infarction in COVID-19, but it appears to be low. Similarly, the incidence of left ventricular systolic dysfunction, acute left ventricular failure and cardiogenic shock have also not been described.
    1. We describe the first case of acute cardiac injury directly linked to myocardial localization of severe acute respiratory syndrome coronavirus (SARS‐CoV‐2) in a 69‐year‐old patient with flu‐like symptoms rapidly degenerating into respiratory distress, hypotension, and cardiogenic shock.
    2. An intra‐aortic balloon pump (IABP) was placed on top of adrenaline (0.07 μg/kg/min), and noradrenaline (0.1 μg/kg/min) was added for worsening hypotension (systolic blood pressure: 80/67/60 mmHg).
    3. The first echocardiography showed a dilated left ventricle [left ventricular (LV) end‐diastolic diameter 56 mm], severe and diffuse LV hypokinesia (LV ejection fraction 34%). Three hours later, LV ejection fraction dropped to 25% and estimated cardiac index was 1.4 L/min/m2. Coronary angiography findings were unremarkable.
    1. By the end of Jan 25, 31 (31%) patients had been discharged and 11 (11%) patients had died; all other patients were still in hospital (table 1). The first two deaths were a 61-year-old man (patient 1) and a 69-year-old man (patient 2). They had no previous chronic underlying disease but had a long history of smoking.
    1. The clinical effects of pneumonia have been linked to increased risk of cardiovascular disease up to 10-year follow-up16 and it is likely that cases infected via respiratory virus outbreaks will experience similar adverse outcomes. Therapeutic use of corticosteroids further augments the possibility of adverse cardiovascular events. However, long-term follow-up data concerning the survivors of respiratory virus epidemics are scarce. Lipid metabolism remained disrupted 12 years after clinical recovery in a metabolomic study amongst 25 SARS survivors,17 whereas cardiac abnormalities observed during hospitalisation in eight patients with H7N9 influenza returned to normal at 1-year follow-up.