Really? This seems kind of far afield. How is SVB due to Trump?
https://www.washingtonpost.com/business/economy/trump-signs-...
See also:
https://www.nbcnews.com/politics/congress/silicon-valley-ban...
Deleted Comment
Really? This seems kind of far afield. How is SVB due to Trump?
https://www.washingtonpost.com/business/economy/trump-signs-...
See also:
https://www.nbcnews.com/politics/congress/silicon-valley-ban...
The first paper used a random forest-based decision tree classifier built on markers in blood assays. Neat.
However, this study has a major flaw. They rated their classifier's accuracy on classifying blood marker profiles of acutely ill COVID patients, long COVID patients experiencing "diffuse symptoms" referred with "no selection process", and a healthy control group. The control group consisted of healthy patients whose blood samples had been banked prior to the COVID-19 pandemic.
It's not clear whether they compared their classifier's results against people who've had COVID and recovered without issue, versus those who had COVID and continued to experience symptoms long after recovery. That is the entire point of developing such a classifier. This paper is worthless without that comparison.
Second paper has the same problem, and is honest about it:
>The healthy control subjects were individuals without disease, acute illness or prescription medications and were previously banked in the Translational Research Centre, London, ON (Directed by Dr. D.D. Fraser; https://translationalresearchcentre.com/). These latter samples were obtained prior to the emergence of SARS-CoV-2 in our region and therefore, were considered not to have been exposed to the virus.
I only added these to say there's enough evidence to be questionable of the null hypothesis with regard to long COVID physiopathology.
Elevated vascular transformation blood biomarkers in Long-COVID indicate angiogenesis as a key pathophysiological mechanism, https://molmed.biomedcentral.com/articles/10.1186/s10020-022...
Plasma Proteome of Long-covid Patients Indicates Hypoxia-mediated Vasculo-proliferative Disease With Impact on Brain and Heart Function (Preprint), https://assets.researchsquare.com/files/rs-2448315/v1/8043bd...
Turns out when I was buying lunch, he was on the phone with a friend who worked at Paytm and that guy gave away my transaction history for shits and giggles.
My trust in private companies has been at it's lowest since then and I absolutely do not trust startups to keep my data safe.
Unfortunately, if you do that, you are going to be outcompeted by the teams that are working to get their first 10,000 paying customers by any means necessary, because privacy planning is less capital efficient.
The companies that do get big enough to overcome their immediate survival constraints often have a harder problem identifying and providing resource needs for privacy assurance because it's less on the minds of the people in charge of making resource decisions because you have other operational scaling issues at the front of mind.
Your engineers and support staff doing dumb things with your data is a risk you can have resources allocated to. But it's not on the critical path to market dominance so it shouldn't be expected to be a priority.
Deleted Comment
"Some parts of Twitter may not be working as expected right now. We made an internal change that had some unintended consequences. We’re working on this now and will share an update when it’s fixed."
https://twitter.com/TwitterSupport/status/163279294226274713...
Median rent in Seattle for a 1 bedroom is $2k. Using the 40x rule someone who makes $80k could easily afford this, which is a low bar for someone with a moderately decent job.
Locking in a low rate alone has nothing to do with whether owning is more affordable than renting. The rate could be 0% but with a sales price high ala 2021-2022 buying mania and then adding property taxes, insurance, maintenance, and HOA the vast majority of "high" cost metros have and will continue to be much more expensive to buy in than rent in whether rates go up or down.
$80k is not a low bar, and this is insulting to really talented people I know stuck in below $40k jobs.
But that definition of effort as it relates to the ability to “survive” does not seem useful to me. It takes a lot of effort to manually dig a ditch compared to using an excavator, but you would not pay the person that shows up with a shovel more than the person that shows up with an excavator.
Edit: this is not intended to say your friend does not deserve a better pay to quality of life (QoL) ratio. However, the fact that you have a comparably favorable pay to QoL and they have an undesirable pay to QoL ratio means society does not want more people to be selling that labor, but rather more people to be selling your labor.
My point is that the disparity is such a chasm that my brain can't reconcile it. We aren't talking about ditch digging, we are talking about serving food to the people of Seattle. All the software engineers in Seattle, in my experience, love to frequent dining establishments. Their quality of life is dependent on the labor of people serving them. There's no way I can accept the disparity as "just the way it is." My gut can't take it.
Plasma Proteome of Long-covid Patients Indicates Hypoxia-mediated Vasculo-proliferative Disease With Impact on Brain and Heart Function (Preprint)
https://assets.researchsquare.com/files/rs-2448315/v1/8043bd...
An excerpt:
> In Fig. 7A, hierarchical clustering heatmaps reflect the levels of neurological markers across the patient groups (markers have been curated by OLINK). The values of the PEA expression levels were hierarchically clustered based on Pearson correlation algorithms. Markers selected through the above methodology were investigated for functional annotation using tools from the GSEA platform and MSigDB data positories (Fig. 7B). This latest analysis demonstrated that functional clusters were formed around leukocyte migration, positive immune signals, glial cell differentiation, neurogenesis and MAPK regulatory modules. Taken together, these pathways predict a possible brain-blood barrier dysfunctionality grounded on cell proliferation. Graphs in Fig. 7C illustrate the expression levels of individual markers from the functional groups presented in Fig. 7B. One of the highly expressed markers, was the amyloid precursor protein (APP; Supplementary Fig. 10) which is known to be a pathognomonic marker for both Alzheimer disease and brain inflammation [61–65]. Additional markers for brain dysfunction include JAM2 (endothelial tight junctions protein), SNAPIN (a mediator of neuronal autophagy-lysosomal function in developing neurons), KCNH2 (potassium channel), S100A14 (involved in cell motility adhesion and growth), KIAA0319 (language impairment biomarker), and IROR1 (a receptor tyrosine kinase like orphan receptor 1, which regulates neurites growth in the central nervous system having also WNT-signaling pathway functions, and being crucial for the auditive apparatus maintenance).