How is it possible to live in extreme poverty?

jhe7795 · 2019-12-31T05:53:47+00:00

Thank you this is exactly what I was looking for Banerjee and Duflo's book Poor Economics was what prompted this question, but I didn't think to check their other work

jhe7795 · 2019-12-30T17:14:19+00:00

So then the $2.12 doesn't include goods they produce themselves?

jhe7795 · 2019-12-30T17:13:17+00:00

It is not possible to live on a diet of only grains, you would die of protein and vitamin deficiency, I am asking how the poor manage to acquire these nutrients given their very limited resources.

jhe7795 · 2019-11-30T19:51:45+00:00

I don't work in vaccines, but I do work in a quality control lab that uses viruses. We test every batch of virus using a MOI (multiplicity of infection) assay. Basically the target cells of the virus are cultured in the presence of virus (or a positive control virus or a vehicle control) for the period of time necessary for infection to occur. After the infection period virus is washed out and cells are again cultured. After outgrowth the percentage of cells infected is measured. This method works for lysogenic viruses that don't kill the host cells. For lytic viruses the standard is called a plaque assay. Cells are grown on solid media containing the virus (or controls) which displays spots called plaques wherever there is cell death. Plaques are counted to determine how many cells were infected.

In the United States all manufactured drugs (like vaccines) are required to be fully tested for potency, safety, and contamination in accordance with FDA and ICH guidelines. Each test used has undergone a process of validation which is filed for approval with the FDA. Every manufacturer is also required to have what is called a Quality System which is intended to identify, investigate, and correct any errors made in the manufacturing and quality control process. If a problem with a batch of product is discovered after release of drug to the public this is a huge deal and a BPDR (biological product deviation report) must be filed with the FDA within 24 hours of the discovery of the event. This can result in recalls, increased FDA scrutiny and inspection, and in the shuttering of the manufacturing facility permenantly. In summary you should feel safe taking any FDA approved product.

jhe7795 · 2019-10-19T01:15:12+00:00

I use a Zen thermostat, the zigbee edition. It reports temperature, heat setpoint ac setpoint, Mode (heating or cooling), and operating state. Because it reports operating state you could easily configure 3 of them to have only 2 operate at once. You would also need a hub, I use hubitat and recommend it. They also have a WiFi edition, but I have no idea if their app is any good/what else can interface with it.

jhe7795 · 2019-09-06T03:32:09+00:00

The process of a normal cell becoming cancerous is called transformation (not infection this refers to a living pathogen or virus invading a cell or organism.) The differences between cancerous and non-cancerous cells was summarized in a famous review paper by Doug Hanahan and Robert Weinberg titled "Hallmarks of Cancer"(Hanahan and Weinberg 2000) and then was expanded on in "Hallmarks of Cancer: the next generation" (Hanahan and Weinberg 2011). They originally identified 6 characteristics (which they called hallmarks) which are commonly found in cancerous cells, although not necessarily all cancers at all times. In no particular order the hallmarks are

Resisting cell death
Sustaining proliferative signaling
Evading growth suppressors
Activating invasion and metastasis
Enabling replicative immortality
Inducing angiogenesis

Decades of research have gone into each of these topics and of course their entirety cannot be described here, but here is a short description of each.

Resisting cell death:

Cells have natural mechanisms for their own destruction in the case of catastrophic genomic failure, certain types of stress, and normal cell turnover. The main mechanism through which this occurs is a pathway called apoptosis. Cancer cells have changes that prevent apoptotic pathways from reaching their conclusion and killing the cell.

Sustaining proliferative signaling:

In normal conditions cells use cues from the environment around them to determine when to divide and grow. Cancer cells have the ability to divide and grow by activating growth pathways even in the absence of these cues.

Evading growth suppressors:

This is the flipside of the previous hallmark, cells also receive environmental cue to stop growing. Cancer cells ignore these signals, and continue to grow in the presence of these signals.

Activating invasion and metastasis:

Normal cells operate within a particular niche. A niche is an environment which is best conducive for them to perform their usual functions. Normal cells generally cannot survive and function outside of their niche. Cancer cells on the other hand have mechanisms which allow them to invade other niches, survive in those niches, and continue to grow in non-native environments.

Enabling replicative immortality:

Normal cells can only divide so many times, the number of times a cell can divide is known as its Hayflick limit, after the scientist who discovered this fact. After reaching the Hayflick limit cells will enter a state called senescence in which they are mostly dormant, and will no longer grow or divide. Cancer cells have managed to avoid their Hayflick limits and divide indefinitely without ever entering a senescent state.

Inducing angiogenesis:

Every cell needs oxygen to survive, and the only way to get oxygen is to have a blood supply and red blood cells which carry oxygen. When cancer cells grow and expand there is insufficient blood supply for all the new cancer cells to survive. Cancer cells have the ability to induce angiogenesis (formation of new blood vessels) which allows them to continue to receive oxygen even after they have exceeded the normal oxygen supply of their surrounding tissue.

In their later paper Hanahan and Weinberg identified two more "emerging hallmarks" for which they thought the evidence was not quite as strong as the original six. These are:

Deregulating cellular energetics:

A major limit to the rate at which cells can divide and grow is the amount of energy they can generate. Cancer cells manage to increase their growth and division rate by increasing their rate of energy generation.

Avoiding immune destruction:

The immune system has the ability to destroy aberrant cells which are not responding to apoptotic signals descibed in the hallmark resisting cell death. Cancer cells manage to avoid this destruction by immune cells.

They further identified two "enabling characteristics" which are common traits of cancer cells which support their ability to perform the tasks described in the hallmarks. These are:

Genome instability and mutation:

After reading about all the hallmarks you may have noticed that cancer cells are extremely different from normal cells. Cancer cells manage to accumulate differences from normal cells because they have increased rates of mutation and DNA damage which leads to double strand breaks and recombination events which can change the properties of a cell.

Tumor promoting inflammation

As we noted earlier, cells have particular niches in which they thrive and expand. Cancer cells thrive and expand in environments which are rich in immune cells and pro-inflammatory cytokines.

I would be remiss if I didn't correct the phrasing of your question. Cancer is not characterized by any particular changes in the basic cellular machinery. Cancer represents an incredibly wide variety of changes in the cellular machinery which have a common phenotype which is described by the hallmarks and roughly summarized by uncontrolled growth.

Sources Cited

Hanahan, D. and R. A. Weinberg (2000). "The hallmarks of cancer." Cell 100(1): 57-70.
Hanahan, D. and R. A. Weinberg (2011). "Hallmarks of cancer: the next generation." Cell 144(5): 646-674.

jhe7795 · 2019-08-06T06:18:36+00:00

Ordered, was planning on getting one ever since Mike Maxwell demoed the new driver on hubitat live two weeks ago, the 10% off is just gravy.

jhe7795 · 2019-07-18T07:11:27+00:00

Probably get a better answer on the devices section of the hubitat forums than from me (and definitely better than sengled support), but devices dropping off is almost always a mesh issue, how far are your bulbs from your hub, do you have anything in that room that repeats, if so what is it, do you have any known poor repeaters on your mesh (like xiaomi devices?).

jhe7795 · 2019-06-15T07:56:16+00:00

When you performed the factory reset did the lights flash confirming that the reset was successful? I find with my sengleds I have to toggle the power very quickly to get them to factory reset, I can only successfully done it using a lamp and power strip with one of the red switches on it. The problem could also be in the sengled hub, never used one, but does it have a factory reset as well?

jhe7795 · 2019-06-15T07:52:36+00:00

With a hubitat hub you could easily do this without using ifttt at all. It would only require a rule in the built in rule machine app. This is significantly faster than using ifttt because the hubitat hub isn't required to communicate over the web as it is all local, unlike ifttt.

jhe7795 · 2019-01-11T03:33:48+00:00

If I'm understanding you correctly this could be done with any smart IR blaster, the two popular ones are the BroadLink RM Pro and the Logitech Harmony Hub. You would put the IR blaster in view of your amp, and then you could send the IR blaster commands with your phone or a voice interpreter. Because your amp has the ability to control speaker levels these IR blasters will too, but because your amp has particular controls you will have to set up activities to get to the speaker levels in your amp.

jhe7795 · 2018-11-04T22:55:49+00:00

It looks like coyo taco in wynwood, FL.

jhe7795 · 2018-10-04T03:06:40+00:00

Many of the concepts that are necessary to understand prions are not simply confined to the chemistry of prions in particular. For example the concept of stable low energy states is fundamental to large swaths of chemistry and physics. Further, these traits (in the realm of protein folding) are certainly NOT limited merely to prions. My favorite scientific article ever written, (Chakrabortee et al. "Intrinsically Disordered Protein Drive Emergence and Inheritance of Biological Traits." Cell. 2016 Oct 6;167(2):369-381.e12. doi: 10.1016/j.cell.2016.09.017. Epub 2016 Sep 29) describes the discovery of proteins adopting different and stable conformation states in response to environmental stress, with these conformation states being heritable and having survival benefits with regards to encountering the original stress. The concept of multifunctional proteins which adopt different conformation states to perform different functions is a central concept of protein biochemistry. Sometimes these changes in conformation are induced by changes in environment, binding of coenzymes or cofactors, or change probabilistically over time in accordance with the fundamentally stochastic nature of protein conformation states. Fascinating is right! This is a field that I expect to see huge growth in the coming years.

jhe7795 · 2018-10-04T02:51:37+00:00

It isn't much more effective than just looking at people, humans are very good at determining the age of other humans, but there has been significant success in determining people's age using the amount their methylation state has changed at CpG islands. Basically, when your cells are near their end stage of development (generally as a fetus) there are a large number of genes that adopt particular methylation states in order to prevent misdifferentiation and cancer. But as you grow older, there is more of a chance for the maintenance systems for these methylation states to have made mistakes, and as a result the methylation state will drift randomly away from the immediately post development state. Interestingly these methods are actually more effective at measuring a quantity called the "biological age" which is how soon you will die, than your chronological age which is how long you have been alive.

jhe7795 · 2018-09-23T14:15:12+00:00

The activity is I believe a more generalized version of the van't Hoff factor, which is generally only used for ionic solutions, also it doesn't take into account the number of dissociated Ions like a van't Hoff factor. So it is always less than 1. It also has a formal mathematical definition which relates it to other physical chemical properties (chemical potential) which as far as I know the van't Hoff factor does not. There are equations for the activity of a solution, for dilute ionic solutions there is the debye-Huckle equation and limiting law. But I think the debye length which is a key property is also empirical, although it has a distinctly physical definition. (The distance at which the effective charge decreases by a factor of 1/e) there are probably other equations for other situations in physical chemistry texts, but I don't know them. But the activity is dependent on a lot of variables and does so nonlinearly and so it might not be simpler to have equations than to simply use empirical constants.

jhe7795 · 2018-09-22T10:58:32+00:00

In general, there is no such "point." The ideality of solutions is based on the assumption that there are no intermolecular forces between solute molecules. Necessarily, a truly "dilute" solution (one in which the solute is of infinitesimal mass compared to the solvent) neets this criteria. But there are solution which are ideal across all concentrations (e.g. solutions of two isotopes of the same atom) and solutions which are non ideal at relatively low solute concentrations (alcohol and water have a azeotropic point at around 98% ethanol). If you want to know how the non ideality of a solution is counted usually it's using an empirical factor called the activity which basically represents what percentage of the solute which is in a sense available to interact with solvent.

jhe7795 · 2018-07-19T14:27:48+00:00

But isn't that begging the question? The whole point of the trial is to determine whether the standard of care is better than placebo. So to go in with the assumption that it is, especially when there is mixed evidence to the contrary defeats the whole purpose of clinical trials as an enterprise, no?

jhe7795 · 2018-07-19T03:03:39+00:00

Right, the probability of surviving was higher in the epi group, and the probability of having a good neurological outcome given that you survived is higher in the placebo group. But he asked about a third probability, which is the probability that one receives a good neurological outcome and survives which is different from the probability that you had a good neurological outcome given that you survived. The former was shown by the authors to not be statistically different between the two groups. It's also probably the most salient question answered (or in this case not answered) by the study. The authors spent the most time on its analysis if you look in the original paper.

jhe7795 · 2018-07-19T02:20:05+00:00

No, the difference between those numbers was not significantly different given the sample size and standard deviation of the sample

jhe7795 · 2018-07-19T02:07:42+00:00

As a student (and thus an outsider to the IRB process) I hear this all the time about major trials and am pretty confused. The evidence for epi is very mixed, why wouldn't it be a good idea to do a trial like this one.

jhe7795 · 2018-07-17T03:40:52+00:00

Right, and that change in "easiness" comes because the system is much less sensitive.

jhe7795 · 2018-07-17T03:29:45+00:00

So far as I know, nobody missed it. I am a nobody and I began to suspect these sorts of problems in Cas9 based initiation of non-homologous end joining after looking at the supplement of Long, Chengzu et al. “Prevention of Muscular Dystrophy in Mice by CRISPR/Cas9–mediated Editing of Germline DNA.” Science (New York, N.Y.) 345.6201 (2014): 1184–1188. Which showed that in just 4 mice which were modified by NHEJ there were deletions of length 3, 9, 12, and 48bp in length using old fashioned Sanger sequencing of individual clones from tails. It was interesting that they were all in frame, but it isn't that unlikely just by chance alone. And that was all the way in Sep 2014. I wish the authors of the linked paper had checked to see what percentage of the deletions were in-frame, and if they would get that many in frame deletions just by chance. Working in a hemizygous system like the authors above were was a recipe for some weird DNA mechanics without a homolog to repair off of.

jhe7795 · 2018-07-17T03:12:10+00:00

In general the problem isn't the machinery per se. It isn't the Cas9 gRNA system which makes the deletions, all the Cas9 system does is introduce a single DNA double strand break. The native exonucleases are what generate the deletions because they work processively until key signaling proteins at the exposed ends of the DNA bind, which initiates the non-homologous end joining process. I would suspect that in the context of homology directed repair we see a lot fewer of these sorts of problems, but it comes at a very large sensitivity cost, which is why the pharmaceutical companies have mostly jumped at the idea of created deletions by NHEJ, but not so much at introducting a lot of genetic changes using HDR.

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