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NNadir
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August 21, 2021
Charlie Haden on Bass.
Only Charlie Haden could do this.
The best communist bass player from Iowa in the world.
Seriously, a giant. My favorite part of his career, if one has to choose a favorite, was his years with Keith Jarrett, Dewey Redman, and Paul Motion.
Something a little outside mainstream jazz, as only Charlie Haden could do it:
August 21, 2021
Mexico City was like another world.
August 18, 2021
Beneath an Evening Sky
August 18, 2021
New York Times Book Review Suite Française
I sort of have to read it, but I won't tell by sons, since I'm trying, hard as it is, to be consistent.
My sons are annoyed by my refusal to read fiction, but without telling them, I may read...
...Irène Némirovsky's Suite Française
...Born in Ukraine, Irène Némirovsky had lived in France since 1919 and had established herself in her adopted country's literary community, publishing nine novels and a biography of Chekhov. She composed "Suite Française" in the village of Issy-l'Evêque, where she, her husband and two young daughters had settled after fleeing Paris. On July 13, 1942, French policemen, enforcing the German race laws, arrested Némirovsky as "a stateless person of Jewish descent." She was transported to Auschwitz, where she died in the infirmary on Aug. 17.
The date of Némirovsky's death induces disbelief. It means, it can only mean, that she wrote the exquisitely shaped and balanced fiction of "Suite Française" almost contemporaneously with the events that inspired them, and everyone knows such a thing cannot be done...
The date of Némirovsky's death induces disbelief. It means, it can only mean, that she wrote the exquisitely shaped and balanced fiction of "Suite Française" almost contemporaneously with the events that inspired them, and everyone knows such a thing cannot be done...
New York Times Book Review Suite Française
I sort of have to read it, but I won't tell by sons, since I'm trying, hard as it is, to be consistent.
August 18, 2021
It sounds dangerous, that Piranha solution. If you're going to use it, be careful! ...Especially if you're misappropriating the ethanol.
Be careful with that Piranha solution.
So I'm reading this paper:
Lipidomic Profiling of Algae with Microarray MALDI-MS toward Ecotoxicological Monitoring of Herbicide Exposure (Peter V. Shanta, Bochao Li, Daniel D. Stuart, and Quan Cheng Environmental Science & Technology 2021 55 (15), 10558-10568)
...and then something scary shows up, something of which I've never heard, Piranha solution!!!!?!!.
The gold microchip array was fabricated in the Cleanroom Facility at UCR, following our previously published procedure.(30) The physical parameters of the finished gold microchips are as follows: each well on a gold microchip has a diameter of 800 ?m, with the well bottom covered with 50 nm thick gold and the edges of wells covered with 200 nm gold. In brief, glass slides (1 × 3 inches) were cleaned with Piranha solution (H2SO4/H2O2, 3:1, Caution!), rinsed with ultrapure water and ethanol, and dried under nitrogen.
It sounds dangerous, that Piranha solution. If you're going to use it, be careful! ...Especially if you're misappropriating the ethanol.
August 13, 2021
A graphic from the article:
There are people selling, in my view, panic.
On this website, I have twice encountered the name of Dr. Eric Topol, who seems to be selling panic for the reward of some kind of fame.
Not all scientists are immune from human frailty, including the spread of hype and outright misinformation.
While I am not claiming to be a Covid expert myself - surely I am not - as a scientist involved in the treatment of human disease, I have been closely monitoring the scientific literature. It may be true that at some point, variants will arise that will require booster or new vaccines. My view is that we're nowhere near that, and that our chief responsibility is to get other human beings, the stupid resistant types as well as the poor vaccinated.
As for media "experts:" I expressed my view of the need for critical thinking when listening to self declared "experts" elsewhere:
In general, the media's job no longer to provide information, but rather to sell advertising.
Be safe, be well.
COVID boosters for wealthy nations spark outrage
The news item I'll discuss in this post comes from the prominent scientific journal Nature. It's here: COVID boosters for wealthy nations spark outrage: COVID boosters for wealthy nations spark outrage. It's probably open source, no subscription required.
It is important to note that like Climate Change, another international disaster that has become highly politicized, Covid involves all humanity. In my view, it is our responsibility in the first world to attend to the third world. We can do this because we are good and noble people, or we can do this for selfish self-interest; it doesn't matter.
The Delta variant, for which the mRNA vaccines are highly effective at saving lives, arose in India, probably among the poor but certainly among the unvaccinated.
Some text from the news item:
Israel has announced plans to begin giving booster shots to older adults next week, in the hope of increasing their protection against COVID-19 — and a number of other wealthy countries are considering the same. But global-health researchers warn that this strategy could set back efforts to end the pandemic. Each booster, they say, represents a vaccine dose that could instead go to low- and middle-income countries, where most citizens have no protection at all, and where dangerous coronavirus variants could emerge as cases surge.
Data do not yet show that extra doses are needed to save lives, researchers say, except perhaps for people with compromised immune systems, who might fail to generate much of an antibody response to the initial COVID-19 shots.
COVID vaccines to reach poorest countries in 2023 — despite recent pledges
An internal analysis from the World Health Organization (WHO) estimates that if the 11 rich countries that are either rolling out boosters or considering it this year were to give the shots to everyone over 50 years old, they would use up roughly 440 million doses of the global supply. If all high-income and upper-middle-income nations were to do the same, the estimate doubles.
The WHO maintains that these shots would be more useful for curbing the pandemic if they were sent to low- and lower-middle-income countries, where more than 85% of people — some 3.5 billion — haven’t had a single jab. “The priority now must be to vaccinate those who have received no doses,” said WHO director-general Tedros Adhanom Ghebreyesus at a briefing on 12 July.
All of the COVID-19 vaccines authorized by most high-income countries reduce a person’s risk of hospitalization and death by more than 90%. Scientists don’t yet know how much more a booster — typically an extra jab of an mRNA-based vaccine on top of the standard doses — would protect the average person, although data are beginning to trickle in. The effects of not receiving any vaccine are more certain. On the African continent, where only 2% of people have been vaccinated, COVID-19 rates are escalating, with fatality rates higher than the global average...
...What’s more, evolutionary biologists say that countries with low vaccination coverage are ripe for the emergence of further dangerous variants of the coronavirus SARS-CoV-2. “Right now, our destiny relies on distributing vaccines so that continued transmission doesn’t occur,” says Nahid Bhadelia, director of the Center for Emerging Infectious Diseases Policy and Research at Boston University in Massachusetts. “We don’t want to be chasing our tail in terms of new variants.”
Contemplating boosters
Israel is not alone in considering boosters for older people. Spurred partly by data1 suggesting that antibody levels wane over time, the United Kingdom has drawn up plans — but not given final approval — for a booster programme to begin in September for older people, front-line health workers and others at high risk of COVID-19...
Data do not yet show that extra doses are needed to save lives, researchers say, except perhaps for people with compromised immune systems, who might fail to generate much of an antibody response to the initial COVID-19 shots.
COVID vaccines to reach poorest countries in 2023 — despite recent pledges
An internal analysis from the World Health Organization (WHO) estimates that if the 11 rich countries that are either rolling out boosters or considering it this year were to give the shots to everyone over 50 years old, they would use up roughly 440 million doses of the global supply. If all high-income and upper-middle-income nations were to do the same, the estimate doubles.
The WHO maintains that these shots would be more useful for curbing the pandemic if they were sent to low- and lower-middle-income countries, where more than 85% of people — some 3.5 billion — haven’t had a single jab. “The priority now must be to vaccinate those who have received no doses,” said WHO director-general Tedros Adhanom Ghebreyesus at a briefing on 12 July.
All of the COVID-19 vaccines authorized by most high-income countries reduce a person’s risk of hospitalization and death by more than 90%. Scientists don’t yet know how much more a booster — typically an extra jab of an mRNA-based vaccine on top of the standard doses — would protect the average person, although data are beginning to trickle in. The effects of not receiving any vaccine are more certain. On the African continent, where only 2% of people have been vaccinated, COVID-19 rates are escalating, with fatality rates higher than the global average...
...What’s more, evolutionary biologists say that countries with low vaccination coverage are ripe for the emergence of further dangerous variants of the coronavirus SARS-CoV-2. “Right now, our destiny relies on distributing vaccines so that continued transmission doesn’t occur,” says Nahid Bhadelia, director of the Center for Emerging Infectious Diseases Policy and Research at Boston University in Massachusetts. “We don’t want to be chasing our tail in terms of new variants.”
Contemplating boosters
Israel is not alone in considering boosters for older people. Spurred partly by data1 suggesting that antibody levels wane over time, the United Kingdom has drawn up plans — but not given final approval — for a booster programme to begin in September for older people, front-line health workers and others at high risk of COVID-19...
A graphic from the article:
There are people selling, in my view, panic.
On this website, I have twice encountered the name of Dr. Eric Topol, who seems to be selling panic for the reward of some kind of fame.
Not all scientists are immune from human frailty, including the spread of hype and outright misinformation.
While I am not claiming to be a Covid expert myself - surely I am not - as a scientist involved in the treatment of human disease, I have been closely monitoring the scientific literature. It may be true that at some point, variants will arise that will require booster or new vaccines. My view is that we're nowhere near that, and that our chief responsibility is to get other human beings, the stupid resistant types as well as the poor vaccinated.
As for media "experts:" I expressed my view of the need for critical thinking when listening to self declared "experts" elsewhere:
In general, the media's job no longer to provide information, but rather to sell advertising.
This requires the use of click bait in internet times.
It is reasonable to ask who exactly "Eric Topol" is, and what is his area of expertise?
I did this, since I never heard of him, by entering his name in Google Scholar and looking at his most recent publications. He's done a lot of work on telemedicine.
While some of his primary papers in the last year relate to Covid, many do not. Opening a few of them leads me to suspect that he is not the world expert in virology.
There is lots and lots and lots and lots and lots of papers published on the subject of the Delta variant, and his remarks do not strike me, even remotely, as consistent with what I read in broader scientific publications.
As for the Nymag reporter, and his choice of whom to designate as the absolute authority, I stand by my claim that one can usually not get a degree in journalism of one has passed a college level science course with a grade of C or better.
Dr. Topol may be a fine scientist, but he is certainly not the only scientist on the planet studying Covid-19, by a long stretch.
If one searches "Delta variant" and BNT162b2 one can see hundreds of papers. The one that comes up for me "Since 2021," is this one from the New England Journal of Medicine, published a week or so ago: Effectiveness of Covid-19 Vaccines against the B.1.617.2 (Delta) Variant
It's a little less panicked than Dr. Topol, with all due respect.
It is reasonable to ask who exactly "Eric Topol" is, and what is his area of expertise?
I did this, since I never heard of him, by entering his name in Google Scholar and looking at his most recent publications. He's done a lot of work on telemedicine.
While some of his primary papers in the last year relate to Covid, many do not. Opening a few of them leads me to suspect that he is not the world expert in virology.
There is lots and lots and lots and lots and lots of papers published on the subject of the Delta variant, and his remarks do not strike me, even remotely, as consistent with what I read in broader scientific publications.
As for the Nymag reporter, and his choice of whom to designate as the absolute authority, I stand by my claim that one can usually not get a degree in journalism of one has passed a college level science course with a grade of C or better.
Dr. Topol may be a fine scientist, but he is certainly not the only scientist on the planet studying Covid-19, by a long stretch.
If one searches "Delta variant" and BNT162b2 one can see hundreds of papers. The one that comes up for me "Since 2021," is this one from the New England Journal of Medicine, published a week or so ago: Effectiveness of Covid-19 Vaccines against the B.1.617.2 (Delta) Variant
It's a little less panicked than Dr. Topol, with all due respect.
Be safe, be well.
August 12, 2021
There is a rather detailed report on the experimental procedures which I will not repeat in detail here, as I haven't much time for detailed discussion.
The authors did not utilize discarded solar cells as the model for the concentrations at which they tested, but rather modeled their work on the known tellurium concentrations associated with silver and gold mine tailings in Japan, and tellurium concentrations measured near a nickel refinery in the UK.
The cells were treated with disodium telluride, similar to the chemical species one would expect to leach from cadmium telluride.
The determination of the proteome of the Bacillus subtilis strain 168 utilized in the experiment was not determined experimentally, but rather the proteome was downloaded from Uniprot as FASTA text files and the cysteine residues therein were counted. This is a relatively simple procedure. I've done it lots of times myself. If you've worked with Uniprot using mass spectrometry to confirm results, it's incredibly accurate.
They considered the sequences of 739 bacterial proteins.
The authors also used a program with which I'm not familiar, CELLO, to localize the proteins within the bacterial cell walls.
Cool...
Some results:
Figure 1:
The caption:
Another picture involving tellurium speciation using two x-ray absorption techniques, XANES and EXAFS
The caption:
Table 1 is rather technical, but for completeness, is below:
The caption:
Another figure:
The caption:
The authors argue that the tellurium adhering to the surface of bacterial walls will not be transported into cells, killing them:
They conclude:
Solar cells can be expected to become landfill in about 20-25 years, and since their massive production has only provided trivial energy, the expectation of increasing their distribution by orders of magnitude will involve massive amounts of distributed electronic waste on a scale dwarfing the already intractable amounts of this waste.
Note that the release of tellurium from cadmium telluride will also mobilize cadmium, the toxicity of which is also connected with cysteine residues in zinc proteins important for respiration.
Have a nice day tomorrow.
Bacterial driven mechanism for tellurium transport from discarded solar cells in landfills.
The paper I'll discuss in this post is this one: Tellurite Adsorption onto Bacterial Surfaces (Jennifer L. Goff, Yuwei Wang, Maxim I. Boyanov, Qiang Yu, Kenneth M. Kemner, Jeremy B. Fein, and Nathan Yee Environmental Science & Technology 2021 55 (15), 10378-10386).
I think it should be pretty clear, stripped of delusions anyway, that all of the cheering for the solar industry for the last half a century has had no effect whatsoever on climate change. If you haven't noticed, as I have, the whole planet is on fire. That hasn't stopped such cheering, of course, but reality is reality and it is a fact that the rate of degradation of the atmosphere is accelerating, not ameliorating.
Besides the popular lie we tell ourselves that solar energy will save the day, there is a related lie we tell ourselves that involves the widespread belief that solar cells are environmentally benign.
This paper suggests otherwise for a particular solar technology; similar considerations apply to other solar technologies.
The paper refers to the mobilization of tellurium, defined as an "emerging contaminant" via proteomic interactions with bacteria, common organisms in landfills.
A cartoon about what's going on in the paper:
From the introduction:
Tellurium (Te) is a chalcogen used in photovoltaic technologies for the production of low-cost cadmium telluride (CdTe) solar cells(1) and the disposal of CdTe solar panels contributes to environmental contamination when soluble Te is released from buried waste.(2?4) Upon decommissioning and disposal of CdTe photovoltaic devices, Te undergoes redox transformations that form dissolved tellurite [Te(IV), TeO32–] and tellurate [Te(VI), TeO42–] in landfill leachate.(2,3) Tellurite is more toxic than tellurate to the microorganisms involved in biodegradation, and the accumulation of tellurite in landfill leachate causes the inhibition of acetoclastic and hydrogenotrophic methanogenesis.(4) Because tellurite is also toxic to humans,(5,6) there is significant interest in understanding its environmental fate(7,8) and transport to drinking water sources.(2?4)
Microbial interactions can alter the chemical speciation of tellurite in the environment.(9) Diverse microorganisms are able to reduce tellurite to elemental tellurium [Te(0)] and precipitate nanoparticulate Te rods and spheres.(10?12) Microbes also uptake tellurite into their cells,(13?15) where it interacts with intracellular thiols and depletes cytoplasmic reservoirs of glutathione.(16,17) Furthermore, experimental studies with other organisms have shown that tellurite binds to proteins(18) and reacts with cellular enzymes that contain sulfhydryl functional groups.(19)
Bacterial cell surfaces are known to harbor sulfhydryl functional groups(20,21) that adsorb environmental contaminants,(22?25) including selenium (Se),(26) a chalcogen that is chemically similar to Te. A recent spectroscopic investigation by Yu et al.(26) revealed that selenite [Se(IV), SeO32–] binds to bacterial surface thiol sites via the formation of R1S–Se–SR2 organo-selenium complexes. Thiol site densities on bacterial surfaces are generally low, but sulfhydryl-selenium complexes are significantly more stable than Se adsorbed to carboxyl and phosphoryl functional groups.(27) Thus, at environmentally relevant contaminant concentrations, sulfhydryl functional groups on cell surfaces can control bacterial adsorption reactions.(28) Currently, the molecules on bacterial surfaces that host reactive sulfhydryl functional groups are poorly understood, and the adsorption of tellurite onto bacterial cells has not been characterized.
The objective of this study was to examine the mechanism of tellurite binding onto bacterial surfaces. Because tellurite reacts with sulfhydryl-containing molecules,(29,30) and the common soil bacterial species Bacillus subtilis is known to produce cell surface sulfhydryl sites,(21,23,26) we selected B. subtilis to test the hypothesis that bacterial tellurite adsorption is controlled by cell surface thiols...
...The results indicate that sulfhydryl-containing molecules in extracellular polymeric substances (EPS) play a key role in tellurite adsorption onto bacterial surfaces...
Microbial interactions can alter the chemical speciation of tellurite in the environment.(9) Diverse microorganisms are able to reduce tellurite to elemental tellurium [Te(0)] and precipitate nanoparticulate Te rods and spheres.(10?12) Microbes also uptake tellurite into their cells,(13?15) where it interacts with intracellular thiols and depletes cytoplasmic reservoirs of glutathione.(16,17) Furthermore, experimental studies with other organisms have shown that tellurite binds to proteins(18) and reacts with cellular enzymes that contain sulfhydryl functional groups.(19)
Bacterial cell surfaces are known to harbor sulfhydryl functional groups(20,21) that adsorb environmental contaminants,(22?25) including selenium (Se),(26) a chalcogen that is chemically similar to Te. A recent spectroscopic investigation by Yu et al.(26) revealed that selenite [Se(IV), SeO32–] binds to bacterial surface thiol sites via the formation of R1S–Se–SR2 organo-selenium complexes. Thiol site densities on bacterial surfaces are generally low, but sulfhydryl-selenium complexes are significantly more stable than Se adsorbed to carboxyl and phosphoryl functional groups.(27) Thus, at environmentally relevant contaminant concentrations, sulfhydryl functional groups on cell surfaces can control bacterial adsorption reactions.(28) Currently, the molecules on bacterial surfaces that host reactive sulfhydryl functional groups are poorly understood, and the adsorption of tellurite onto bacterial cells has not been characterized.
The objective of this study was to examine the mechanism of tellurite binding onto bacterial surfaces. Because tellurite reacts with sulfhydryl-containing molecules,(29,30) and the common soil bacterial species Bacillus subtilis is known to produce cell surface sulfhydryl sites,(21,23,26) we selected B. subtilis to test the hypothesis that bacterial tellurite adsorption is controlled by cell surface thiols...
...The results indicate that sulfhydryl-containing molecules in extracellular polymeric substances (EPS) play a key role in tellurite adsorption onto bacterial surfaces...
There is a rather detailed report on the experimental procedures which I will not repeat in detail here, as I haven't much time for detailed discussion.
The authors did not utilize discarded solar cells as the model for the concentrations at which they tested, but rather modeled their work on the known tellurium concentrations associated with silver and gold mine tailings in Japan, and tellurium concentrations measured near a nickel refinery in the UK.
The cells were treated with disodium telluride, similar to the chemical species one would expect to leach from cadmium telluride.
The determination of the proteome of the Bacillus subtilis strain 168 utilized in the experiment was not determined experimentally, but rather the proteome was downloaded from Uniprot as FASTA text files and the cysteine residues therein were counted. This is a relatively simple procedure. I've done it lots of times myself. If you've worked with Uniprot using mass spectrometry to confirm results, it's incredibly accurate.
They considered the sequences of 739 bacterial proteins.
The authors also used a program with which I'm not familiar, CELLO, to localize the proteins within the bacterial cell walls.
Cool...
Some results:
Reaction of aqueous tellurite with B. subtilis cells resulted in the loss of dissolved tellurium from solution (Figure 1). Adsorption experiments showed that the concentration of adsorbed tellurite increased linearly with the aqueous tellurite concentration with a Kd value of 19.5 ± 5.4 L kg–1. To test if sulfhydryl sites are involved in tellurite adsorption, the membrane-impermeable thiol-specific probe qBBr was used to block the sulfhydryl sites on the bacterial surface. The adsorption isotherms showed significantly less tellurite adsorption by qBBr-treated cells compared to untreated cells. The partition coefficient of the qBBr-treated cells was Kd = 6.6 ± 2.6 L kg–1. The decrease in the tellurite binding constant was attributed to tellurite binding to low-affinity sites on the bacterial surface due to the loss of sulfhydryl complexation on the qBBr-treated cells...
Figure 1:
The caption:
Figure 1. Tellurite adsorption isotherms. Adsorption of tellurite (Te[IV]) on to untreated Bacillus subtilis cells ( ● ) ; cells treated with resin to desorb surface attached EPS ( ? ) ; and cells treated with qBBr to block surface thiol sites ( □ ). All experiments conducted at pH = 7.2.
Another picture involving tellurium speciation using two x-ray absorption techniques, XANES and EXAFS
The caption:
Figure 2. Te K-edge XAS of Te standards and Te adsorbed to B. subtilis. (A) XANES spectra. Arrows indicate the position and amplitude of the white lines for the different Te species; (B) k2-weighed ? (k) EXAFS spectra; (C) Fourier transform of the EXAFS data in the range ?k = 2.5–10.5 Å–1; (D) Shell-by-shell fits of the EXAFS data. Letter designations (A–G) correspond to the EXAFS model listed in Table 1. The ball-and-stick models to the right illustrate the starting tellurite ion and the structure of the binding of the adsorbed Te atoms bound to S-based groups in the biomass.
Table 1 is rather technical, but for completeness, is below:
The caption:
N, R, and ?^(2_ are coordination number, radial distance, and Debye-Waller factor, respectively, for each path used in the fit. ?E is the energy shift relative to the calculated Fermi level. DF = degrees of freedom in the fit, i.e., the difference between the number of independent data points and the number of fit parameters (data were fit between R + ? = 1.1–2.2 Å for Na2-tellurite, 1.5–3.0 Å for metallic Te, 1.0–3.8 Å for TeO2, 1.5–3.0 Å for the Te(IV)-thiol and Te-biomass data). The R-factor is the fractional misfit of the data relative to its amplitude, and is a goodness-of-fit indicator. More details on these fit parameters can be found in FEFFIT’s documentation(43).
bThe amplitude suppression factor S02 was determined to be 0.93 based on the fit of this standard where the O coordination is known to be 3.0; this S02 was then used in all other fits to refine the coordination numbers.
cDue to the overlapping contributions in this spectral region there was significant correlation between the coordination number and the Debye–Waller factor of this shell, so the latter was fixed to the value shown to stabilize the fit.
dThe ?E variables for the two O shells were constrained to be the same.
bThe amplitude suppression factor S02 was determined to be 0.93 based on the fit of this standard where the O coordination is known to be 3.0; this S02 was then used in all other fits to refine the coordination numbers.
cDue to the overlapping contributions in this spectral region there was significant correlation between the coordination number and the Debye–Waller factor of this shell, so the latter was fixed to the value shown to stabilize the fit.
dThe ?E variables for the two O shells were constrained to be the same.
Another figure:
The caption:
Figure 3. Protein and thiol content of B. subtilis EPS. (A) Protein concentration in EPS; (B) Thiol content of EPS collected from early stationary phase cultures. (C) Surface site concentrations of cells with intact EPS (+EPS) and cells with EPS removed (?EPS). Error bars represent the standard deviation of triplicate measurements.
The authors argue that the tellurium adhering to the surface of bacterial walls will not be transported into cells, killing them:
Bioenvironmental Implications
The adsorption of Te(IV) and formation of stable RS–Te–SR components in the EPS are expected to affect bacterial Te(IV) uptake and microbial Te interactions. Previous studies of microbial Te(IV) reduction have largely focused on the chemical reactions that occur after Te enters the cells(16,17,64,65) and have neglected the mechanisms that control Te(IV) binding to the cell surface. Microorganisms can import tellurite into the cell and reduce Te(VI) to Te(0).(13,14) In environmental microbial systems, cell surface adsorption and uptake of tellurite are likely to co-occur to varying degrees depending on EPS production. Our results suggest that microorganisms that produce thiol-rich EPS would bind a significant portion of tellurite outside of the cell, thus limiting the translocation of Te into the cytoplasm and potentially mitigating the deleterious effects of tellurite uptake...
The adsorption of Te(IV) and formation of stable RS–Te–SR components in the EPS are expected to affect bacterial Te(IV) uptake and microbial Te interactions. Previous studies of microbial Te(IV) reduction have largely focused on the chemical reactions that occur after Te enters the cells(16,17,64,65) and have neglected the mechanisms that control Te(IV) binding to the cell surface. Microorganisms can import tellurite into the cell and reduce Te(VI) to Te(0).(13,14) In environmental microbial systems, cell surface adsorption and uptake of tellurite are likely to co-occur to varying degrees depending on EPS production. Our results suggest that microorganisms that produce thiol-rich EPS would bind a significant portion of tellurite outside of the cell, thus limiting the translocation of Te into the cytoplasm and potentially mitigating the deleterious effects of tellurite uptake...
They conclude:
...Finally, our findings have important implications for understanding the environmental fate of Te adsorbed to bacterial surfaces. If high-affinity tellurite binding sites on bacteria are associated with loosely attached molecules on the cell surface, then the adsorbed organo-tellurium components can be released into aqueous solution as soluble organic matter when the EPS is destabilized. The attachment of EPS to cells is controlled, in part, by electrostatic interactions.(68) Thus, changes in environmental factors such as pH, salinity, and groundwater composition can trigger EPS detachment from the cell surface and render the organo-tellurium species mobile for transport. Of particular interest is the stability of cysteine-rich proteins in the EPS which have high thiol site densities and likely have the greatest contribution to tellurite binding. The results of our study indicate that quantification of these sulfhydryl-containing molecules and the incorporation of protein-specific complexation reactions into surface complexation models will enable better predictions of how bacterial adsorption affects tellurite transport in landfills and other contaminated sites.
Solar cells can be expected to become landfill in about 20-25 years, and since their massive production has only provided trivial energy, the expectation of increasing their distribution by orders of magnitude will involve massive amounts of distributed electronic waste on a scale dwarfing the already intractable amounts of this waste.
Note that the release of tellurium from cadmium telluride will also mobilize cadmium, the toxicity of which is also connected with cysteine residues in zinc proteins important for respiration.
Have a nice day tomorrow.
August 7, 2021
I recently listened to a lecture by one of the authors of the paper from this graphic who explained that San Diego's subjects were ethnically diverse, Denver's mostly Caucasian, Baltimore's mostly African American, and Cape Town, of course, African although whether the Cape Town subjects were mostly native African and/or Euro-Africans. The near homology with the Baltimore subjects suggests the former. (Note this data was accumulated in the context of other studies, and was not generated in studies connected with determining allele frequency.)
"Tregitope" is a compound word; like German, although not quite as broadly, English allows for compound words. "Tregitope" is a compound word of "Treg" for regulatory T-Cells, T-cells that shut off immune responses after the antigen insult has been addressed. The "-itope" is a truncation of "epitope," an "epitope" being the business sequence of a protein, a short sequence of those amino acids that actually bind to a target, whether the target is actually an antigen like, say, the S-Protein of SARS-Cov-2 of Covid frame, or a physiological target for instance for the release of digestive enzymes, or binding to a receptor that increases heart rate during exercise. The bulk of many proteins is actually involved in exposing, hiding, or changing the geometry of epitopes.
Anyway, Cockroach immune responses - in this case allergies - can make you feel horrible, and/or even kill you.
From the introductory text of the open sourced paper:
I added the bold so you can see the good...I mean bad...part.
A picture of mouse lung cells from cockroach allergic mice and normal mice and those injected with the vehicle but not the allergen (sham mice):
Figure 3
The caption:
As for the word "poverty" in the title of this post, coupled with the (hopefully recognized as sarcastic) word "fun," I don't know whether you've ever lived around cockroaches, but I have, but only in those "fun" portions of my life where I was, um, "down and out."
This rather ignored issue, allergies to cockroaches, may be just one reason that life-expectancy is lower for the impoverished than for the relatively wealthy or, for that matter, the super wealthy.
If this paper is to be believed, cockroach exposure can kill people.
I have convinced myself, to the extent that I consider social issues and recognizing some over-simplification, that many of the world's most intractable problems are related to poverty. There is a difference between a person who parks his shiny new Tesla electric car in the driveway of his McMansion, its roof strewn with solar cells, so all his or her neighbors know how "green" she or he is, and a person who is trying to keep the babies alive by pouring contaminated water over them in an extreme heat outbreak. If the latter person has to burn coal to run a pump to get the water, or have someone else burn coal to do so, they are not likely to have the time or energy to worry about climate change.
I often hear from people whose per capita climate impacts are greater than those of 50 citizens of the Central African Republic that "population" is the problem. In cultures where the future of elderly adults in entirely contingent on care by their offspring, and where infant and child mortality is high, one may be inclined to have more children to address the probability of having someone to care for them. This is why, I suspect, that birthrates are below the replacement rate in precisely those countries where people can feel secure with healthcare, are secure in their homes, and have access to health care, generally.
Simplistic, to be sure, but I may be on to something.
Bill Gates's children didn't have a cockroach allergy problem. Neither did mine.
But I'd guess billions of people do.
Have a pleasant weekend.
Fun With Poverty: The Immunology of How Cockroaches Make People Sick.
The paper to which I'll refer in this post is this one: Prangtaworn, P., Chaisri, U., Seesuay, W. et al. Tregitope-linked Refined Allergen Vaccines for Immunotherapy in Cockroach Allergy. Sci Rep 8, 15480 (2018). The article is open sourced, anyone can read it.
There's therefore no need for me to excerpt a lot of it, but I'll make a few editorial comments before posting some brief excerpts and a graphic or two.
It is my privilege to be asked serious questions to explain subjects about which I know nothing at all. This inspires me to find things out. This brief post is about one of those adventures.
Over the years, I've garnered some impressions of immunology by osmosis, mostly connected with proteomics issues in my work, and of course, Covid has inspired additional desultory interest in the subject, but effectively, I know nothing at all. So this weekend I'm watching recorded lectures on the topic and reading lots and lots of papers on the subject. It really is fascinating, thrilling actually, particularly since the immune system, as recorded on chromosome six, can illuminate the disease history of various ethnic groups, going back tens of thousands, hundreds of thousands of years. There are very real genetic differences between ethnic groups with respect to their immune systems.
This is shown in a graphic, with some explanation required, from this paper: McKinney, D.M., Southwood, S., Hinz, D. et al. A strategy to determine HLA class II restriction broadly covering the DR, DP, and DQ allelic variants most commonly expressed in the general population. Immunogenetics 65, 357–370 (2013):
The caption:
Allelic coverage. The HLA class II alleles represented in the panel of 46 single transfected cell lines provide coverage of the majority of HLA class II types expressed in a cohort of 190 donors recruited for two different studies in the San Diego area. The fraction of all donors for which the panel provides coverage of zero to eight possible class II types expressed is shown in the bar graph (a). The cumulative fraction of donors covered is shown in the line plot (a). This coverage is consistent across different donor cohorts from geographically disparate regions (b)
I recently listened to a lecture by one of the authors of the paper from this graphic who explained that San Diego's subjects were ethnically diverse, Denver's mostly Caucasian, Baltimore's mostly African American, and Cape Town, of course, African although whether the Cape Town subjects were mostly native African and/or Euro-Africans. The near homology with the Baltimore subjects suggests the former. (Note this data was accumulated in the context of other studies, and was not generated in studies connected with determining allele frequency.)
"Tregitope" is a compound word; like German, although not quite as broadly, English allows for compound words. "Tregitope" is a compound word of "Treg" for regulatory T-Cells, T-cells that shut off immune responses after the antigen insult has been addressed. The "-itope" is a truncation of "epitope," an "epitope" being the business sequence of a protein, a short sequence of those amino acids that actually bind to a target, whether the target is actually an antigen like, say, the S-Protein of SARS-Cov-2 of Covid frame, or a physiological target for instance for the release of digestive enzymes, or binding to a receptor that increases heart rate during exercise. The bulk of many proteins is actually involved in exposing, hiding, or changing the geometry of epitopes.
Anyway, Cockroach immune responses - in this case allergies - can make you feel horrible, and/or even kill you.
From the introductory text of the open sourced paper:
Cockroach (CR) is a pestiferous source of human pathogen and allergen1,2. Exposure to CR-derived proteins is associated with high risk of developing allergies, including allergic dermatitis, allergic rhinitis, and atopic asthma3. It has been reported that 26–61% of allergic patients have positive skin test to cockroach extract4,5,6,7. Morbidity caused by CR allergens is usually more severe and prolonged than morbidity caused by other indoor allergens, such as house dust mites (HDM) and pets8. After allergen exposure, the sensitized subject develops predominant Th2 immune response9,10,11. Specifically, naïve CD4+ T cells transform to Th2 cells, which produce the following Th2 cytokines: interleukin (IL)-4, IL-5, IL-9, and IL-13. The immune response may be aggravated by IL-25, IL-31, and IL-33 produced by activated T cells, alveolar macrophages, epithelial cells, and dendritic cells (DCs)10,11,12,13,14. Secreted IL-4 and IL-13 influence class-switching of B cells to secrete an excessive amount of specific IgE that fixes to Fc epsilon receptors (Fc?RI) on the surface of tissue mast cells and blood basophils. The sensitized subject also has allergen-specific memory B and Th2 cells, and a high level of serum IgE. Upon re-exposure, the allergen cross-links IgE located on the surface of sensitized mast cells and basophils, causing the cells to release mediators that result in allergic symptoms that can be as severe as atopic asthma or life-threatening immediate anaphylaxis...
I added the bold so you can see the good...I mean bad...part.
A picture of mouse lung cells from cockroach allergic mice and normal mice and those injected with the vehicle but not the allergen (sham mice):
Figure 3
The caption:
Histological appearances and grades of lung sections of mice after staining with Periodic Acid-Schiff (PAS). (A–D) Grades 0–3, respectively, of goblet cells (stained pink/red; black arrow heads) in the lung epithelia. (E) Comparative average goblet cell grades of normal, sham and allergenized mice. The allergenized mice had significantly higher average goblet cell grade than the normal and sham mice (p??0.05).
As for the word "poverty" in the title of this post, coupled with the (hopefully recognized as sarcastic) word "fun," I don't know whether you've ever lived around cockroaches, but I have, but only in those "fun" portions of my life where I was, um, "down and out."
This rather ignored issue, allergies to cockroaches, may be just one reason that life-expectancy is lower for the impoverished than for the relatively wealthy or, for that matter, the super wealthy.
If this paper is to be believed, cockroach exposure can kill people.
I have convinced myself, to the extent that I consider social issues and recognizing some over-simplification, that many of the world's most intractable problems are related to poverty. There is a difference between a person who parks his shiny new Tesla electric car in the driveway of his McMansion, its roof strewn with solar cells, so all his or her neighbors know how "green" she or he is, and a person who is trying to keep the babies alive by pouring contaminated water over them in an extreme heat outbreak. If the latter person has to burn coal to run a pump to get the water, or have someone else burn coal to do so, they are not likely to have the time or energy to worry about climate change.
I often hear from people whose per capita climate impacts are greater than those of 50 citizens of the Central African Republic that "population" is the problem. In cultures where the future of elderly adults in entirely contingent on care by their offspring, and where infant and child mortality is high, one may be inclined to have more children to address the probability of having someone to care for them. This is why, I suspect, that birthrates are below the replacement rate in precisely those countries where people can feel secure with healthcare, are secure in their homes, and have access to health care, generally.
Simplistic, to be sure, but I may be on to something.
Bill Gates's children didn't have a cockroach allergy problem. Neither did mine.
But I'd guess billions of people do.
Have a pleasant weekend.
August 5, 2021
It came up under my Google Scholar alert for "liquid plutonium."
I downloaded it, and hope I'll find time to at least excerpt it. It's rather long, over 800 pages. I seldom read any book from cover to cover.
Issues considered:
About the author:
I never heard of him until now.
Now this looks like an interesting read...
The History and Future of Technology: Can Technology Save Humanity from Extinction?It came up under my Google Scholar alert for "liquid plutonium."
I downloaded it, and hope I'll find time to at least excerpt it. It's rather long, over 800 pages. I seldom read any book from cover to cover.
Issues considered:
Benefits
Along the way, you will consider
If the human race can survive without fossil fuels
If we can decarbonize completely
If we can stabilize the global climate before it is too late
If solar and wind power alone can be self-sufficient
If we will need conventional nuclear power
If our descendants in 2120 will have thermonuclear fusion
If our descendants in 2120 will ride in private automobiles
If nuclear families will live in private suburban houses
If there is a viable technological strategy to recovering biological diversity
What technologies can protect us from future mutant viruses
If artificial intelligence will permit robots to become our future masters
Along the way, you will consider
If the human race can survive without fossil fuels
If we can decarbonize completely
If we can stabilize the global climate before it is too late
If solar and wind power alone can be self-sufficient
If we will need conventional nuclear power
If our descendants in 2120 will have thermonuclear fusion
If our descendants in 2120 will ride in private automobiles
If nuclear families will live in private suburban houses
If there is a viable technological strategy to recovering biological diversity
What technologies can protect us from future mutant viruses
If artificial intelligence will permit robots to become our future masters
About the author:
Professor Ayres holds a PhD in Mathematical Physics from Kings College, University of London, a MSc in Physics from the University of Maryland and a BA, BSc from the University of Chicago. He is currently Emeritus Professor of Economics and Political Science and of Technology and Operations Management at INSEAD, the international graduate business school.
He joined INSEAD in 1992, becoming the first Sandoz (now Novartis) Chair of Management and the Environment, as well as the founder of CMER, Center for the Management of Environmental Resources. He directed CMER from 1992-2000. Since retirement he has been a visiting professor at Chalmers Institute of Technology in Sweden (where he was also a King's Professor) and Institute Scholar at the International Institute for Applied Systems Analysis (IIASA) in Austria. He remains active, producing publications on topics ranging from Industrial Metabolism and Industrial Ecology, through Environmental Policy and Environmental Economics, to Energy. Professor Ayres is the author or coauthor of 21 books, most recently including The Economic Growth Engine (2009, with Benjamin Warr), Crossing the Energy Divide (2009, with Edward Ayres) and Bubble Economy (2014), Energy, Complexity and Wealth Maximization (2018) and “On Capitalism and Inequality” (2020).
He joined INSEAD in 1992, becoming the first Sandoz (now Novartis) Chair of Management and the Environment, as well as the founder of CMER, Center for the Management of Environmental Resources. He directed CMER from 1992-2000. Since retirement he has been a visiting professor at Chalmers Institute of Technology in Sweden (where he was also a King's Professor) and Institute Scholar at the International Institute for Applied Systems Analysis (IIASA) in Austria. He remains active, producing publications on topics ranging from Industrial Metabolism and Industrial Ecology, through Environmental Policy and Environmental Economics, to Energy. Professor Ayres is the author or coauthor of 21 books, most recently including The Economic Growth Engine (2009, with Benjamin Warr), Crossing the Energy Divide (2009, with Edward Ayres) and Bubble Economy (2014), Energy, Complexity and Wealth Maximization (2018) and “On Capitalism and Inequality” (2020).
I never heard of him until now.
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