1/ #LBBB generates often a classical pattern on #EchoFirst. The pattern is very distinctive in Tissue Doppler of the septum.

The classical pattern arises from the time lapse of the activation and relaxation of the two walls, creating a pattern of interaction due to a sequence temporal imbalances of the tension between the two walls.
2/ As the septum is activated first, it contracts (shortening - septal flash) without activation of the lateral wall, which stretches. This generates slower pressure build up than a normal IVC, which then is prolonged.
3/ During ejection, the LV volume decreases, so both walls shorten. Tension, however, declines first in the septum, as this was activated first. This leads to a tension imbalance, so the lateral wall continues to shorten, the more relaxed septum stretches.
4/ The stretching of the septum builds up an elastic tension in the septum, which is released as recoil, when tension declines in the lateral wall, showing a post systolic shortening in the septum which is due to elasticity.
5/ This classical pattern is also very evident in the strain curves, and an integrated strain analysis will show this, in a semi quantitative way describing how work is wasted by looking at the opposing wall. https://t.co/8DS2F1S0BW
6/ This classical interaction pattern explains all changes seen in apical velocities (apical rocking), basal velocity curves, strain and strain rate.
7/ Applying estimated LV pressure do not add information, simply because the pressure curve is the same for both walls, so the different strain-pressure loops arises from plotting different strain curves against the same pressure curve, the differences lie in the strain.
This is the CLASSICAL pattern. This is dependent on a normally functioning lateral wall (except for the delay) https://t.co/fQ83cMGI3k
@threadreaderapp unroll

More from Science

@mugecevik is an excellent scientist and a responsible professional. She likely read the paper more carefully than most. She grasped some of its strengths and weaknesses that are not apparent from a cursory glance. Below, I will mention a few points some may have missed.
1/


The paper does NOT evaluate the effect of school closures. Instead it conflates all ‘educational settings' into a single category, which includes universities.
2/

The paper primarily evaluates data from March and April 2020. The article is not particularly clear about this limitation, but the information can be found in the hefty supplementary material.
3/


The authors applied four different regression methods (some fancier than others) to the same data. The outcomes of the different regression models are correlated (enough to reach statistical significance), but they vary a lot. (heat map on the right below).
4/


The effect of individual interventions is extremely difficult to disentangle as the authors stress themselves. There is a very large number of interventions considered and the model was run on 49 countries and 26 US States (and not >200 countries).
5/
https://t.co/hXlo8qgkD0
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get


A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from

The Taq.
https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals

Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.

The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process

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