Buyback Blackout Period Is Over, And 10 More Reasons Why Goldman Calls The End Of The Market Carnage

 Two weeks ago, when looking at a recent matrix of market bull and bear cases, we asked if it was time to get bullish on stocks and concluded that the since fundamentals leaned in either direction, the answer was most likely “not yet” for one simple reason: JPM’s resident permabull, Marko Kolanovic, had just turned from modestly bearish – an extremely rare stance for him – to bullish again, urging his clients to reverse from taking profits (unclear on what exactly since he had been bullish all the way down from the market’s all time high)…

… to buying the dip again. Meanwhile, at roughly the same time, the far more accurate strategists at Goldman’s flow desk – in this case Tony Pasquariello - had just warned that the market was likely to be well lower in several weeks time, not higher. After last week’s furious rout in the market they were right.

Which is why we find it worth mentioning that after correctly calling the market’s downward inflection point in April, those same Goldman folks are once again leaning bullish, and in a Friday note from Goldman Scott Rubner (which is not for mass distribution to the bank’s entire client base and instead is reserved for a handful of the bank’s top client as it indicate what the bank’s traders actually do believe, it is also available to zero hedge professional subscribers), he says that the worst is behind us and gives 11 reasons why the late April rout may have been the market bottom for the time being.

Rubner’s argument in a nutshell: pointing to Thursday’s explosive move higher as testament of the market’s extremely negative sentiment and low positioning (which of course was followed by Friday’s rout), the Goldman trader thinks that global stocks will rally “significantly” in May as the flow-of-funds is set to improve starting on Monday (even though the closely watched 50bps rate hike FOMC meeting is due on May the 4th).

Below we lay out Rubner’s bullish 11-point checklist in greater detail.

• 1. US Corporates return back to the open window on Monday with dry powder. Rubner calculates $5BN of demand per day, every day until mid-June. US corporates are the largest buyer of equities in 2022 and have authorized record YTD (AAPL = $90bn; GOOG = $70bn; MSFT = $60bn; FB = $50bn, etc).
• 2. Pensions flipped to buy given the recent outperformance of bonds vs stock. This should carry over into next week.
• 3. S&P Index gamma turned negative on Thursday for the first time since March.
• 4. Synthetic Short Gamma through CTA and Vol-Control strategies supply will fade over the next week (Thursday’s move will lower some of the supply expectations and Goldman’s estimates will dramatically change next week).
• 5. Liquidity is simply not available to try to cover liquid macro. As we noted on several occasions last week [insert hyperlink to liquidity tweet], top book liquidity in the S&P 500 futures is $2.8M. This ranks in the 1st percentile in the last 10-years. This is as low as it gets.
• 6. Sentiment is the most bearish since the market crash lows in March 2009. Rubner says that he has done “more bearish zoom calls these past two weeks, than I can recall.” The bears (AAIIBEAR) published a reading of 59.40 today. This was the highest level since March 5th 2009 (70.27). S&P500 rallied 8.54% in March 2009 and 9.39% in April of 2009. That was the generational market bottom.
• 7. Money Market Inflows Logged a massive +$60B inflows last week, which was the largest weekly inflow since Covid 2020 (and typically another fear gauge).

• 8. For the fixed income watchers, Goldman’s CTA models show some impressive demand. Goldman has +$20B of bonds to buy in a flat tape, but +$117B of bonds to buy in an up tape, and $37B of bonds to buy in a down tape. This should ease some of the pressure on long duration equities and largest construction of market cap.
• 9. Goldman’s Prime Desk notes that hedge funds exposure is dismal. Gross and Net Exposure are currently at 2-year lows. And vs the past 5 years, Gross ranks in the 21st and Net ranks in the 38th. US TMT Megacap L/S ratio declined by -48% in the past 1-month. (~right before earnings)
• 10. Everyone is short: Short leverage (with options) ranks in the 98th percentile in the last 5 years.
• 11. New month = New Inflows. There should be some decent inflows to start May per normal rebalancing cycle in retirement accounts.

* * *

Rubner then does a more detailed breakdown of what the latest flows indicate for markets. We excerpt from the main points below (professional subscribers have access to the full note).

1. Passive USA Large Cap Outflows (and resulting MOC 3:50pm imbalances): = “you ask me for money and I sell”

• US Equity Funds registered their largest outflows of 2022.

• b) US large cap Equity funds registered the largest outflows since 2018.

• c) this is LIFO (last in, first out) behavior. This is where all of the new repatriated safe haven has flowed.

* * *

2. “Everything cross-asset outflow” - this is rare. Stocks, Bonds, and Cash all saw outflows this past week

• You don't see this very often. This is what we call an everything outflow. No lines saw inflows, and its back to checking accounts.

* * *

3. Retail Investors buyers of 0-1 DTE (days-to-expiry) puts are largest on record – does retail start buying calls again?

• Friday's same-day SPX were the highest dollar-volume ever traded for a single expiry on a single day
• $225bln of puts and $160bln notional of calls traded
  • Already in 12 figures on Friday’s SPX expiration - $105bln in just the the first hour. Keep an eye on DTEs
• Daily option volume Notional volume ($bln) traded in listed US equity options

Final-day trading volume: Notional SPX option volume traded on the day of expiration, excluding Third Friday and end-of-month expirations

* * *

4. Both Professional and Retail Sentiment have reached new lows. Rules and Tools have historically marked a contrarian indicator.

• GS sentiment indicator (SI) current reading of -2.2 is a signal of extremely light positioning and typically acts as a solid contra indicator for the market. Out of 687 weekly readings (first recording: 2/27/09), there have only been 14 instances in which the sentiment indicator was more negative (below -2.2).

• AAIIBULL (bullish investors) reached the 9th lowest reading since 1987 (1820) observations (zeroth percentile).

• Market returns after such extremely negative readings have been uniformly bullish, and the hit rate six months after such a reading is 100% (14 of 14 occasions), leading to a median 19% return!

 * * *

5. Futures Positioning has been unwound and ranks in the 15th percentile over the past 10 years.

• For context, the high futures position for 2022 was +$138.4B (January 25th ) vs. +$10B currently.

* * *

6. Peak Blackout is behind us. US Corporates return from the blackout window on May 2nd (Monday). The largest buyer of equities in 2022 has been out of the market for much of April and is now back.

• 51% of the S&P 500 reported last week. This is the largest week for earnings in Q1. Corporates are slowing re-emerging from the blackout.

• 2022 US corporate authorizations are off to the best year on record. Do they come back to buy stocks at these levels having already authorized? Do we hear about more big authorizations this week?

• GS buyback activity last week was 2.4x the bank’s average 2021 levels - despite being in the earnings 'blackout window.’ the bank estimates ~59% of companies will emerge by this time next week

* * *

7. S&P Index Gamma (no longer long) given institutional “forced hedging” of May puts – do we see monetization of puts after the big FOMC event next week?

Dealer long gamma has been unwound, and works in both directions. This will exacerbate, not buffer moves in the same direction as the market.

* * *

8. Systematic Equity Supply is far smaller than some have feared given recent deleveraging.

• Goldman calculates that CTA strategies have to sell $8B over the next 1 week and $21B to sell over the next month.
• In an up tape, CTA strategies have up to buy $78B vs. down tape -$81B to sell. Said otherwise, they will continue to trade negative synthetic gamma in the same direction as the market

* * *

9. Synthetic fixed income short gamma (CTA strategies) have triggered flip levels. Does FI demand ease pressure on rate move and long duration equities?

• Bond yields lower = SPX construction higher? This might be important chart for equity traders given the large cap tech weighting of the indices.

* * *

10. S&P 500 Top Book Liquidity “works in both directions”

• Liquidity in the most liquid equity future in the world ranks in the 7th percentile in the past 10 years, and offers just $6M to trade on the screens.

* * *

12. Seasonals – “Sell in May and Go Away” this year? Positioning is already too low to sell from here. (30-yr look back)

• This chart will matter if and when May inflows come back.

* * *

13. HF Leverage Exposure remains at cycle lows, does May the 4th become another clearing event and quick adding back of exposure?

• Overall book Gross leverage +1.0 pts to 228.4% (5th percentile one-year) and Net leverage -0.6 pts to 72.9% (lowest since May ‘20). Overall book L/S ratio -0.9% to 1.937 (lowest since May ‘20).
• Fundamental L/S Gross leverage +1.3 pts to 172% (6th percentile one-year) and Fundamental L/S Net leverage -1.1 pts to 49.3%, near the lowest levels since Apr ‘20.

As Rubner concludes, “choppy and wide trading range continues but market technicals flip in favor of the bulls for may.” One thing is clear: the market can’t take much more pain without the Fed having to step in – we are talking the proverbial “flush” - no matter how much Biden berates Powell into standing to the side as stocks crash if it somehow means that inflation will shrink – and boost Biden’s approval rating - just because we enter a bear market. Incidentally, we wonder if Biden’s handlers have considered what will happen to the president’s approval rating if in additional to a stagflationary recession, the president were to also add a market crash to his list of achievements.

https://www.zerohedge.com/markets/buyback-blackout-period-over-and-10-more-reasons-goldman-calls-end-market-carnage

RI Bill Fines Parents For Unvaxxed Kids And Doubles Income Taxes

 An absurd COVID-19 bill by radical leftist Road Island Senator Samuel W. Bell says that residents who refuse the vaccine and its booster shots are subjected to fines and pay more income tax unless they receive an exemption. 

Bell introduced Rhode Island Senate Bill S2552 on March 1. As of last week, the bill had not been passed into law is currently in review by the Senate Health and Human Services committee. 

S2552 states eligible Rhode Island residents would have to be vaccinated against COVID. If they reject, they could face a $50 monthly fine and pay double the state income tax. There are also fines for unvaccinated children under the age of 16 that would be imposed on the parents. Text from the bill reads:

This act would mandate all residents sixteen (16) years or older to be vaccinated against COVID-19. If a resident is under sixteen (16) years of age, the resident would be required to be immunized against COVID-19, with the responsibility for ensuring compliance falling on all parents or guardians with medical consent powers.

Additionally, any person who violates this chapter would be required to pay a monthly civil penalty of fifty dollars ($50.00) and would owe twice the amount of personal income taxes.

Talking about the bill, Bell told the Boston Globe:

"The reason I introduced the bill is we have a crisis with the pandemic.

"Thousands of Rhode Islanders have died. I've had really painful calls from constituents who can't go to the store because they're immuno-compromised, who have lost loved ones to this pandemic, who are really ill and not fully recovered, suffering long-term effects."

Bell has faced harsh criticism for the introduction of the bill. He tweeted this email he received from one angry Rhode Islander. 

Subjecting adults to fines and more taxes for not being vaxxed or even their kids not being vaxxed is a significant overreach by government. Also, the vaccine is not risk-free, especially for children.

Dr. Robert Malone, a virologist and immunologist who has contributed to the technology of mRNA vaccines, recently said: "Think twice before you vaccinate your kids. Because if something bad happens, you can't go back and say, 'whoops, I want a do-over.'"

https://www.zerohedge.com/political/new-covid-bill-fines-parents-unvaxxed-kids-and-doubles-income-taxes

California Expands Medi-Cal To Adults 50 And Up, Regardless Of Immigration Status

 by Vanessa Serna via The Epoch Times (emphasis ours),

California will extend Medi-Cal health care coverage to more than 185,000 residents 50 years and older, regardless of their immigration status starting May 1.

“This is an investment in our people, our economy, and our future,” Gov. Gavin Newsom said in an April 29 statement.

This Medi-Cal coverage extension was a part of Assembly Bill 133, which was voted into law in July 2021, following Newsom’s proposal to expand health care to low-income residents and address “health disparities and inequities, especially among populations of color” during the COVID-19 pandemic, according to the statement.

Medi-Cal currently provides low-income individuals under the age of 25 or above the age of 65, pregnant women, and those with disabilities with free or low-cost medical and dental care.

Until recently, Medi-Cal was only available for U.S. citizens in the state, except for refugees staying in the country temporarily.

“We’re delivering concrete results for Californians, continuing to fulfill the promise of a Healthy California for All, and I encourage all those eligible to take advantage of these essential health services,” Newsom said.

Looking forward, Newsom has also proposed expanding Medi-Cal coverage to about 700,000 people from ages 26 to 49, regardless of their immigration status by January 2024.

https://www.zerohedge.com/political/california-expands-medi-cal-adults-50-and-older-regardless-immigration-status

Spinal oxygen sensors critical sensors for when body has low to no oxygen

 University of Calgary researchers have identified a new oxygen sensing mechanism in a small population of spinal cord neurons capable of protecting the brain and other vital organs from low oxygen (hypoxia). As blood oxygenation decreases mammals mount a cardiorespiratory response and prioritize oxygen supply to vital organs. The team discovered the kick-start to that rescue response are spinal oxygen sensors (SOS) that trigger activation of the sympathetic and respiratory nervous system.

"Understanding how the central nervous system regulates oxygen supply is of considerable scientific and medical importance," say Dr. Nicole Barioni, PhD, first author on the study. "Hypoxia can lead to cognitive decline, memory impairment and in extreme circumstances such as heart attack, stroke or sudden infant death syndrome (SIDS), can be fatal."

The study, published in Science Advances, is the first to definitively demonstrate the existence of spinal oxygen sensors. The result of eight years of research by Barioni and principal investigator, Dr. Richard Wilson, PhD.

"What started with a late-night experiment in the lab with some mates and a post-pizza surprise discovery turned into an epic multi-year international science project to determine mechanism. Without the tireless energy and brilliance of Nicole and the rest of the team, this important contribution would not have been possible," says Wilson.

Due to the unique way in which the SOS work, they are geared to be important for wide-ranging physiological regulation in health, chronic disease, spinal cord injury and cardiorespiratory crisis.

The study suggests the SOS use a novel oxygen sensing mechanism involving two yin and yang-like oxygen-dependent enzymes. These enzymes compete for the same molecules. When oxygen is abundant one enzyme wins. Only when oxygen falls does the other enzyme take over, using the remaining oxygen to generate signaling factors. These signalling factors then activate a cascade of events leading to neuronal excitation and sympathetic activation.

"Unlike brainstem neuronal networks controlling breathing, which are largely suppressed by acute hypoxia, sympathetic networks are strongly excited," says Wilson, "Prior to this study identifying the sensors, the way in which these sympathetic networks function in low to no oxygen was not well understood."

Using several novel experimental approaches that isolate different parts of the rodent nervous system to test physiological responses to spinal cord oxygen levels, this study determines that the SOS contribute to sympathetic activation and under extreme circumstances are critical for auto resuscitative reflexes.

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Story Source:

Materials provided by University of Calgary. Original written by Shea Coburn, Hotchkiss Brain Institute. Note: Content may be edited for style and length.

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Journal Reference:

1. Nicole O. Barioni, Fatemeh Derakhshan, Luana Tenorio Lopes, Hiroshi Onimaru, Arijit Roy, Fiona McDonald, Erika Scheibli, Mufaddal I. Baghdadwala, Negar Heidari, Manisha Bharadia, Keiko Ikeda, Itaru Yazawa, Yasumasa Okada, Michael B. Harris, Mathias Dutschmann, Richard J. A. Wilson. Novel oxygen sensing mechanism in the spinal cord involved in cardiorespiratory responses to hypoxia. Science Advances, 2022; 8 (12) DOI: 10.1126/sciadv.abm1444

https://www.sciencedaily.com/releases/2022/04/220422161541.htm

Genetic changes in patients who progress to esophageal cancer

 More and more mutations clutter up our DNA as we age. Mostly, these don't cause problems. But sometimes, a switch will flip, and a mutated cell turns cancerous. Can we see this shift in time to prevent or treat cancer before it starts?

Led by researchers at Fred Hutchinson Cancer Research Center, a scientific team who studies a precancerous condition of the esophagus (called Barrett's esophagus or BE) are working to answer this question. In work published April 28 in Nature Communications, the team revealed that DNA changes in BE cells that presage esophageal cancer can be spotted years before cancer develops.

The characteristic changes include rearrangements of large chunks of DNA and damage to both copies of a tumor-suppressing gene called TP53.

"Most patients who progressed [to esophageal cancer] had two 'hits' [changes that likely inactivate normal gene function] to TP53," said Dr. Thomas Paulson, a senior staff scientist in the Grady Lab who co-led the project. "Cells with altered TP53 had spread to larger regions of the esophagus and persisted over longer periods of time compared to patients who didn't progress to cancer."

Though the team's ultimate goal is to improve diagnostics and screening for esophageal cancer, Paulson emphasized that this study compares the mutations and DNA changes that occurred in patients who progressed to cancer with those that occurred in patients with stable, benign BE. While the findings are significant and are based on analysis of over 400 tissue samples, results from this 80-patient study would need to be validated in other patient groups before they could be used clinically to predict whether other BE patients will progress to cancer, he said.

Winding back the clock to cancer's earliest stages

In some people with long-term acid reflux, Barrett's esophagus arises as a new type of esophageal lining that better resists the damage caused by reflux. Even though it's often accompanied by DNA mutations, most people will never need treatment for their BE, which will remain benign and stable. But for about 5% of patients with BE, their condition will progress to a kind of cancer called esophageal adenocarcinoma. Though esophageal cancer is relatively rare (about 20,000 new cases are diagnosed each year in the U.S.), it's aggressive: Only 20% of patients survive five years past diagnosis.

"Once you progress to an advanced esophageal adenocarcinoma, treatment options are quite limited," Paulson said. "If you can find the tumor when it's very small, even microscopic, the treatment options are much better."

However, 95% of patients with BE will never get cancer. For them invasive screening and preventive measures expose them to risks without benefits.

To address this, Hutch researchers set up the Seattle Barrett's Esophagus Study in the early 1980s to learn more about BE, how it progresses, and find any genetic characteristics that flag patients at high or low risk of progressing to cancer. The ability to sort patients into risk categories, also known as risk stratification, would help doctors give patients the right amount of screening and intervention.

Because the team has studied patients for years, they have a long runway along which they can hunt for clues before cancer takes off.

Previous studies of the genetics of BE and esophageal cancer focused more on changes to specific genes, but now advances in technology allow scientists to understand DNA changes outside genes (where most of our DNA lies). To learn more, the BE team undertook a sequencing study that covers all the DNA in a cell (known as the genome) in 427 tissue samples.

Highlighting the changes in esophageal cancer

The team looked at small changes that altered just a few letters of DNA, and big changes that added, removed or moved around large swaths of DNA. First, they found that all BE is accompanied by lots of mutations, whether a patient eventually gets cancer or not.

"One of the critical results was how many genes were altered in patients who will never go on to cancer, that people think of as cancer-driver genes," said project co-lead Patty Galipeau, a Public Health Sciences research program manager now in Dr. Gavin Ha's lab, who helped shepherd the years-long project to completion.

In the researchers' analyses, one cancer-associated gene in particular, TP53, stood out. It encodes a protein that regulates a lot of important cellular processes, including recognizing damaged DNA, repair and cell growth. It's one of the most frequently mutated genes in all kinds of cancer -- but the team found that some BE patients that didn't progress to cancer also had a TP53 mutation.

However, their deeper dive into BE DNA revealed that the idea that any TP53 alteration leads to cancer is too simplistic. Humans get two copies of each gene (one from each parent). A person can have a mutation in one copy (one "hit") or mutations in both copies (two hits).

"Most progressors had two hits in TP53," said Paulson. Two hits would suggest a person is at very high risk for progressing from BE to cancer, though occasionally a person with one hit may also progress, he said. Patients who progressed to cancer also had TP53 mutations in larger regions of tissue, compared to the single-hit, localized lesions in non-progressing patients.

If both copies of TP53 in a person's cells are broken, it's very difficult for them to fix damaged DNA. This leads to duplications, deletions or reshuffling of large pieces of DNA. In fact, the team saw that BE cells in patients who progressed to esophageal cancer were much more likely to contain these large, complex changes than cells from those who never progressed.

Looking to the future

Even though the current findings on their own aren't enough to change diagnostic strategies for patients, the work has important insights that researchers who want to develop a biomarker test should keep in mind, such as that single TP53 mutations aren't likely to help separate high-risk and low-risk patients, Galipeau said.

Led by senior author Dr. Xiaohong Li, the group is working to integrate these findings with other data, including different types of genetic analyses, to develop an algorithm that can optimize screening times and predict which BE patients are at risk of developing cancer.

A better future for BE patients will not merely rely on genetic analyses, but on new technologies that make taking biopsies easier or even unnecessary, Galipeau said. With Ha, she, Paulson and the rest of the team are exploring the possibility of developing a screening test based on DNA released into the blood from BE cells that would indicate high risk of cancer, which ends up circulating in the blood. Such a test would allow doctors to evaluate patient status less invasively, using a blood draw rather than a scope down the throat.

The team also hopes their findings provide insights to other cancer researchers. They think that the genetic changes they spotted may reveal insight into how cells evolve to cope with stressful conditions -- and how those coping mechanisms can backfire -- and go beyond esophageal-specific cancer mechanisms.

"I think this study emphasizes that when mutations are happening, they're often happening in a tissue-specific context that's not specific to cancer itself," Galipeau said.

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Story Source:

Materials provided by Fred Hutchinson Cancer Research Center. Original written by Sabrina Richards. Note: Content may be edited for style and length.

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Journal Reference:

1. Thomas G. Paulson, Patricia C. Galipeau, Kenji M. Oman, Carissa A. Sanchez, Mary K. Kuhner, Lucian P. Smith, Kevin Hadi, Minita Shah, Kanika Arora, Jennifer Shelton, Molly Johnson, Andre Corvelo, Carlo C. Maley, Xiaotong Yao, Rashesh Sanghvi, Elisa Venturini, Anne-Katrin Emde, Benjamin Hubert, Marcin Imielinski, Nicolas Robine, Brian J. Reid, Xiaohong Li. Somatic whole genome dynamics of precancer in Barrett’s esophagus reveals features associated with disease progression. Nature Communications, 2022; 13 (1) DOI: 10.1038/s41467-022-29767-7

https://www.sciencedaily.com/releases/2022/04/220428103908.htm

Potential cure for carbon monoxide poisoning

 Carbon monoxide is an odorless and colorless gas made when fossil fuels burn incompletely. It's also a silent killer.

According to the Centers for Disease Control (CDC), more than 400 deaths and 20,000 emergency room visits can be attributed to carbon monoxide (CO) poisoning every year. While CO detectors and making sure your fireplace and heaters work correctly can help prevent exposure, treatment options are limited for those suffering from CO poisoning.

That's why Tim Johnstone, an assistant professor of chemistry and biochemistry at UC Santa Cruz, has been working to develop an easy-to-administer antidote.

"If you are exposed to carbon monoxide, the primary treatment right now is fresh air," said Johnstone. "It is a question of time. In fresh air, you need four to six hours for the level of CO in your blood to be cut in half. With 100 percent oxygen or hyperbaric oxygen, the half-life shortens further. Even then, the high blood levels of CO can persist long enough to lead to long-term deficits and neurological problems."

Johnstone has been studying the chemistry of carbon monoxide, which is made of one oxygen atom and one carbon atom joined by a triple bond. In a biological context, CO binds to metal centers like the iron in hemoglobin, which then prevents this protein from functioning as it normally would, transporting oxygen from the lungs to tissues in the rest of the body.

To mitigate this, Johnstone has designed small molecules that possess many of the features of the active site of hemoglobin but can bind CO much more tightly than the protein. In a recent paper published in Chemical Communications, his group described the ability of one such molecule to bind CO, sequester CO that is already bonded to hemoglobin, and rescue red blood cells exposed to CO, all promising signs for a future antidote.

Johnstone says these are early results, but the hope is to create a point-of-care treatment that can be administered quickly. The most common carbon monoxide poisoning symptoms are headache, dizziness, weakness, upset stomach, vomiting, chest pain, and confusion. Because it mimics the flu, people may experience symptoms without realizing the danger and delay seeking treatment.

Graduate student Daniel Droege has been the point person on this project and is first author of the paper.

In addition to the research on carbon monoxide poisoning, Johnstone's Lab is also working on antimony-containing drugs used to treat the neglected tropical disease Leishmaniasis, developing novel arsenic-based anticancer agents, and discovering new main-group bonding motifs. His work has been supported by the Hellman Foundation, the National Science Foundation, and the University of California Cancer Research Coordinating Committee.

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Story Source:

Materials provided by University of California - Santa Cruz. Original written by Elisa Smith. Note: Content may be edited for style and length.

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Journal Reference:

1. Daniel G. Droege, Timothy C. Johnstone. A water-soluble iron-porphyrin complex capable of rescuing CO-poisoned red blood cells. Chemical Communications, 2022; 58 (16): 2722 DOI: 10.1039/D1CC05542A

https://www.sciencedaily.com/releases/2022/04/220429144907.htm

Future wearable health tech could measure gases released from skin

 Scientists have taken the first step to creating the next generation of wearable health monitors.

Most research on measuring human biomarkers, which are measures of a body's health, rely on electrical signals to sense the chemicals excreted in sweat. But sensors that rely on perspiration often require huge amounts of it just to get a reading.

A new study suggests that a wearable sensor may be able to monitor the body's health by detecting the gases released from a person's skin.

"It is completely non-invasive, and completely passive on the behalf of the user," said Anthony Annerino, lead author of the study and a graduate student in materials science and engineering at The Ohio State University.

Some wearable devices, like smartwatches or fitness trackers, are already capable of measuring pulse rates or temperatures, but this team's method would allow the technology to sense biomarkers related to metabolic disorders, like heart disease or diabetes.

Their research is published in the journal PLOS One.

"Discerning health issues through the skin is really the ultimate frontier," said study co-author Pelagia-Iren Gouma, professor of materials science and engineering. Gouma also leads the Smart Connected Health project, which aims to support research in health and medicine.

"The project still has a couple of years to go," said Gouma. "But in six months, we should have proof of concept and in a year, we'd like to have it tested in people."

The final product of the team's research would be a small device a person could wear on low-sweat body locations, like behind the ear or on the nails, she said. And as more people become familiar with using wearable devices in their everyday lives, Gouma expects technology and medicine to become even more intertwined.

"We are developing a new generation of skin sensors, and it will really be the new norm," Gouma said.

Scientists, including Gouma, have a long history of measuring the concentration of organic compounds in our breath -- a type of gas -- as indicators of health. One example would be blowing into a breathalyzer, a device which can measure the amount of alcohol in a person's blood or be used to detect viruses.

But such a gadget requires "active intent" and only provides a "momentary snapshot" of the body, Annerino noted. Compared to the amount of chemicals we release when we breathe, he said, this team's sensors can operate on much smaller amounts of gaseous acetone released from the skin.

Acetone is one of the substances secreted from the skin that can tell researchers a lot about the inner workings of the human body. Concentrations of acetone in the breath have also been shown to be related to blood sugar levels and fat-burning rates.

"This is an area of research that hasn't been nearly as well developed yet, because we're just now producing the technology to measure lower concentrations of these gases with high selectivity," Annerino said.

To test whether their sensors could detect varying amounts of these enlightening chemicals (which would signal the presence of the gaseous molecules), the researchers created a film material made out of derivatives of plant cellulose and electroactive polymers. This film can bend dramatically in response to how much of the acetone is detected in its environment.

Annerino's team then placed the film over solutions containing ethanol (alcohol), acetone and water to gauge its sensitivity, selectivity and repeatability.

"We found significant bias toward bending more upon exposure to certain chemicals over others," said Annerino. This bending happens in milliseconds, and the researchers used machine learning and complex computational algorithms to accurately record and track the film's bending response to the different chemical solutions.

Their findings showed that the films are sensitive enough to track long-term changes in the body. While focusing on a metabolic rate sensor, another possible use would be to track ethanol which, in the body, can spell signs of liver disease. More work needs to be done on how the films used in this study would work as actual sensors worn on the body, the researchers said.

The opportunity to make someone's life easier was one of the reasons Annerino said he was so eager to get involved with the study. "Not every research study has an obvious impact on society and people's lives, but that's something that this project in particular really has," he said.

Other co-authors were Manoj Srinivasan, an associate professor of materials science and engineering, and Michael Faltas, a recent graduate of the materials and aerospace engineering program. This work was funded by the National Science Foundation.

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Story Source:

Materials provided by Ohio State University. Original written by Tatyana Woodall. Note: Content may be edited for style and length.

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Journal Reference:

1. Anthony Annerino, Michael Faltas, Manoj Srinivasan, Pelagia-Irene Gouma. Towards skin-acetone monitors with selective sensitivity: Dynamics of PANI-CA films. PLOS ONE, 2022; 17 (4): e0267311 DOI: 10.1371/journal.pone.0267311

https://www.sciencedaily.com/releases/2022/04/220429144924.htm