Objectives The aims of this study were to analyze in a large series of patients undergoing transcatheter aortic valve implantation (TAVI): 1) the accuracy of 3-dimensional transesophageal echocardiographic (3DTEE) measurement of left coronary cusp (LCC) length and of the distances from left main coronary ostium (LM) to the aortic annulus (AA) pre-operatively and to the aortic prosthesis post-operatively; and 2) the role of the 3DTEE measurements in predicting the prosthetic deployment and the association between prosthesis position and aortic regurgitation (AR) and/or prosthesis-patient mismatch (PPM).
Background Coronary ostia occlusion is a possible complication in TAVI; therefore, the careful pre-operative evaluation of AA-LM and LCC length, and the post-operative analysis of the relationship between the prosthesis and LM, may influence the procedural outcomes. Even though multidetector computed tomography (MDCT) is the gold standard pre-operatively, sometimes it cannot be performed and it is rarely repeated post-operatively.
Methods In 122 patients undergoing TAVI, pre-operative AA-LM and LCC measurements obtained by 3DTEE and MDCT were compared. Post-operatively, the feasibility of 3DTEE evaluation of the prosthesis-LM distance was performed. The relationship between 3DTEE overlap of the prosthesis with the anterior mitral leaflet and AR/PPM was assessed.
Results Pre-operatively, 3DTEE AA-LM (r = 0.83) and LCC (r = 0.69) significantly correlated with MDCT. Post-operatively, 3DTEE prosthesis-LM distance was 2.1 ± 1.9 mm. The prosthesis reached or exceeded LM in 6 and 10 cases, respectively. Prosthesis overlap with mitral leaflet was 4.7 ± 1.8 mm. Significant correlation between the 3DTEE computed and nominal length of the prosthesis was found (r = 0.61). No correlations were found between prosthesis–mitral leaflet overlap and aortic regurgitation or PPM.
Conclusions AA-LM distance and LCC length may be accurately estimated by 3DTEE, which may represent a valid alternative to MDCT. Pre- and post-3DTEE data concerning the aortic root, such as LM, aortic valve, and prosthetic morphology, give new insights into TAVI and its complications.
Transcatheter aortic valve replacement (TAVI) has become a valid alternative to conventional surgery in selected high-risk patients with severe and symptomatic aortic valve stenosis (1,2). One of the major complications reported after TAVI is coronary ostia impairment (3–7) due to the presence of low coronary ostia and/or the occluding effect of aortic leaflets displacement by prosthetic percutaneous implantation.
Therefore, a careful pre-operative evaluation of the distance between aortic annulus (AA) and left main coronary ostium (LM) and of left coronary cusp (LCC) is necessary, and an accurate analysis of the critical relationship between the prosthesis and LM post-operatively should be performed.
Pre-operatively, AA-LM distance and LCC length estimation are generally obtained through multidetector computed tomography (MDCT), which is the gold standard in this context, allowing an accurate assessment of aortic root geometry (7–9). Unfortunately, MDCT cannot be performed in arrhythmic patients or in cases with severely impaired renal function, and it is rarely repeated post-operatively for clinical reasons. Moreover, immediate post-procedural imaging inside the surgical suite is possible only by using echocardiographic or angiographic techniques.
Three-dimensional transesophageal echocardiography (3DTEE) has been demonstrated to be very useful in the management of TAVI in the pre-operative evaluation of AA dimensions (8,10) and may be used as a substitute for MDCT in AA measurement. The incremental value of its application in procedural monitoring of TAVI and of post-procedural result assessment is also well known (11,12). Moreover, few data are available concerning the immediate post-operative relationship between the device and coronary ostia.
Our aims were to study in a large series of patients: 1) the feasibility of pre-operative AA-LM distance and LCC length measurements by 3DTEE; 2) its accuracy in comparison with MDCT-derived measurements; 3) the feasibility of post-operative 3DTEE evaluation of the distance between the prosthesis and LM; 4) the accuracy of 3DTEE-derived measurements in predicting the stent landing zone as defined by the overlap of the prosthesis with mitral leaflet; and 5) the association between prosthesis deployment and regurgitation, positioning, and spatial relation with LM.
From January 2008 to June 2011, 276 consecutive patients underwent TAVI using the Edwards Sapien prosthesis (Edwards Lifesciences, Irvine, California) at the Centro Cardiologico Monzino Istituto di Ricovero e Cura a Carattere Scientifico, Milan, Italy.
In all patients, a transthoracic echocardiography was performed before surgery to confirm the severity of the aortic valve stenosis (mean transaortic pressure gradient ≥40 mm Hg or an aortic valve area <1 cm2) (13) and to assess the feasibility of the percutaneous procedure (absence of aortic bicuspid valve, AA dimensions between >18 mm and 26 mm) (12,14). After the TAVI procedure but before hospital discharge, transthoracic echocardiography was repeated and the effective orifice area of the prosthesis was obtained using the continuity equation approach and indexed to body surface area. Prosthesis-patient mismatch (PPM) was defined as the presence of an orifice area ≤0.85 cm2/m2 (15–17).
Before the TAVI procedure, invasive coronary and peripheral vascular angiography was performed according to guidelines (14) in order to rule out coronary and peripheral disease. In 190 of 276 patients, a MDCT exam was performed. In 268 patients, periprocedural 2-dimensional (2D) TEE monitoring, completed with 3DTEE acquisitions, was performed. Exclusion criteria were atrial fibrillation or other arrhythmias, impaired renal function, inability to sustain a 10-s breath-hold, presence of esophageal diseases or clinical contraindication to general anesthesia during the procedure, or stenosis of the LM and/or the proximal descending coronary artery. Therefore, 122 of 276 patients were enrolled in this study.
The study protocol was approved by the ethics committee and, prior to participation, informed consent was obtained from all patients.
Patients were imaged during the TAVI procedure using a commercially available echocardiographic system (iE33, Philips Medical Systems, Andover, Massachusetts) equipped with an X7-2t probe, allowing 2D multiplane, real-time 3D, and full volume TEE acquisitions. Image acquisition was performed by an experienced cardiologist. Pre-operatively, in accordance with current clinical practice, a 2DTEE acquisition in zoom mode of the left ventricular outflow tract from the mid-esophageal position with scanning planes from 115° to 160° was performed in all patients in order to assess precise measurements of the AA and aortic root. Moreover, real-time zoomed 3D or full volume images containing the whole aortic apparatus and the proximal ascending aorta were acquired both pre- and post-TAVI for quantitative analysis performed with a commercially available software package (3DQ, Q-Lab version 7.0, Philips Medical Systems). Briefly, before TAVI, the 3D dataset was analyzed moving 3 different orthogonal cut planes. The first cut plane was transversal, oriented to visualize a short-axis view of the AA, and on this plane the maximum diameter (Max-D), the minimum diameter (Min-D), and the area of AA were measured. The second and the third were both longitudinal planes, 1 adjusted orthogonal to the short axis in order to obtain a sagittal view of the ascending aorta. The other longitudinal plane was gradually rotated until the LM appeared, allowing the measurement of AA-LM distance (Fig. 1). In addition, in the same plane, LCC length was assessed as the distance between the tip of the leaflet and the AA (Fig. 2).
Example of 3-dimensional (3D) transesophageal echocardiography (TEE) measurement of the distance between the aortic annulus (AA) and left main coronary ostium (LM). The 3D dataset was analyzed through 3 different orthogonal cut planes: green plane (A) is a short-axis view of aortic root crossing the LM; red (B) and blue (C) planes are sagittal views of the ascending aorta. The blue plane was gradually rotated until the LM appeared, allowing the measurement of the distance between the AA and LM (white arrow). (D) The position and the relationship of each plane in the 3D dataset are shown.
(Top) Example of 3DTEE measurement of the left coronary cusp (LCC) length. A short-axis view (A1) at the level of AA (top, left); a short-axis view (A2) at the level of the tip of the leaflets (top, middle); a sagittal view of the ascending aorta with the LCC length (white line) measured as the distance between plane A1 and A2 (top, right). (Bottom) Example of multidetector computed tomography (MDCT) measurement of the LCC length. A short-axis view (B1) at the level of AA (bottom, left); a short-axis view (B2) at the level of the tip of the leaflets (bottom, middle); a sagittal view of the ascending aorta, with the LCC length (red line) measured as the distance between plane B1 and B2 (bottom, right). Abbreviations as in Figure 1.
In the post-TAVI 3D dataset, we evaluated: 1) L1 = the overlap of the prosthesis with the anterior mitral valve leaflet, defined as the distance between the ventricular edge of the aortic prosthesis and the native AA; and 2) L2 = the distance between the distal edge of the prosthesis and the LM. The 3DTEE prosthesis length was calculated as [(AA-LM distance + L1) – L2], and this computed measurement was compared with the nominal prosthesis length (14, 17, and 19 mm for a 23-, 26-, and 29-mm device, respectively) (Fig. 3).
Example of a 3DTEE post-operative evaluation of the aortic root and prosthesis. Three different orthogonal views are shown: (left) a short-axis view of aortic root at the level of the aortic prosthesis and the LM; (middle) a longitudinal view of the ascending aorta showing the aortic prosthesis length and the overlap of the prosthesis with the anterior mitral valve leaflet; and (right) a longitudinal view of the ascending aorta crossing the LM; this view allows the measurement of the distance between the upper edge of the prosthesis and the LM. Abbreviations as in Figure 1.
A 3D dataset was considered unsuitable for analysis if it contained artifacts or if the LM was not clearly visible due to artifacts or poor quality of the image.
Finally, after the device deployment and after removal of the catheters, the presence of post-procedural paravalvular aortic regurgitation (AR) was evaluated. Post-procedural AR was quantified according to standard echocardiographic color-Doppler method using the jet width and extension and graded as: 0 (absent) 1 (mild); 2 (mild to moderate); 3 (moderate to severe); or 4 (severe). Paravalvular AR was considered significant if ≥2.
All examinations were performed with a LightSpeed VCT XT Scanner (GE Healthcare, Milwaukee, Wisconsin). Scanning parameters were: slice configuration, 64 × 0.625 mm; gantry rotation time, 350 ms; tube voltage, 120 kVp; and effective tube current, 650 mA. Contrast enhancement was achieved with a triphasic injection of an 80-ml bolus of Iomeron 400 mg/ml (Bracco Imaging S.p.A., Milan, Italy) through an antecubital vein at a 5-ml/s infusion rate, followed by 50 ml of saline solution, and a further 50-ml bolus of contrast at 3.5 ml/s. After the threshold level of 200 Hounsfield units (HU) in the right ventricle was achieved, patients were instructed to hold a deep breath, and the scan was started when a threshold of 200 HU was reached in the left atrium, allowing the synchronization of the arrival of the contrast media and the scan. Data acquisition was performed with retrospective electrocardiogram triggering.
Image analysis was performed on a separate computer workstation. AA was defined as a virtual ring formed by joining the basal attachments of the aortic leaflets (18). Max-D, Min-D, and the area of AA were measured in an orthogonal plane on the center line of the aorta in systole. The distance between the AA and the LM was defined as the distance between the short axis at the level of the LM and the short axis at the level of AA (Fig. 4). The LCC length was defined as the distance between 2 orthogonal planes on the center line of the aorta, centered at the basal attachment and apex of the LCC in the end-diastolic phase (Fig. 3).
Example of MDCT measurement of AA to LM distance. (A) A sagittal view of the ascending aorta; AA-LM was measured as the distance between the short axis at the level of the LM and the short axis at the level of the AA. (B) A short-axis view at the level of the LM. AN AO = aortic annulus; L Coro = left coronary artery; other abbreviations as in Figures 1 and 2.
Data are presented as mean ± SD for continuous variables and frequencies and relevant percentages for categorical variables. Linear regression analysis with Pearson correlation coefficient was used to evaluate the relationship between computed and nominal prosthesis length, LCC length and AA-LM distance, and 3DTEE and MDCT measurements. Also, Bland-Altman analysis was used to assess the intertechnique agreement by calculating the bias (mean difference) and the 95% limits of agreement (defined as 1.96 SD around the mean difference). A chi-square test was performed to investigate the associations among prosthesis-mitral leaflet overlap, the entity of paravalvular AR, and the presence of PPM. To determine the reproducibility of the AA-LM distance, intraobserver and interobserver variability were assessed in a subset of 30 patients as coefficient of variation, defined as the ratio between the SD and the mean of the 2 measurements, expressed as a percentage. During these repeated analyses, investigators were blinded to each other's and prior measurements. A Bland-Altman analysis was performed to evaluate the concordance between the 2 observers and between the first observer and himself. All statistical analyses were performed using SPSS version 17.0 (SPSS Inc., Chicago, Illinois).
All patients underwent TAVI with a balloon-expandable Edwards Sapien valve using the transapical (n = 43) or transfemoral (n = 79) approach. The procedures were performed under general anesthesia with TEE and fluoroscopic guidance. Twenty-three–, 26-, and 29-mm prostheses were implanted in 58, 59, and 5 patients, respectively. Clinical baseline characteristics of the study population are reported in Table 1. Paravalvular AR immediately after TAVI was graded as: 0 in 54 patients (44%); 1 in 52 patients (43%); 2 in 14 patients (11%); 3 in 1 patient (1%); and 4 in 1 patient (1%). Therefore, AR was ≥2 in 16 patients (13%). The incidence of PPM after TAVI was 45% (n = 55), as assessed by transthoracic echocardiography before hospital discharge.
The measurement of AA-LM distance was feasible in 119 of 122 patients (97.5%) with a 3DTEE acquisition focused on the aortic apparatus and in all of the patients with MDCT. 3DTEE estimation of the distance between the LM and the prosthesis was feasible in 110 cases (90%).
Table 2 shows the mean values of the AA-LM distance, LCC length, Min-D, Max-D, and area of AA obtained by 3DTEE and MDCT for all patients and separately for each size of prosthesis implanted. All measurements were significantly correlated, as depicted in the scatterplots of Figure 5, together with the results of Bland-Altman analysis, which showed good agreement between the 2 techniques and minimal underestimation of 3DTEE measurements compared with MDCT.
Results of linear regression (left) and Bland-Altman analysis (right) for (A) AA-LM distance, (B) LCC length, (C) AA area, (D) minimum (min-D), and (E) maximum (max-D) diameters, measured by 3DTEE and MDCT. Abbreviations as in Figures 1 and 2.
3DTEE measurements of AA-LM distance were found to be highly reproducible on both intraobserver and interobserver variability analysis as depicted by lower coefficients of variation, 2.1% and 2.6%, respectively. Figure 6 shows the results of Bland-Altman analysis of the agreement between repeated measurements of AA-LM distance together with relevant bias and limits of agreement.
Results of Bland-Altman analysis of the agreement between repeated 3DTEE measurements of the AA-LM distance for interobserver (left) and intraobserver (right) variability obtained in a subset of 30 randomly selected patients. Abbreviations as in Figure 1.
The mean value of overlap with the anterior mitral valve leaflet (L1) was 4.5 ± 1.9 mm (range –2.0 to 9.5 mm) and the distance between the distal edge of the prosthesis and the LM (L2) was 2.1 ± 1.9 mm (range –2.0 to 6.5 mm). The upper edge of the prosthesis reached (6 cases) or overlapped (10 cases) the LM. Table 3 shows 3DTEE-derived anatomic data regarding AA-LM distance (pre-operatively) and the characteristics of the prosthesis implantation (post-operatively) in each of these 16 cases. Figure 7 shows 3DTEE reconstruction of the distance between the upper edge of aortic prosthesis and LM in 2 different cases.
3DTEE reconstruction of the aortic root and LM in 2 patients before (A, C) and after (B, D) transcatheter aortic valve replacement. Solid arrows indicate the LM; dotted arrows indicate the upper edge of the prosthesis in the post-operative reconstruction. (A, B) Pre- and post-operative reconstruction in a patient with the LM in a high position; the upper edge of the prosthesis is a few millimeters distance from the LM. (C, D) Pre- and post-operative reconstruction in a patient with the LM in a low position; in the post-operative image, the upper edge of the prosthesis is partially superimposed on the LM. Abbreviations as in Figure 1.
There was a good correlation (r = 0.64; p < 0.001) between the 3DTEE computed and nominal lengths of the prosthesis (Fig. 8). No differences in echocardiographic parameters were found in patients with suboptimal hemodynamic results (PPM or AR >2) and cases with optimal hemodynamic results. In particular, no correlations were found between prosthesis–mitral leaflet overlap and paravalvular AR or PPM. Moreover, no significant correlation was found between LCC length and AA-LM distance.
Correlation between prosthesis nominal length and prosthesis length as measured by 3-dimensional transesophageal echocardiography. Median values are depicted as squares; whiskers extend from the first quartile to the third quartile; outliers are shown as + symbols.
Currently, TAVI is a valid alternative to surgical aortic valve replacement for the treatment of high-risk surgical candidates with severe aortic valve stenosis. As in traditional surgical aortic valve replacement, after prosthesis implantation, an immediate decrease of transvalvular pressure gradient and of systolic left ventricular pressure is expected. These changes are generally associated with a significant increase in coronary flow (19,20).
However, coronary ostia impairment, due to the presence of low coronary ostia and/or to the occluding effect of the calcified native cusps crushed against the aortic wall after the prosthesis deployment, is included between the possible life-threatening complications of the procedure (3–5). Moreover, operator-related factors, such as high valve positioning or implantation of an oversized prosthesis, may also lead to post-operative complications.
Several investigators (8,10,21) have demonstrated the importance of an accurate pre-operative evaluation of the distance between the AA and coronary ostia in the selection of candidates for TAVI in order to avoid LM occlusion due to covering of coronary ostium by the upper part of the prosthesis or by LCC displacement. Therefore, even in the absence of defined guidelines, an AA-LM distance less than 10 to 11 mm is generally indicated as the cutoff value under which a TAVI with Edwards Sapiens prosthesis may be contraindicated (7,12,18).
Because MDCT provides precise information about the aortic valve anatomy, it is considered the gold standard for the pre-operative assessment of TAVI candidates. However, in these critical patients, impaired renal function, severe breathlessness, atrial fibrillation, or other arrhythmias are frequently present and may contraindicate the employment of MDCT or limit its image quality.
The position of the coronary arteries relative to the AA can also be assessed using invasive angiography, which is often performed in most of the patients pre-operatively in order to study coronary arteries and peripheral vessels. However, the angiographic procedure shows the bias due to its 2D nature, and, in some cases, it may carry a high risk of complications. Therefore, MDCT has been reported as a valid alternative to angiography (9).
The role of echocardiography in the assessment of TAVI patients is well known. The incremental value of 3D echocardiographic technology and its accuracy in comparison to MDCT in the measurement of the AA and ascending aorta dimensions has been demonstrated previously (8,12,22). Otani et al. (23) evaluated 3DTEE AA-LM in a large series of patients; however, 3D accuracy in comparison with MDCT was calculated only in a few cases, all without aortic valve stenosis. Unfortunately, in aortic valve stenosis, AA-LM is generally shorter than in control subjects, and the presence of leaflets and AA calcifications may markedly impair the accuracy of 3DTEE measurements. Moreover, few post-operative data have been reported concerning the distance between the LM and aortic prosthesis (8).
The main findings and novelties of our study are 2-fold. First, we demonstrated in a large series of patients with aortic valve stenosis that a 3DTEE pre-operative estimation of AA-LM distance is possible in most cases (97%). Only in 3 of 122 cases was the LM not adequately visualized due to poor quality of TEE images. AA-LM measurement was accurate, comparable to MDCT data, and highly reproducible on intraobserver and interobserver variability. As expected, patients with larger AA dimensions had longer AA-LM distances, and, for this reason, larger prostheses could be implanted without coronary impairment.
The second important result is that 3DTEE allows an immediate evaluation of the distance between the LM and aortic prosthesis after the implantation. This measurement is feasible in most of the cases (90%) and also accurate. In fact, the 3DTEE-computed prosthesis length (calculated as the difference between 3DTEE AA-LM distance plus prosthesis–anterior mitral leaflet overlap, and the distance between the LM and the prosthesis) is similar to the prosthetic nominal value. Interestingly, in 16 cases, the upper edge of the prosthesis exceeded the LM, even though none of the enrolled patients had signs or symptoms of ischemia. These data are in accordance with the radiologic (MDCT) observation of Delgado et al. (8). A possible explanation is the limited extension of the overlap in our cases (≤2 mm) involving a portion of the prosthesis where its struts allow coronary inflow, without reaching the reinforced inferior part of the structure where the pericardial leaflets are inserted.
No relationship was found between the presence of prosthesis/LM overlap and the prosthesis size or the AA-LM pre-operative distance, which supports the importance of a correct implantation procedure, because even very small changes in the prosthesis positioning may interfere with the coronary flow. This result does not detract much from the necessity of an accurate evaluation of AA-LM distance. In fact, in high-risk patients, the knowledge of a small AA-LM distance is important information for the operator who may consequently adapt the prosthesis implantation. Indeed, our data demonstrate the absence of a significant relationship between prosthesis overlap and clinical variables such as PPM or paravalvular AR. This observation reinforces the importance of a correct and precise knowledge of the AA-LM distance, facilitating optimal and safe procedural maneuvers by the operator.
Moreover, after prosthesis deployment in the case of abrupt coronary artery occlusion, the pre-operative awareness of a high occlusion risk may favor the immediate recognition of this life-threatening complication, inducing a prompter circulatory support and the hemodynamic procedure of percutaneous recanalization in order to restore normal coronary flow. In this regard, even though the LCC length has been postulated to be involved in this complication, in our patients we did not find prospectively any correlation between this measurement and AA-LM.
3DTEE may estimate the AA-LM distance as an alternative technique to MDCT. Pre- and post-3DTEE data concerning the valve and prosthesis morphology and simultaneous real-time evaluation of the aortic root, including the LM, give new insights regarding TAVI and its complications.
Even though we included in the study a large number of cases, only a few patients received a 29-mm prosthesis, and, for this reason, the statistical analysis for this group has an important bias as shown in Table 2 (no significant correlation was observed between 3DTEE and MDCT for Max-D and area of AA measurements). However, the high correlation in the overall population between 3DTEE and MDCT measurements confirms the value of the 3D modality, and the reported limitation does not detract much from our results.
The right coronary artery was not evaluated in our study, and we chose to focus our analysis only on the LM. Few data concerning the measurement by 2DTEE and not 3DTEE have been published regarding the measurement of the distance between the right coronary ostium and the AA (12); moreover, the right ostium is generally more distant from the AA in comparison with the LM, and its occlusion post-TAVI procedure is very uncommon. Right coronary artery imaging by real-time 3DTEE is more difficult in comparison with imaging the LM. Even though the incidence of right coronary artery occlusion is low, future studies may define the role of 3DTEE, particularly with the new technologies in the evaluation of both coronary ostia before and after TAVI.
(2010) Left main coronary artery occlusion after percutaneous aortic valve implantation. Ann Thorac Surg 89:953–955.
(2011) Feasibility and accuracy of a comprehensive multidetector computed tomography acquisition for patients referred for balloon-expandable transcatheter aortic valve implantation. Am Heart J 161:1106–1113.
(2000) Hemodynamic performance during maximum exercise in adult patients with the Ross operation and comparison with normal controls and patients with aortic bioprotheses. Am J Cardiol 86:982–988.
(2011) Hemodynamic and clinical impact of prosthesis–patient mismatch after transcatheter aortic valve implantation. J Am Coll Cardiol 58:1910–1918.
(1996) Influences of aortic pressure gradient and ventricular septal thickness with systolic coronary flow in aortic valve stenosis. Am J Cardiol 78:1303–1306.
(2009) Effects of percutaneous aortic valve replacement on coronary blood flow assessed with transesophageal Doppler echocardiography in patients with severe aortic stenosis. Am J Cardiol 104:850–855.
(2006) Comparison of feasibility and accuracy of transthoracic echocardiography versus computed tomography in patients with known ascending aortic aneurysm. Am J Cardiol 98:966–969.
(2010) Assessment of the aortic root using real-time 3D transesophageal echocardiography. Circ J 74:2649–2657.


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Volker Winkler (nascido em 20 de julho de 1957) é um ex-ciclista alemão que competiu no ciclismo nos Jogos Olímpicos de Verão de 1980 em Moscou, onde ganhou a medalha de prata na perseguição por equipes.

Ciclistas olímpicos da Alemanha Oriental
Ciclistas nos Jogos Olímpicos de Verão de 1980
Medalhistas nos Jogos Olímpicos de Verão de 1980
Medalhistas olímpicos do ciclismo
Medalhistas olímpicos da Alemanha Oriental
Campeões mundiais de ciclismo em pista

redpajama_set_name: RedPajamaWikipedia


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George P. Bush, Commissioner of the Texas General Land Office, speaks to members of College Republicans in March of 2014. Despite many House District 49 candidates focusing on student outreach as a part of their campaigns, College Republicans has yet to receive outreach from any candidate.
While most of the Democrats running for House District 49 have reached out to several campus organizations in an effort to gain student support, there are still some groups — such as College Republicans — who have yet to recieve any form of outreach.
Five of the candidates — Austin ISD School Board member Gina Hinojosa, former legislative aide Huey Rey Fischer, UT law professor Heather Way, attorney Aspen Dunaway, former NARAL Pro-Choice Texas counsel Blake Rocap — have actively spent time on campus reaching out to student voters through forums with University Democrats and Student Government. All have previously stated they would focus on the concerns of the large student population trhoughout the district, if elected.
Whichever candidate wins the Democratic primary on March 1 will face no opposition in the November general election, ensuring the nominee is a freshman representative once the legislature reconvenes in January 2017.
Over the weekend, the candidates — except attorneys Kenton Johnson and Matt Shrum — attended forums with University Democrats and Central Austin Democrats. After the forum, UDems members voted to endorse Fischer and Central Austin Democrats endorsed Hinojosa.
In addition to his recent UDems endorsement, the Fischer campaign on Monday released a list of student leader endorsements on campus, which includes Student Government President Xavier Rotnofsky and Vice President Rohit Mandalapu as well as leaders of Students Against Animal Cruelty.
Fischer, who has run on a platform focused on student voters, said as a previous UDems president, he had a healthy relationship working with College Republicans and other groups on campus in trying to increase voter turnout on campus, and he said he hopes that relationship continues if elected to the legislature.
While some candidates have reached out to Student Government and other nonpartisan organizations on campus, Robert Guerra, College Republicans communications director, said he believes candidates haven't spent time talking to more conservative student organizations because of partisanship.
Throughout the campaign, Hinojosa has locked up the endorsements of more than 200 Democratic organizations and other groups, including the Austin American-Statesman and Central Austin Democrats.
Although Hinojosa did not get the UDems endorsement, supporters of Hinojosa say her campaign will still be active on campus leading into March 1.


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Understanding Pandemics & COVID-19 | Health Newsletter
Written by: Jon Barron
COVID-19: So Much Bad Information
Understanding pandemics throughout history and what we have learned from them
What the data really means
Let's talk about masks
The important number that no one is talking about
Going to school
Using a natural antipathogen formula as a prophylactic to prevent ever getting the virus
If you are from a country that has the coronavirus somewhat under control, then this newsletter is not for you. That said, feel free to read it for entertainment value, but for the most part, it does not apply to you.
Some History
I have had to do a number of rethinks on this newsletter. There were issues relative to the coronavirus that were important to explore, but it has become obvious, especially since the last newsletter, that we have reached the limits of science-based arguments supported by studies. It turns out that bad information is even more contagious than the coronavirus, and there is no way to counter it. Science is no longer an effective counter when so many people choose to believe scientists are lying to them and opt instead to believe in the most extreme theories circulating on the internet. When it comes to COVID-19, people have staked out their territory and pitched their camps based on their beliefs. There are those who automatically believe what scientists and medical experts tell us about the virus–even when they are repeatedly shown to be wrong. On the other hand, there are those who choose to disbelieve the mainstream scientific community and choose to follow the advice of more fringe "experts," even when those experts also tell us that people are getting sick because they have sex with astral demons in their sleep and that vaccines are dangerous because they are made with alien DNA (and no, I am not talking about the aliens who come to the United States by migrating across the border).
I was planning to do my usual thing and write a newsletter filled with citations and scientific references, but things have changed so much in the last three months. For a huge swath of the public, science no longer works as an explanation for what's happening with the coronavirus. People are looking for a bigger, grander, more all-encompassing explanation for the chaos we now face–an explanation far beyond the reach of science.
So, a different approach is required. Instead of arguing the science, let me present a narrative that might inform how we look at the facts on the ground. And the best place to begin is with a little history about pandemics. This also happens to be a freebie for me since I can cut and paste from the section on pandemics that I just put together for the rewrite of Lessons from the Miracle Doctors. Incidentally for those of you who are interested, I have now finished 28 of what will be 30 chapters in the book. With just two chapters to go, the book is now over 350,000 words and has over 1700 clickable citations. I expect to finish by the end of August at which point I will turn it over to the editors for proofing and formatting for Kindle and Apple Books, etc., which will likely take 2-3 months. But enough about me.
Let's take a quick look at some of the great pandemics in human history to get a sense of how long they lasted, how many they killed, and how they ended.
Plague of Justinian (Bubonic plague)
Lasted 200 years (The bulk of the deaths occurred between 541 and 542, but this pandemic was stubborn and did not fade entirely until 750.)
Killed upwards of half the world's population
Ended when there was no one left to infect. Half the world had died, and the other half had been infected, survived, and was now immune.
The bubonic plague returned to Europe in 1347. It lasted on and off for about 300 years.
In just four years, it killed half the population of Europe. The plague resurfaced roughly every 20 years from 1348 to 1665–40 outbreaks in 300 years. And with each new plague epidemic, 20 percent of the men, women, and children living in London were killed.
It ended essentially by locking away the sick so they could not infect the healthy and by burying the dead in mass graves.
Smallpox in the New World
Smallpox was endemic to Europe, Asia, and Arabia for centuries. It killed 30% of all those infected and left survivors with pockmarked faces. It was carried to the New World in the 15th century with the first European explorers. The indigenous populations had zero resistance. To them, it was a "novel" virus.
Over the next hundred years, it wiped out 90-95% of the native population. In Mexico, the population dropped from 11 million pre-conquest to just one million. Smallpox in the New World is far and away the deadliest pandemic in human history.
It ended when there were no more native Americans left to infect.
The smallpox vaccine, introduced by Edward Jenner in 1796, was the first successful vaccine to ever be developed. It took 200 years of vaccinations to eradicate smallpox. In 1980, the World Health Assembly declared smallpox eradicated. No cases of naturally occurring smallpox have happened since. Other pathogens such as bubonic plague have had ebbs and flows throughout history, but smallpox is the only pathogen, so far, that has ever been eliminated from the face of the earth!
We came close with polio, but fear of vaccination in a handful of countries in Africa and Asia is causing the number of cases to increase. One disturbing thought is that if the disease breaks out of the handful of countries in which it is now contained, no one in the developed world any longer has any immunity to the disease. It would spread rapidly.
Cholera originated in the Ganges delta in India.
During the 19th century, it spread across the world. Six subsequent cholera pandemics have killed millions of people across all continents. The current (seventh) pandemic started in South Asia in 1961 and reached Africa in 1971 and the Americas in 1991. It is still active.
In the mid-19th century, cholera killed tens of thousands in London. John Snow, a British Doctor figured out that it was being transmitted by contaminated water. Specifically, people were being infected by drinking water contaminated by sewage flowing near the infected wells.1 Kathleen Tuthill. "John Snow and the Broad Street Pump." UCLA Department of Epidemiology. Nov 2003. (Accessed 20 Jul 2020. https://www.ph.ucla.edu/epi/snow/snowcricketarticle.html) Improving urban sanitation in the developed world led to an end of cholera pandemics in the developed world. Unfortunately, it is still a persistent killer in third-world countries lacking adequate sewage treatment and access to clean drinking water.
HIV/AIDS: Sub Saharan Africa
1981 to the present.
Between 56 and 100 million people have become infected with HIV since the start of the pandemic.2 "Global HIV & AIDS statistics–2020 fact sheet." UNAIDS. (Accessed 20 Jul 2020.) https://www.unaids.org/en/resources/fact-sheet. (Note: WHO actually defines HIV as a "global epidemic," whatever that means. And between 25 and 42 million people have died from AIDS-related illnesses since the start of the epidemic.
It is far from gone, but HIV can be well managed in the developed nations so it doesn't progress to AIDS. Nevertheless, AIDS is still incredibly deadly in developing nations without access to adequate health care and preventative measures.
A number of deadly flu outbreaks have occurred over the years, but the 1918 Spanish flu is the worst in history. Although called the Spanish Flu, scientists are mostly sure it didn't start there. Best guess is that it originated in the United States, with China a strong runner up possibility.
It is estimated that in just two years 500 million people, or one-third of the global population was infected. It is also estimated that 40-50 million died.
There were no vaccines and no therapeutics. In the end, it disappeared as the result of wearing masks and social distancing.
So, What Have We Learned About Pandemics?
Yes, all pandemics eventually end, at least for a while. But not all pandemics end in a few months like the flu. Many can continue for several hundred years before they seem to "magically disappear"–only to circle back every generation as herd immunity disappears with the next generation, to strike again and again. However, even though we are unable to eliminate most pandemic pathogens, we have several major advantages over the ancients.
We are much better at understanding how pathogens infect, spread, and kill.
This allows us to implement policies that inhibit their ability to spread and develop therapeutics that can significantly reduce mortality rates or even help patients live for decades while infected. People infected with HIV can now live mostly symptom free indefinitely. And in the last six years, newly developed therapeutics have dropped the mortality rate for Ebola from 74% to as low as 6% if treated early enough.
We also have options for testing and contact tracing on a massive scale that were not available to peoples of the past.
And despite the resistance of many to their use, vaccines of varying efficacy (20% to 90%, with benefits lasting as little as a few months to as long as several decades) and varying side effects (ranging from mild to occasionally deadly) are sometimes available.
As human civilizations have flourished, so too have infectious diseases. It is the inevitable result of large numbers of people living in close proximity to each other–and to animals–often with poor sanitation and nutrition. This provides fertile breeding grounds for disease. In ancient times, overseas and land-based trading routes slowly spread novel infections from country to country, creating the first global pandemics. Today, it is international air travel which can spread a pandemic to opposite ends of the world in a matter of hours!!
Finally, in order, here is a list of the tools we now have at our disposal for combatting pandemics.
1. Vaccines
A low-risk, effective vaccine is the most efficient way to stop the spread of pandemic. Unfortunately, that is easier said than done. In the entire history of humankind, only one pandemic has ever been wiped from the face of the earth through a vaccine. Every other vaccination program has come up short of that in terms of efficacy and/or lack of harm. Some highly effective vaccines have produced significant harm at various times as they have evolved. Specifically, I am talking about the polio vaccine. Yes, it is now highly effective and close to wiping polio off the face of the earth, but along the way, versions of the vaccine caused both polio and brain cancer in patients until those issues were discovered and resolved. To be clear, neither of those issues are present in current iterations of the vaccine–but they were at one time.
The other problem with vaccines, of course, is convincing people to use them. According to a national survey designed and analyzed by Tufts University's Research Group on Equity in Health, Wealth, and Civic Engagement, only 57% of Americans say they would get a COVID-19 vaccine if it were available. That is not enough to develop herd immunity.
Of course, when it comes to COVID-19, no vaccine is currently available. We have no idea how effective any vaccine in the pipeline will be. And we have no idea what its side effects might be on the population as a whole. Nevertheless, there is a political imperative to get a vaccine injected into everyone's arm ASAP–cutting the evaluation time from a standard 18 months to as little as six months. What could possibly go wrong developing a vaccine at warp speed?
2. Testing, quarantine, and contact tracing
This can be highly effective. Countries like South Korea and all of the Nordic countries have used this to great effect during the coronavirus pandemic. If you can quickly test for possible infections, quarantine anyone who tests positive, and then trace and quarantine anyone who was in direct contact with the infected person, you can control a pandemic with minimal inconvenience to the population as a whole. In fact, this method alone has kept the infection rate so low that only 5-10% of citizens in the Nordic countries bother to wear a mask in public settings, a figure that has remained stable since the start of the outbreak.
In the United States, this is no longer an option.
We were late getting into the testing game.
We are five months into the pandemic, and we still don't have adequate testing on a per capita basis.
Test results for most people take far too long to be useful when it comes to either quarantining or contact tracing.
Accuracy for many of the tests has been dubious, at least so far.
Too many citizens in the U.S. consider tracing an invasion of their personal freedom and refuse to cooperate with authorities. And the use of a mandatory phone app that would make contact tracing simple, automatic, and require minimal manpower is a non-starter in the United States for privacy reasons. And to tell the truth, given the government's track record when it comes to monitoring its citizens and invading privacy, I can't say I disagree. Nevertheless, for those countries that have used them, these apps have been extremely effective at limiting the spread of the virus without requiring an army of trackers and general lockdowns.
Even if we wanted to now, we have allowed the pandemic to get so out of control and infect so many people that it would be impossible to implement any kind of effective testing, selective quarantine, and contact tracing program at this stage of the game.
The President does not like any aspect of testing, quarantines, or contact tracing–so this is likely a non-starter, at least on a national basis, at this time.
3. Social distancing
The idea of American exceptionalism is built into our culture. It has always been linked to the idea of freedom. The identification of the United States as a unique embodiment of liberty in a world overrun by oppression goes back to the American Revolution. It has served us well when it comes to things that benefit from innovation, out of the box thinking, and the entrepreneurial spirit. Think business, science, entertainment, and technological innovation. If we were having a political discussion, I would now launch into a discussion of how it shapes our world view and our relationships with other countries throughout the world, but that is for another day and another writer. The issue for us today is that American exceptionalism also has a downside. It serves as the justification for people to take steps on behalf of their own personal freedom over the wellbeing of society as a whole. Here is a picture of Coney Island on July 4th–no social distancing and not a facemask in sight. What more needs be said?
4. Masks and other PPE
When you have already eliminated vaccines, testing, quarantines, contract tracing, and social distancing as options, masks are the next line of defense. Unfortunately, 30% of Americans say they either sometimes, rarely, or never wear a mask when they leave home. At that rate of noncompliance, the virus will spread rapidly. (We will talk more about masks later.)
5. Lockdowns
Lockdowns are the last line of defense. When people are not following the already mentioned guidelines, you end up issuing orders for entire communities to stay at home and lock down for an indefinite period. Just a few days ago, the President said that "lockdowns do not prevent infection in the future," and he's absolutely right. I said the same thing in early March. (Makes you wonder if he's now reading my newsletters.) Since no one gains immunity while in lockdown, all this approach does is buy you time. Time to prepare hospitals and spread out infections so your medical response is not overwhelmed. But as soon as you lift the lockdown, the pandemic is likely to surge as people burst forth from their homes and break all the rules in an orgy of "liberation." (See picture above.) Also, mass lockdowns are incredibly disruptive to life, mental wellbeing, employment, and the economy. They are a well that can only be drawn from so many times before people refuse to comply. We are probably already at that point.
6. Natural herd immunity
This is what happens when everything else you have tried has failed. There are three problems with it:
It can take a long time. It took 200 years for natural immunity to take hold during the Plague of Justinian.
It can be costly in terms of human life. When smallpox tore through the indigenous peoples of North and South America, over 90% of the population died before the 10% that survived the disease gained herd immunity, along with horrible disfigurement.
It doesn't last. People have this nasty habit of creating copies of themselves. The problem is that the copies (often called children) do not share their parents' immunity, and thus the pandemic can resurface again and again and again. As we saw with the Black Death, the plague resurfaced roughly every 20 years from 1348 to 1665–40 outbreaks in 300 years. And with each new plague epidemic, 20 percent of the men, women, and children living in London were killed.
7. Waiting for the pandemic to magically go away
The belief that pandemics magically go away as part of their natural cycles is mostly not true for two reasons.
So far, no pandemic has permanently disappeared on its own without human intervention. Many have run for hundreds of years, then disappeared, only to surface again years later. This is mostly the result of fading herd immunity.
Some, like the flu, appear to magically disappear each summer, only to return again each fall. This is the result of viral mutation that renders any existing herd immunity obsolete.
The only pandemic that has completely disappeared from the face of the earth is smallpox, and that was not the result of magically going away, but as a result of the development of a vaccine.
8. Therapeutics
Therapeutics, essentially, are what we do when we cannot get rid of the pandemic. HIV is a great example. We cannot yet stop the spread of the virus, but through the use of therapeutics, we have been able to turn a certain death sentence into decades of relatively normal life. We have learned to co-exist with the pandemic.
A major problem we now face is that many people question the numbers they see in the news. They are convinced that the death toll is far less than the numbers shown on TV. According to a July 21st poll, nearly one in three Americans are skeptical of the official death count.3 Margaret Talev. "Axios-Ipsos poll: The skeptics are growing." AXIOS. Jul 21, 2020. (Accessed 30 Jul 2020.) https://www.axios.com/axios-ipsos-poll-gop-skeptics-growing-deaths-e6ad6be5-c78f-43bb-9230-c39a20c8beb5.html They consider the coronavirus pandemic a hoax. The primary claim is that hospitals are inflating the numbers by claiming that if someone dies of a heart attack but was merely in contact with someone who had COVID-19, the hospital will list it as death by COVID-19 not a heart attack because they get reimbursed more for coronavirus deaths. It also does not help that the President is constantly claiming that if there were less testing, the numbers would be less.
Surprisingly, both these claims are partially true. However, even though they contain an element of truth, the parts that aren't true make them highly misleading and totally irrelevant.
How the Cause of Death is Determined
Let's start with how hospitals determine the cause of death. Big surprise, everyone, there is nothing new here. Hospitals do this all the time and have done so for years–and no, not to claim higher reimbursement. It's very simple; in most cases when someone dies, there are comorbidities. Let me give you a very-common example. Someone gets the flu. It causes inflammation of the lung tissue and weakens their immune system. This opens the door for them to catch pneumonia. The pneumonia inflames their arteries, destabilizing plaque on the arterial wall, which then breaks loose and causes a blockage that leads to a heart attack and death.
So, what does the doctor list on the death certificate: flu, pneumonia, arterial inflammation, plaque, arterial blockage, or heart attack. Guess what: there is a protocol for this. It is called the "underlying cause of death," which is defined as the disease or injury that initiated the train of events leading directly to death. In this case, the death certificate will list the flu as the underlying cause of death.
And that's how COVID-19 gets listed as the underlying cause of death regardless of any pre-existing comorbidities–because it initiated the "train of events" that led directly to death. Make sense? There is no inflating of numbers here. It's how the cause of death has been determined for years.
Now to be clear, there are examples of states and/or hospitals:
Labeling some deaths as COVID related even when an alternative cause is clearly the more likely underlying cause.
Labeling every death in which someone tested positive for the virus as a COVID death, even when the actual cause of death was totally unconnected, such as an automobile accident or suicide.
And sometimes labeling deaths as COVID related even when postmortem testing subsequently showed that the deceased never actually had the coronavirus.
But these appear to be very much the exception and not the rule. That said, these "lapses in judgment" don't add that many deaths to the tally. Also, it should be remembered that we now know the coronavirus was working its way through the United States for at least two months before we knew it was here. That means that it's likely that several thousand people died from COVID-19 before we even knew that we should look for it, which means that all of those deaths were assigned to some other underlying cause–most likely the flu–when in fact it was the coronavirus that killed them. In other words, before you say that the number of deaths in the U.S. from the coronavirus are overstated, you need to add those uncounted deaths back into your tally since the official count may, in fact, be understated.
The bottom line is that whatever the exact number may be, we can clearly state in general terms that too many people have died from COVID-19.
The More You Test, the More Cases You Will Find
The President is absolutely right. It is 100% true that the more people you test, the more cases you will find. However, closing your eyes and not seeing cases of coronavirus does not mean they are not there. But more importantly, holding back testing, in addition to allowing the virus to spread much faster and reach far more people because you are flying blind, makes another, even more important, number look much worse: the incidence of mortality.
Let's make this simple. If you test 1,000 people and 100 test positive for COVID-19 and 10 people die, you are looking at a 10% mortality rate (10 out of the 100 who tested positive). On the other hand, if you had tested 10,000, you would have found ten times as many, or 1,000, who tested positive for the virus. (This is the number the President doesn't like.) However, deaths have nothing to do with testing. In other words, you would still have the same 10 deaths, which means your mortality rate would drop to a mere 1%. In other words, as increased testing reveals more positives (a Presidential bad), your mortality rate drops (a community good).
To put this in simple terms, holding back testing is a bad idea. Flying blind through a major pandemic is a bad idea.
Even Though Cases Are Soaring, Deaths Are Not
As the incidence of COVID-19 has soared over the last few weeks, the number of deaths each day has not kept pace. There may be several reasons for this.
Increased testing is catching more cases, which as we just discussed lowers mortality rates ipso facto.
Increased testing is catching more mild cases.
Younger people are making up a larger share of the cases now. And although they do die, they die at a lower rate than senior citizens.
Doctors now have therapeutics such as remdesivir that are proven to lower mortality rates and speed up recovery.
And the President may be half right yet again. He said that warmer temperatures would make the virus magically go away. Well, warmer temperatures certainly haven't made the virus go away, but they may have made the virus less virulent. If so, unfortunately, we can look for that benefit to disappear in the fall, which means the mortality rate will once again rise, even if just a little, when temperatures drop. That said, COVID-19 does not appear to be a seasonal virus like the flu. Instead it appears to be much more ocean like–just one continuous series of wave after wave after wave–never really going away.
By the way, speaking of deaths, we're now getting a partial answer to a question that I asked in my last newsletter: how many deaths per day are we willing to tolerate before everyone in the country says, "Enough is enough?" Well, we have now reached 1,000 per day, and it hasn't yet triggered that response. So, we now know that whatever that level is, it is going to be substantially higher than 1,000 a day.
Frighteningly, when it comes to COVID-19 in the United States, we may be looking at a frog in the water scenario. I'm talking about how a frog will jump out of boiling water but will allow itself to be boiled alive if the temperature is raised slowly, one degree at a time. If deaths back in March had jumped from one to a thousand a day that month, there would have been panic and a national outcry. But by adding a few deaths every day over five months, we now seem to be accepting a thousand a day as just another fact of life that you live with. And if things keep increasing a little at a time, there is no telling how high that number could go without drawing national outrage.
Now, let's talk about masks. Dr. Fauci is now saying you should wear a mask anytime you leave your house, and he's also recommending that you add goggles, face shields, and gloves to the mix. I understand the intent of the new guidelines: keep things as simple as possible (if you're out of the house wear a mask) and to maximize protection (use everything.) And yes, more is better but not necessarily that much better. We're talking about the law of diminishing returns here. And considering how resistant so many people are to wearing a mask in any situation–let alone adding face shields and goggles–I'm guessing these new guidelines will be followed even less religiously than the previous guidelines.
Look, something is going on here, and it transcends political lines. It is visceral, and it is driven by anger.
In the 1918 flu pandemic, there were no vaccines and no effective therapeutics. Lockdowns, social distancing, and masks were the primary defense against the spread of the pandemic. Sound familiar? And of the three–hold onto your hats–masks were the most hated and the most resisted by the public. In places where mask orders were successfully implemented, noncompliance and outright defiance quickly became a problem. It really is true, isn't it: the more things change, the more they stay the same?
What has changed, though, is the arguments against the use of masks. Back in 1918, things were simple. People didn't like the way they felt. Workers felt they were too uncomfortable to wear all day. They made "their noses fall asleep." Today, the arguments against them are much grander.
Let's quickly deal with them.
They force you to breathe your own air, depriving you of oxygen, and poisoning your body with carbon dioxide. This is only slightly true. Air takes up space. When you blow up a balloon, as air fills the space, the balloon gets bigger. If the balloon does not get bigger, then no air is going into the balloon. That means that if your mask is not getting bigger, the only place "used" air from your lungs can be stored is in the places between the mask and your face. For soft masks that sit close to the face, there just is not much space for holding of used air to be rebreathed. Hard masks, such as N95's that protrude from the face will definitely hold some used air in the space where the mask protrudes out from your nose and mouth. But just look at the space; it's not a lot, but it definitely is some.
Masks "activate" the virus making it more infectious. Yeah, I don't really know what to say about this one. It's not a thing. It's not real. That's not the way viruses work.
Masks hold viruses when you touch them so that you breathe them in later. Not really. Viruses travel on water droplets. If an infected droplet lands on your mask, the water is absorbed by the mask which means the virus now sits on the mask and can only be moved by direct contact, no longer by breathing.
Masks don't protect you. Absolutely true. As I said back in February, masks provide little protection to the wearer. What they do is impede the dispersal of water droplets expelled from your lungs whenever you breathe, talk, yell, cough, or sneeze–and thus impede how far the viruses traveling on those droplets can travel. Unimpeded, those droplets can ride moisture droplets from your lungs six feet in a couple of seconds. Impeded by a mask, they only travel about 18 inches. That's why keeping six feet apart and wearing a mask, works to stop spreading infection.
They are a violation of personal freedom. They are fine to wear for those who want to wear them, but it should be a personal choice. That would be true if we were talking about protecting the wearer. But we are not. We are talking about protecting others from being infected by you. Saying that wearing a mask should be a personal choice is like saying.
Drinking and driving should be a personal choice.
Yelling fire in a theater should be a personal choice.
Going out to a crowded neighborhood bar while infected with Ebola should be a personal choice.
On the other hand, wearing a mask when it doesn't accomplish anything–and in fact makes activities more difficult–is questionable and will lead to noncompliance.
Places to wear a mask:
Pretty much anyplace indoors outside your own home where other people are present.
Anyplace outdoors where you cannot keep socially distant.
Places in which wearing a mask provides only marginal benefit:
Outdoors in general–as long as you can keep socially distant.
While exercising outdoors alone, cycling, or running. (Note: when cycling of running, you can leave a slipstream of droplets trailing as much as 27 feet behind you. However, they tend to be so dissipated in the air as to be minimally infectious.)
Any indoor work situation that significantly increases your breathing rate (in which case your employer will need to allow for 12 feet of social distancing between workers).
Final thought. As we have already discussed, if you have the virus under control with sufficient testing, contact tracing, and social distancing, then very few people out in public are likely to be infected and potentially infecting others, and the need for wearing masks at all is minimal. And as we see in the Nordic countries, very few people wear masks, and they have no problem. Unfortunately, the U.S. is not in that position. In the U.S. masks offer the last line of defense. If enough people in the U.S. choose not to wear masks, we are in for an extended world of hurt.
PS: Since masks tend to reduce droplet travel to about 18 inches, they will not be effective if you can't also keep socially distant.
William Henry Gates III
Poor Bill Gates. Back in 2011, he was accused by conspiracy theorists within the alternative health community of claiming to want to use vaccines to kill off 1 billion children, which, of course, is not what he said at all…or did.
Now, he is being accused of trying to use COVID-19 medical and dental injections to implant tracking chips. I mentioned this "theory" in my last newsletter and received several strongly worded emails accusing me of being naïve and not understanding the truth behind the accusation. In fact, according to a poll, fully half of all Americans who name Fox News as their primary news source believe the story that Bill Gates is looking to use a coronavirus vaccine to inject a microchip into people and track the world's population.4 Andrew Romano. "New Yahoo News/YouGov poll shows coronavirus conspiracy theories spreading on the right may hamper vaccine efforts." Yahoo News. May 22, 2020. (Accessed 31 Jul 2020.) https://news.yahoo.com/new-yahoo-news-you-gov-poll-shows-coronavirus-conspiracy-theories-spreading-on-the-right-may-hamper-vaccine-efforts-152843610.html
But here is a surprise, the poll found that 15 percent of MSNBC viewers also believe this conspiracy theory. They chose to target Gates specifically because of his decade-long advocacy for vaccines.
So, just for fun, I decided to trace this narrative back to its source. And guess what: I found it. As Reuters Fact Check reported:
"This claim was originally posted as satire on May 13, 2020. Its author, Sam Powell ( here ) later described the post on his Facebook profile as "a wild exaggeration of false rumors already circulating" about Bill Gates and microchips.
"I stretched it to a ridiculous extreme to demonstrate just how willing the right wing extremists are to believe slanderous manipulations of the irrational fears of the anti-vaxxer community to demonize the allegedly liberal Gates and support their false tin idol Trump", Powell wrote on Facebook, describing the post as a "subtle parody" ( here ).
He is a tad more demonizing of the right than I would like, but it doesn't change the facts behind what happened next. The parody gained legitimacy and exploded when Fox primetime host Laura Ingraham shared a tweet where she expressed agreement with a user who wrote about the debunked conspiracy theory. She wrote, "Digitally tracking Americans' every move has been a dream of the globalists for years. This health crisis is the perfect vehicle for them to push this."
Thanks to Ingraham's endorsement, different iterations of the claim have now been shared thousands and thousands and thousands of times. Examples of the post are visible here and here.
So, there ya go! I realize the information will not change any of the minds of those who are now emotionally invested in the theory. But at least you now know that it started as parody and how it gained legitimacy. So, there is that.
There Is an Important Number that No One Is Talking About
All the talking heads and politicians talk about testing, the number of people who get COVID-19, and the number who die. Or as the President likes to say, "99 percent of virus cases are harmless."
But that's not true. There's an extremely important missing number here.
First of all, to be precise, the official mortality rate in the U.S. is not 1% as the President claims. It is 3.4%. But that's because we don't test enough. As I mentioned earlier, the mortality rate would go down with adequate testing. In fact, when all is said and done, the real mortality rate for COVID-19 is probably as low as 0.6%–especially now as more therapeutics like remdesivir come into play. But that does not mean the President is correct.
When it comes to COVID-19, we cannot limit our discussion to living and dying. This virus has significant morbidity even for those who do not die. About 40 percent of adults in the U.S. have at least one underlying health condition that would put them at risk for severe complications of COVID-19, according to a report published by the Centers for Disease Control and Prevention.5 Hilda Razzaghi, Yan Wang, Hua Lu, et al. "Estimated County-Level Prevalence of Selected Underlying Medical Conditions Associated with Increased Risk for Severe COVID-19 Illness — United States, 2018." CDC MMWR. July 24, 2020 / 69(29);945–950. (Accessed 4 Aug 2020.) https://www.cdc.gov/mmwr/volumes/69/wr/mm6929a1.htm The bottom line is that some 20% of those who come down with COVID, although they survive, find that the virus is anything but harmless. Many people, even young people, get extremely ill, and their road back to health includes weakness, shortness of breath, loss of muscle mass, and sometimes strokes. As we have discussed previously, COVID-19 can cause brain inflammation, hallucinations, psychosis, delirium, and nightmares. It can scar the lungs horribly, lead to weight loss and loss of lean muscle mass and has even been responsible for strokes in those age 40 and younger and loss of legs due to blood clotting issues. This virus not only affects the lungs and blood, but also the kidneys, liver, and brain–the last potentially resulting in chronic fatigue and major long-term depression, among other symptoms. It may not kill a high percentage, but it does still ravage a significant percentage of people.
A Dutch report published in early July (an excerpt is translated here) surveyed 1,622 Covid-19 patients with an average age of 53 who reported a number of enduring symptoms, including intense fatigue (88%), persistent shortness of breath (75%), and chest pressure (45%). Ninety-one percent of the patients were not hospitalized, suggesting they suffered these side-effects despite their cases of COVID-19 qualifying as "mild". While 85% of the surveyed patients considered themselves generally healthy before having COVID-19, only 6% thought so one month or more after getting the virus.
Conservatively, you are looking at 10 times the number of people who die from COVID-19 having long-term health issues. When you add in those who suffer long-term harm from the virus, we're not talking 160,000. We're talking several million people. So no, it is not "harmless" for 99%.
There is a passionate, raging debate right now when it comes to opening schools. There are parents and teachers on both sides of the question. Some of it is political, but I'm not going to go into that side of it. I just want to talk about the safety aspect.
On the open now side, there are two main points.
There is some evidence that children are less likely to catch the virus versus adults, and when they do, they are less likely to get as sick.6 Jim Morrison. "What Scientists Know About How Children Spread COVID-19." Smithsonian Magazine. July 23, 2020. (Accessed 30 Jul 2020.) https://www.smithsonianmag.com/science-nature/what-scientists-know-about-how-children-spread-covid-19-180975396/ Although the evidence leans in that direction, it is ambiguous at best, and even if true, it only applies to children under 10. At 10 and up, their susceptibility is the same as any adult's. But even for younger children, "less likely" does not mean "not at all."
There is also evidence to suggest that children are also less likely to transmit the virus VS adults.7 Morrison Again, the evidence is highly ambiguous–and again, if true, only for children under 10. At 10 and up, their communicability is the same as any adult's. And again, even for younger children "less likely" does not mean "not at all."
On the stay closed side, there are the facts on the ground.
Two weeks after Israel fully reopened schools, a COVID-19 outbreak swept through classrooms — including at least 130 cases at a single school.8 Daniel Estrin. "After Reopening Schools, Israel Orders Them To Shut If COVID-19 Cases Are Discovered." NPR. June 3, 2020. (Accessed 30 Jul 2020.) https://www.npr.org/sections/coronavirus-live-updates/2020/06/03/868507524/israel-orders-schools-to-close-when-covid-19-cases-are-discovered , 9 TOI Staff. "Almost 10,000 students, teachers quarantined as 217 infected in Israeli schools." The Times of Israel. 2 Jun 2020. (Accessed 30 Jul 2020.) https://www.timesofisrael.com/thousands-more-students-quarantined-as-nationwide-school-infections-continue/
A summer camp in suburban Dallas was forced to close less than two weeks after opening when both children and counselors showed symptoms and tested positive for COVID-19.10 Meredith Yeomans. "Summer Camps Struggle to Keep Out COVID-19." 5 NBCDFW. July 8, 2020. (Accessed 30 Jul 2020.) https://www.nbcdfw.com/news/coronavirus/summer-camps-struggle-to-keep-out-covid-19/2403236/ The camp had put numerous safety precautions in place, including mask wearing, daily temperature checks, social distancing of age groups, no food or material sharing, and much more. Similar outcomes were seen in Oklahoma and Missouri where dozens caught the virus.
Several weeks ago, 260 of the 597 children attending a summer camp in Georgia contracted the coronavirus, adding to a growing body of evidence that minors are both susceptible to infection and serve as vectors of transmission. According to the CDC, the true number of infected campers was probably significantly higher since test results were only available for 58 percent of the group.
As of June 30th, there were 950 reported positive cases of COVID-19 in Texas at 668 childcare locations–307 children and 643 staff members.11 Reese Oxner. "More than 300 children in Texas day cares have caught COVID-19, and the numbers are rising." The Texas Tribune. July 1, 2020. (Accessed 30 Jul 2020.) https://www.texastribune.org/2020/07/01/texas-day-care-coronavirus-cases-rising/ Statewide, 12,207 licensed childcare operations were open at the time, and total reported coronavirus cases had risen from 59 cases in mid-May and 576 on June 23.
One of the first school districts in the country to reopen its doors during the coronavirus pandemic did not even make it a day before a call from the county health department notified Greenfield Central Junior High School in Indiana that a student who had walked the halls and sat in various classrooms had tested positive for the coronavirus. "We knew it was a when, not if," said Harold E. Olin, superintendent of the Greenfield-Central Community School Corp., but were "very shocked it was on Day 1."
And finally, a study published online in JAMA Network found that infected children have at least as much of the coronavirus in their noses and throats as infected adults, according to the research. Indeed, children younger than age 5 may host up to 100 times as much of the virus in the upper respiratory tract as adults.12 Heald-Sargent T, Muller WJ, Zheng X, Rippe J, Patel AB, Kociolek LK. "Age-Related Differences in Nasopharyngeal Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Levels in Patients With Mild to Moderate Coronavirus Disease 2019 (COVID-19)." JAMA Pediatr. Published online July 30, 2020. https://jamanetwork.com/journals/jamapediatrics/fullarticle/2768952
And then there are the teachers.
Thirty percent of elementary school teachers are age 50 or older, which puts them in a high-risk group.
In mid-July, a longtime Arizona elementary school teacher died of coronavirus after sharing a summer classroom with two other teachers who also fell ill with the disease.13 Elisha Fieldstadt. "Beloved Arizona teacher dies of coronavirus, two others sharing classroom also infected." NBC News. July 13, 2020. (Accessed 30 Jul 2020.) https://www.nbcnews.com/news/us-news/beloved-arizona-teacher-dies-coronavirus-two-others-sharing-classroom-also-n1233672 They were teaching virtual summer school lessons, and the educators "took extra precautions" and "followed the CDC guidelines and more," but still got sick. They kept their distance, wore masks, and constantly used hand sanitizer.14 James Doubek. "A Teacher Who Contracted COVID-19 Cautions Against In-Person Schooling." NPR. July 14, 2020. (Accessed 30 Jul 2020.) https://www.npr.org/sections/coronavirus-live-updates/2020/07/14/890716897/teacher-recovering-from-covid-19-says-school-reopening-is-tough-decision
At least 600 Florida teachers have requested living wills as they prepare for schools in the state to reopen even as coronavirus numbers swell.15 J. Edward Moreno. "Hundreds of Florida teachers request living wills as they prepare to return to school amid COVID-19 spike." The Hill. 07/25/20. (Accessed 30 Jul 2020.) https://thehill.com/homenews/state-watch/509026-hundreds-of-florida-teachers-request-living-wills-as-they-prepare-to
So, let's cut to the chase. The primary argument I hear in favor of opening schools is that other countries all over the world are safely opening schools (not counting Israel and France,16 Daniel Cole/AP. "70 cases of COVID-19 at French schools days after reopening." NBC News. May 18, 2020. (Accessed 30 Jul 2020.) https://www.nbcnews.com/health/health-news/70-cases-covid-19-french-schools-days-after-re-opening-n1209591 of course), so why shouldn't the United States?
And the simple answer is lava!
When lava is hot and fresh and flowing, it's not a good idea to walk on it. Once it has cooled, though, there is no problem walking on it. In fact, if you wait long enough, after the lava breaks down into volcanic soil, the lava field is not just safe to walk on, it is absolutely verdant.
So, the simple answer as to why other countries can safely open schools and we cannot in the many, many areas of the country that currently have high infection rates is that they are opening their schools on a cooled lava field, whereas we are trying to open them (at least those in the "hot" districts) on flowing lava fields–metaphorically speaking. (See chart below.)
Note: in the above chart, the numbers are not affected by the number of tests. The numbers reflect an average per hundred thousand people. If you test 100,000, 200,000, 1 million people, it doesn't matter. While the total number of people with the virus would indeed go up, that number never appears in the chart–only the average per 100,000, which would remain unchanged.
Natural Antipathogen Formula as a Prophylactic
One of the things I was challenged on in my last newsletter was that several months earlier I had said there was no need to panic, and now I was preaching doom and gloom and large amounts of dead people. In fact, nothing has changed. I have said from the very beginning that I expected a large number of deaths–and those predictions are proceeding apace. Specifically, what I said is that the coronavirus had a low mortality rate, but that a low rate applied to a large susceptible population (essentially every person living in the United States) would mean a large number of deaths. But what I also said was that there was no need to panic since there are steps you can take that will likely put you on the good side of those numbers. And one of the more essential pieces of that program is an effective natural antipathogen formula.
Since I first mentioned that formula, many people have written in to ask if the natural antipathogen formula could be taken on a daily basis in smaller amounts to prevent ever getting the virus in the first place. The idea would be to use it prophylactically versus waiting until you experience the first symptoms and taking it in larger amounts to throttle back its progression from that point?
Before we go any further, we need to keep in mind that there is no actual proof that the formula works to kill the virus if you have been infected. Yes, there are thousands of anecdotal testimonials over the years as to how well it works in controlling the flu, but none of this constitutes proof. Without the rigors of a large cohort study, there is no proof that people who didn't use the formula wouldn't have had exactly the same experience in terms of either preventing the flu from hitting full on or patients getting well in what appeared to be half the time. And when it comes to the coronavirus, we have far fewer anecdotal reports. There is me, Kristen, and maybe a half dozen others who have written in to say that the formula prevented the virus from progressing. But with the coronavirus, the same might have been claimed by 80% of people who came down with the virus, took nothing to mitigate it, and had no or very mild symptoms.
And if we ever did run a huge cohort study and proved the formula stopped COVID-19 in its tracks, I couldn't talk about those results. If I did, the formula would be classified as a drug and could only be sold by prescription. And Baseline Nutritionals has no network of pharmaceutical reps to convince doctors to do so. In other words, Baseline would no longer be able to sell the formula.
So, where does that leave us?
For the thousands of people who have used the antipathogen formula over the last two decades, they do not need any studies. Based on their personal experience on multiple occasions, they are convinced the formula works. And their experiences are the reason that months of inventory for that formula was cleaned off the warehouse shelves in a matter of days back in March when people suddenly realized the coronavirus was for real. Which brings us to the question at hand: instead of just using it after you notice symptoms, can you use the antipathogen formula prophylactically to prevent ever getting the virus in the first place?
And the answer is: possibly, yes, theoretically?
Again, although there are many reasons to suspect it might work well for this purpose, there are no studies that prove it does so. In fact, such studies would be almost impossible to conduct. When it comes to assessing protection potential, you are talking about a large cohort study in which you analyze the data from a large cohort of people who were exposed to the virus during the course of the study.
Then you compare the infection and mortality results of those who regularly used the formula with those who did not. Unfortunately, no such cohort exists, nor is there ever likely to be one. So, when it comes to the efficacy of using an antipathogen formula to prevent the virus, you are flying blind. Nevertheless, the formula contains several powerful antivirals, and we do have several decades of testimonials vis-à-vis the flu–so again, it's theoretically likely. Which brings up the question: if so, how much do you need to take?
We already know that when you are dealing with an all-out infection, you need to take a bottle a day for three to four days until the infection is somewhat under control. After that, 10 droppers a day is sufficient. So, 10 droppers a day is a reasonable starting point. The problem with 10 droppers a day for prophylactic purposes, though, is that you are talking about 5 bottles a month, which would get expensive over several months. My guess, and this is just a guess, is that 5 droppers a day, two days on and one day off should do the trick, or at the very least make it likely that any infection is minimal. At that rate, each bottle would last about 18 days, so you are talking just under two bottles a month–which is a whole lot more economically feasible than five bottles a month.
Also, keep in mind that if you are using the formula that regularly, you will want to be sure to supplement with a good probiotic. Yes, the ingredients in the formula, although antibiotic, are gentle when it comes to your intestinal bacteria. But if you are taking it that regularly for weeks on end, it will begin to negatively impact your intestinal flora. So yes, you will want to supplement with a good probiotic to balance out that effect.
Unfortunately, thanks to an incoherent response from the highest levels of government, inconsistent messaging from public health officials, the media giving diametrically opposed opinions (depending on what station you listen to), not to mention public antipathy for many of the mitigating recommendations, the fight against COVID-19 in the United States has begun to feel hopeless. As a result, conspiracy theories have replaced science for many, whereas others have simply thrown caution to the wind. Now, instead of working as one country to suppress the virus and emerge slowly and carefully into public life again, people are making up their own rules as they go. And the result is chaos, many more deaths than we should ever have seen, and savage disruption to our economy–not to mention an astonishing number of people who claim the entire thing is a hoax. Without leadership from the top, the national response is fragmenting.
And if you are waiting for a vaccine, don't count on it helping very much. If the new vaccines are 50% effective, like the flu vaccine in a good year, and only 50% of the population is willing to take it, we are going to be living with the coronavirus for a number of years to come.
Some people will be immune because they have already had the virus.
Some will be immune because they got vaccinated and it worked for them.
Some will do nothing, take no precautions, refuse to wear masks and social distance, come down with the virus, and count on their doctors to use therapeutics to get them through.
New therapeutics will help here
And retail businesses and restaurants will find ways to reopen in the new environment by taking steps to kill the virus in the air and prevent its spread from person to person. For example, there are studies to show that air ionizers can kill airborne viruses.17 Hagbom M, Nordgren J, Nybom R, Hedlund KO, Wigzell H, Svensson L. "Ionizing air affects influenza virus infectivity and prevents airborne-transmission." Sci Rep. 2015;5:11431. Published 2015 Jun 23. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477231/. The problem is producing enough negative ions economically to sanitize an entire restaurant or store.18 Plasma Air. "Plasma Air Ionization Proven to Reduce Coronavirus Surrogate MS2 Bacteriophage by 99% in Independent Spanish Testing." PR NewsWire. Jun 16, 2020. (4 Aug 2020.) https://www.prnewswire.com/news-releases/plasma-air-ionization-proven-to-reduce-coronavirus-surrogate-ms2-bacteriophage-by-99-in-independent-spanish-testing-301076955.html And other studies have shown that far-UVC light can kill airborne coronavirus.19 Buonanno, M., Welch, D., Shuryak, I. et al. "Far-UVC light (222 nm) efficiently and safely inactivates airborne human coronaviruses." Sci Rep 10, 10285 (2020). https://doi.org/10.1038/s41598-020-67211-2 Bottom line: there are ways to make the air and surfaces in indoor environments anathema to coronavirus transmission–without the need for masks.
Some will have long-term side effects or die.
And some will proactively build their immune systems and keep a supply of a good natural antipathogen formula on hand to handle any eventuality.
By default, and without consciously choosing it, the United States appears to be heading for a chaotic, slightly modulated, free fall descent into natural herd immunity. If you think I'm exaggerating, then consider that even as I write this, a quarter of a million bikers from every corner of the country are gathering in South Dakota for nine days for the 80th annual Sturgis Motorcycle Rally. And for those nine days, there will be no social distancing and no wearing of masks. As one of the bikers, Rod Woodruff told the Daily Beast on Wednesday, "We're just celebrating good old American freedom."
And they will be bringing whatever they catch in those nine days back to every corner of the country. We are so screwed!
Ultimately, it looks like we're going to have to live with the virus for a long time. The only question is whether you choose to be proactive, reactive, or hope to hide from it. Some day, it would be nice to return to business as normal.
By the way, it's probably worth mentioning that the long-term herd immunity thing (options 1-3) may not work out so well in the near-term as the virus is showing a propensity for mutation.20 Kai Kupferschmidt. "The pandemic virus is slowly mutating. But is it getting more dangerous?" Science. Jul. 14, 2020. (Accessed 4 Aug 2020.) https://www.sciencemag.org/news/2020/07/pandemic-virus-slowly-mutating-it-getting-more-dangerous At least one mutation made the virus 10 times more infectious.21 Mark Terry. "Mutated COVID-19 Viral Strain in U.S. and Europe 10 Times More Contagious than Original Strain." BioSpace Jun 30, 2020. (Accessed 4 Aug 2020.) https://www.biospace.com/article/mutated-covid-19-viral-strain-in-us-and-europe-much-more-contagious/ And a new strain that has just appeared in Vietnam appears to be both more infectious22 TOMOYA ONISHI. "Vietnam fights new COVID-19 strain with higher infection rate." Nikkei Asian Review. August 3, 2020. (Accessed 4 Aug 2020.) https://asia.nikkei.com/Spotlight/Coronavirus/Vietnam-fights-new-COVID-19-strain-with-higher-infection-rate and more severe. 23 "Alarm in Vietnam after new strain of coronavirus." 112 UA. 29 July 2020. (4 Aug 2020.) https://112.international/ukraine-top-news/alarm-in-vietnam-after-new-strain-of-coronavirus-53430.html
Note: There is one small positive here. With people working from home and a large number wearing masks and socially distancing (even if not enough to stop COVID-19), it should be enough to drastically reduce the spread of flu this year–ultimately dropping the influenza death toll by more than half.
Kathleen Tuthill. "John Snow and the Broad Street Pump." UCLA Department of Epidemiology. Nov 2003. (Accessed 20 Jul 2020. https://www.ph.ucla.edu/epi/snow/snowcricketarticle.html)
"Global HIV & AIDS statistics–2020 fact sheet." UNAIDS. (Accessed 20 Jul 2020.) https://www.unaids.org/en/resources/fact-sheet.
Margaret Talev. "Axios-Ipsos poll: The skeptics are growing." AXIOS. Jul 21, 2020. (Accessed 30 Jul 2020.) https://www.axios.com/axios-ipsos-poll-gop-skeptics-growing-deaths-e6ad6be5-c78f-43bb-9230-c39a20c8beb5.html
Andrew Romano. "New Yahoo News/YouGov poll shows coronavirus conspiracy theories spreading on the right may hamper vaccine efforts." Yahoo News. May 22, 2020. (Accessed 31 Jul 2020.) https://news.yahoo.com/new-yahoo-news-you-gov-poll-shows-coronavirus-conspiracy-theories-spreading-on-the-right-may-hamper-vaccine-efforts-152843610.html
Hilda Razzaghi, Yan Wang, Hua Lu, et al. "Estimated County-Level Prevalence of Selected Underlying Medical Conditions Associated with Increased Risk for Severe COVID-19 Illness — United States, 2018." CDC MMWR. July 24, 2020 / 69(29);945–950. (Accessed 4 Aug 2020.) https://www.cdc.gov/mmwr/volumes/69/wr/mm6929a1.htm
Jim Morrison. "What Scientists Know About How Children Spread COVID-19." Smithsonian Magazine. July 23, 2020. (Accessed 30 Jul 2020.) https://www.smithsonianmag.com/science-nature/what-scientists-know-about-how-children-spread-covid-19-180975396/
Daniel Estrin. "After Reopening Schools, Israel Orders Them To Shut If COVID-19 Cases Are Discovered." NPR. June 3, 2020. (Accessed 30 Jul 2020.) https://www.npr.org/sections/coronavirus-live-updates/2020/06/03/868507524/israel-orders-schools-to-close-when-covid-19-cases-are-discovered
TOI Staff. "Almost 10,000 students, teachers quarantined as 217 infected in Israeli schools." The Times of Israel. 2 Jun 2020. (Accessed 30 Jul 2020.) https://www.timesofisrael.com/thousands-more-students-quarantined-as-nationwide-school-infections-continue/
↑10
Meredith Yeomans. "Summer Camps Struggle to Keep Out COVID-19." 5 NBCDFW. July 8, 2020. (Accessed 30 Jul 2020.) https://www.nbcdfw.com/news/coronavirus/summer-camps-struggle-to-keep-out-covid-19/2403236/
Reese Oxner. "More than 300 children in Texas day cares have caught COVID-19, and the numbers are rising." The Texas Tribune. July 1, 2020. (Accessed 30 Jul 2020.) https://www.texastribune.org/2020/07/01/texas-day-care-coronavirus-cases-rising/
Heald-Sargent T, Muller WJ, Zheng X, Rippe J, Patel AB, Kociolek LK. "Age-Related Differences in Nasopharyngeal Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Levels in Patients With Mild to Moderate Coronavirus Disease 2019 (COVID-19)." JAMA Pediatr. Published online July 30, 2020. https://jamanetwork.com/journals/jamapediatrics/fullarticle/2768952
Elisha Fieldstadt. "Beloved Arizona teacher dies of coronavirus, two others sharing classroom also infected." NBC News. July 13, 2020. (Accessed 30 Jul 2020.) https://www.nbcnews.com/news/us-news/beloved-arizona-teacher-dies-coronavirus-two-others-sharing-classroom-also-n1233672
James Doubek. "A Teacher Who Contracted COVID-19 Cautions Against In-Person Schooling." NPR. July 14, 2020. (Accessed 30 Jul 2020.) https://www.npr.org/sections/coronavirus-live-updates/2020/07/14/890716897/teacher-recovering-from-covid-19-says-school-reopening-is-tough-decision
J. Edward Moreno. "Hundreds of Florida teachers request living wills as they prepare to return to school amid COVID-19 spike." The Hill. 07/25/20. (Accessed 30 Jul 2020.) https://thehill.com/homenews/state-watch/509026-hundreds-of-florida-teachers-request-living-wills-as-they-prepare-to
Daniel Cole/AP. "70 cases of COVID-19 at French schools days after reopening." NBC News. May 18, 2020. (Accessed 30 Jul 2020.) https://www.nbcnews.com/health/health-news/70-cases-covid-19-french-schools-days-after-re-opening-n1209591
Hagbom M, Nordgren J, Nybom R, Hedlund KO, Wigzell H, Svensson L. "Ionizing air affects influenza virus infectivity and prevents airborne-transmission." Sci Rep. 2015;5:11431. Published 2015 Jun 23. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477231/.
Plasma Air. "Plasma Air Ionization Proven to Reduce Coronavirus Surrogate MS2 Bacteriophage by 99% in Independent Spanish Testing." PR NewsWire. Jun 16, 2020. (4 Aug 2020.) https://www.prnewswire.com/news-releases/plasma-air-ionization-proven-to-reduce-coronavirus-surrogate-ms2-bacteriophage-by-99-in-independent-spanish-testing-301076955.html
Buonanno, M., Welch, D., Shuryak, I. et al. "Far-UVC light (222 nm) efficiently and safely inactivates airborne human coronaviruses." Sci Rep 10, 10285 (2020). https://doi.org/10.1038/s41598-020-67211-2
Kai Kupferschmidt. "The pandemic virus is slowly mutating. But is it getting more dangerous?" Science. Jul. 14, 2020. (Accessed 4 Aug 2020.) https://www.sciencemag.org/news/2020/07/pandemic-virus-slowly-mutating-it-getting-more-dangerous
Mark Terry. "Mutated COVID-19 Viral Strain in U.S. and Europe 10 Times More Contagious than Original Strain." BioSpace Jun 30, 2020. (Accessed 4 Aug 2020.) https://www.biospace.com/article/mutated-covid-19-viral-strain-in-us-and-europe-much-more-contagious/
TOMOYA ONISHI. "Vietnam fights new COVID-19 strain with higher infection rate." Nikkei Asian Review. August 3, 2020. (Accessed 4 Aug 2020.) https://asia.nikkei.com/Spotlight/Coronavirus/Vietnam-fights-new-COVID-19-strain-with-higher-infection-rate
"Alarm in Vietnam after new strain of coronavirus." 112 UA. 29 July 2020. (4 Aug 2020.) https://112.international/ukraine-top-news/alarm-in-vietnam-after-new-strain-of-coronavirus-53430.html
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text:
Blood Money är Mobb Deeps sjunde album och den första produktionen i samarbete med G-Unit Records. Skivan släpptes den andra maj 2006 och debuterade på Billboard Top 200:s tredjeplats och som listetta på både Top Rap Albums och Top R&B/Hip Hop Albums.

Låtlista
Smoke It
Put Em in Their Place
Stole Something  (med Lloyd Banks)
Creep  (med 50 Cent)
Speakin So Freely
Backstage Pass
Give It to Me  (med Young Buck)
Click Click  (med Tony Yayo)
Pearly Gates  (med 50 Cent)
Capital P, Capital H
Daydreamin'''The Infamous  (med 50 Cent)  In Love With the Moula It's Alright (med 50 Cent & Mary J. Blige) Have a Party (med 50 Cent & Nate Dogg)  Outta Control (Remix)''  (med 50 Cent)

Musikalbum 2006
Album producerade av Dr. Dre


After trying to acquire the consulting arm of PWC, HP has decided to swallow EDS HP Press Release: HP to Acquire EDS for $13.9 Billion. This is a large transaction by all means. From the press release HP is seeing an opportunity to improve the operational sides of EDS by consolidating, but all in all the two businesses will stay the way they are.


text:
Wolves forced into re-think as Italians make U-turn over star forward
Wolves may now have to look elsewhere after news emerged in the Italian media that Milan are set to keep hold of forward Rafael Leao.
Wolves were first linked with the 22-year-old back in April when Nuno Espirito Santo was in charge. The Portuguese connection was strong and it made the West Midlanders among the favourites to sign the youngster. Nuno has now departed but, with Bruno Lage at the helm, there still seemed hope of a deal.
And with super-agent Jorge Mendes in control of proceedings, things were looking good. As recently as last week, reports claimed the clubs were in discussions over the sale of Leao.
It was thought that Milan were open to the idea of cashing in on the former Portugal Under-21 star. But, ahead of the Rossoneri's friendly clash with French club Nice on Saturday, news broke of a change of heart.
MilanNews (via sportslens) are reporting that the San Siro giants are not willing to let the youngster leave for any club this summer. Wolves were not the only outfit thought to hold an interest in the former Sporting ace.
Everton's name has been mentioned although that was when it was felt Nuno would replace Carlo Ancelotti. It is not clear if Toffees chief Rafa Benitez is a fan of the frontman but that trail seems to have gone cold.
Leao the man to unlock defences
It is clear that Wolves need more firepower in the final third. Last season's woeful goal return was behind their below-par campaign.
Raul Jimenez's injury absence was a huge factor and proved just how much the Black County outfit rely on the Mexican. Leao is not a prolific goalscorer but that part of his game is likely to develop as he matures.
Likened to both Cristiano Ronaldo and Kylian Mbappe, he has bagged 13 times in 73 Milan appearances. But he is certainly a provider, with six Serie A assists in 2020-21 to add to his six league goals.
There is still time for the Italians to change their minds and allow the starlet to leave. However, with Norway international Jens Petter Hauge edging toward a summer exit, they will need Leao on board.
He is highly regarded at the club and has made 61 league starts across the past two seasons. Wolves would have loved to see him at Molineux but hopes appear to be fading.
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