Researchers Discover How Force Dynamics Affect Cells, And Living Tissues (Medicine)

Researchers, led by Pere Roca-Cusachs at the Institute for Bioengineering of Catalonia (IBEC) discover how force dynamics affect cells, and living tissues. The results give an insight into the critical mechanical processes that occur in different diseases such as cancer.

From the vocal cords that produce our voice, to our heartbeat, our body’s cells are constantly subjected to mechanical forces that steadily change their response to these stimuli, regulating vital processes, in healthy individuals and in diseases such as cancer alike. Nevertheless, despite their importance, we remain largely ignorant of how cells sense and respond to these forces. 

Image 1: Isaac Almendros and Pere Roca-Cusachs (from left to right) leaders of the research. © IBEC

Now, an international team co-led by the researcher Pere Roca-Cusachs, from the Institute for Bioengineering of Catalonia (IBEC), and Isaac Almendros, a researcher at the Respiratory Diseases Networking Biomedical Research Centre (CIBERES) and IDIBAPS, both professors at the Faculty of Medicine and Health Sciences of the University of Barcelona, has just proven that what determines mechanical sensitivity in cells is the rate at which the force is applied, in other words, how fast the force is applied. The paper has been published in the prestigious journal Nature Communications and shows, for the first time in vivo, the predictions of the “molecular clutch” model.

These results will help, for example, to gain a better understanding of how a cancerous tumour proliferates, as well as how the heart, the vocal cords or the respiratory system respond to the constant variation of forces to which they are repeatedly exposed.  

A constant cellular “push and pull” 

The researchers observed that there are two responses to the force applied to a cell, using state-of-the-art techniques such as Atomic Force Microscopy (AFM) or so-called “optical tweezers”.  

On the one hand, the cytoskeleton, the dense network of fibres (mainly actin), which has, among others, the function of maintaining the shape and structure of the cell, is reinforced when the cell is subjected to a moderate force. In this regard, the cell is able to sense and respond to mechanical force, and the reinforcement of the cytoskeleton leads to a stiffening of the cell, and the localisation of the YAP protein in the nucleus. When this occurs, the YAP protein controls and activates genes related to cancer development.  

On the other hand, if the rate of force applied is repeatedly applied above a certain value, a reverse effect occurs; the cell no longer senses the mechanical forces. In other words, instead of the cytoskeleton and the cell becoming more rigid, a partial breakdown of the cytoskeleton occurs, leading to a softening of the cell.  

Like stretching and shrinking chewing gum, we have subjected cells to different forces in a controlled and precise manner, and we have seen that the rate at which the force is applied is of the utmost importance in determining the cellular response. 

Ion Andreu (IBEC), co-lead author of the study.

A model corroborated by in vivo experiments 

 To understand how the reinforcement and softening effects of the cytoskeleton are related, the researchers developed a computational model that considers the effect of the progressive application of force on the cytoskeleton and the “couplings” (proteins involved in binding the cell to the substrate, such as talin and integrin). These “couplings” are somewhat akin to the effect of the clutch of a car, in tightening the mechanical connection between the engine and the wheels, which is why the model is known as the “molecular clutch”.  

Next, the scientists performed experiments on laboratory rats to prove that the results observed in single cells also occur in in-vivo whole organs. To do so, the researchers studied the lungs, which naturally undergo cyclical mechanical stretching during breathing. Specifically, the two lungs were ventilated at different rates, with one lung filling and emptying faster (hyperventilation) and the other more slowly, while maintaining a normal total ventilation rate.  

After analysing and comparing cells from both lungs, they observed that the YAP protein increased its nuclear localisation only in cells from the lung subjected to hyperventilation. This increase in YAP in in-vivo samples, caused by the “cellular tug-of-war”, was akin to that found in proliferating cancer tumours. 

Our results demonstrate, at organ level, the role of force application rate in the transduction of the ventilation-induced mechanical signal in the lungs.  

Bryan Falcones (IBEC-UB), co-lead author of the study.

The paper sets out a mechanism by which cells respond, not only to direct forces, but also to other passive mechanical stimuli, such as the stiffness of the substrate on which they are located. The results give an insight into understanding how a priori opposite phenomena, such as reinforcing and softening of the cytoskeleton, can go hand in hand with controlling cell mechanics and respond specifically to different situations.  

Featured image: Rat lung responding to ventilation with YAP protein staining © IBEC


Reference article:  

Ion Andreu, Bryan Falcones, Sebastian Hurst, Nimesh Chahare, Xarxa Quiroga, Anabel-Lise Le Roux, Zanetta Kechagia, Amy E. M. Beedle, Alberto Elósegui-Artola, Xavier Trepat, Ramon Farré, Timo Betz, Isaac Almendros & Pere Roca-Cusachs. The force loading rate drives cell mechanosensing through both reinforcement and cytoskeletal softening. Nature Communications, 2021. 


Provided by IBEC

Scientists Divide Cancer Into Two Groups Based On Presence Or Absence Of Protein (Medicine)

All cancers fall into just two categories, according to new research from scientists at Sinai Health, in findings that could provide a new strategy for treating the most aggressive and untreatable forms of the disease.

In new research out this month in Cancer Cell, scientists at the Lunenfeld-Tanenbaum Research Institute (LTRI), part of Sinai Health, divide all cancers into two groups, based on the presence or absence of a protein called the Yes-associated protein, or YAP.

Rod Bremner, senior scientist at the LTRI, said they have determined that all cancers are present with YAP either on or off, and each classification exhibits different drug sensitivities or resistance. YAP plays an important role in the formation of malignant tumours because it is an important regulator and effector of the Hippo signaling pathway.

“Not only is YAP either off or on, but it has opposite pro- or anti-cancer effects in either context,” Bremner said. “Thus, YAPon cancers need YAP to grow and survive. In contrast, YAPoff cancers stop growing when we switch on YAP.”

Many YAPoff cancers are highly lethal. In their new research, Bremner and fellow researchers from the Roswell Park Comprehensive Cancer Center in Buffalo, NY, show that some cancers like prostate and lung can jump from a YAPon state to a YAPoff state to resist therapeutics.

When cancer cells are grown in a dish in a lab setting, they either float or stick down. The team of researchers found that YAP is the master regulator of a cell’s buoyancy, where all the floating cells are YAPoff, and all the sticky cells are YAPon. Changes in adhesive behavior are well known to be associated with drug resistance, so their findings implicates YAP at the hub of this switch, explained Bremner.

Joel Pearson, co-lead author and a post-doctoral fellow in the Bremner Lab at the LTRI, said therapies that tackle these cancers could have a profound effect on patient survival.

“The simple binary rule we uncovered may expose strategies to treat many cancer types that fall into either the YAPoff or YAPon superclasses,” Pearson said. “Moreover, since cancers jump states to evade therapy, having ways to treat either the YAPoff and YAPon state could become a general approach to stop this cancer from switching types to resist drug treatments.”

The researchers hope by deducing common vulnerabilities of these types of cancer, it may be possible to develop new therapeutic approaches and improve patient outcomes.

The work was funded primarily by the Canadian Institutes of Health Research (CIHR), the Cancer Research Society, and the Krembil Foundation.

The study, “Binary pan-cancer classes with distinct vulnerabilities defined by pro- or anti-cancer YAP/TEAD activity”, Cancer Cell, 2021. DOI: https://doi.org/10.1016/j.ccell.2021.06.016

Featured image: Lunenfeld-Tanenbaum Research Institute scientists Joel Pearson, left, and Rod Bremner, right, divided all cancers into two groups, based on the presence or absence of a protein called the Yes-associated protein, or YAP. © Sinai Health


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NIH-funded Study Finds Gene Therapy May Restore Missing Enzyme in Rare Disease (Medicine)

Results provide hope for children with aromatic L-amino acid decarboxylase deficiency

A new study published in Nature Communications suggests that gene therapy delivered into the brain may be safe and effective in treating aromatic L-amino acid decarboxylase (AADC) deficiency. AADC deficiency is a rare neurological disorder that develops in infancy and leads to near absent levels of certain brain chemicals, serotonin and dopamine, that are critical for movement, behavior, and sleep. Children with the disorder have severe developmental, mood dysfunction including irritability, and motor disabilities including problems with talking and walking as well as sleep disturbances. Worldwide there have been approximately 135 cases of this disease reported.

In the study, led by Krystof Bankiewicz, M.D., Ph.D., professor of neurological surgery at Ohio State College of Medicine in Columbus, and his colleagues, seven children received infusions of the DDC gene that was packaged in an adenovirus for delivery into brain cells. The DDC gene is incorporated into the cells’ DNA and provides instructions for the cell to make AADC, the enzyme that is necessary to produce serotonin and dopamine. The research team used magnetic resonance imaging to guide the accurate placement of the gene therapy into two specific areas of the midbrain.

Positron emission tomography (PET) scans performed three and 24 months after the surgery revealed that the gene therapy led to the production of dopamine in the deep brain structures involved in motor control. In addition, levels of a dopamine metabolite significantly increased in the spinal fluid.

The therapy resulted in clinical improvement of symptoms. Oculogyric crises, abnormal upward movements of the eyeballs, often with involuntary movements of the head, neck and body, that can last for hours and are a hallmark of the disease, completely went away in 6 of 7 participants. In some of the children, improvement was seen as early as nine days after treatment. One participant continued to experience oculogyric crises, but they were less frequent and severe.

All of the children exhibited improvements in movement and motor function. Following the surgery, parents of a majority of participants reported their children were sleeping better and mood disturbances, including irritability, had improved. Progress was also observed in feeding behavior, the ability to sit independently, and in speaking. Two of the children were able to walk with support within 18 months after receiving the gene therapy.

The gene therapy was well tolerated by all participants and no adverse side effects were reported. At three to four weeks following surgery, all participants exhibited irritability, sleep problems, and involuntary movements, but those effects were temporary. One of the children died unexpectedly seven months after the surgery. The cause of death was unknown but assessed to be due to the underlying primary disease.

This study was supported by NINDS (R01NS094292, NS073514-01).

Featured image: MR-guided delivery of AAV2-hAADC into the midbrain, baseline DaTscan and changes in FDOPA PET biomarker after gene delivery. © Authors


Article: Pearson, T.S., Gupta, N., San Sebastian, W. et al. Gene therapy for aromatic L-amino acid decarboxylase deficiency by MR-guided direct delivery of AAV2-AADC to midbrain dopaminergic neurons. Nat Commun 12, 4251 (2021). https://doi.org/10.1038/s41467-021-24524-8


Provided by NINDS

Ludwig Cancer Research Study Reveals Even Transient Chromosomal Mistakes Can Initiate Cancer (Medicine)

A Ludwig Cancer Research study has found that inducing random chromosome instability (CIN) events in mice for as little as one week is enough to trigger harmful chromosomal patterns in cells that spur the formation of tumors.

“We show that you don’t need chronic, lifelong chromosomal mistakes to produce tumorigenesis at a quite respectable frequency,” said Don Cleveland, Member of the Ludwig Institute for Cancer Research, San Diego, who led the study with Floris Foijer of the University of Groningen, in The Netherlands. “A very transient exposure would likely be sufficient to drive a very substantial increase in tumorigenesis.”

The finding, detailed this week in the journal Genes & Development, confirms a nearly 120-year-old hypothesis by the German biologist Theodor Boveri that aneuploidy—an abnormal number of chromosomes—and tumorigenesis are linked.

“Boveri hypothesized that there would be specific combinations of gains and losses of chromosomes that could lead to cancer. We’ve now tested that and shown that not only was he right, but that even a short burst of chromosome instability is enough to induce these combinations,” said Ofer Shoshani, a postdoctoral researcher in Cleveland’s lab and the study’s first author.

In the study, Shoshani and his colleagues overexpressed the gene polo-like kinase 4 (Plk4) in mice. Plk4 is a master regulator that controls the number of centrosomes present inside a cell. Centrosomes play an important role in cell division by helping separate replicated chromosomes into two daughter cells. Normally, two centrosomes are present inside a cell during division, one at each pole of the cell.

“However, when you overexpress Plk4, you have more than two, and this leads to chromosome missegregation, whereby the chromosomes are not being pulled correctly and the daughter cells inherit an unequal number of chromosomes,” Shoshani explained.

The scientists overexpressed Plk4 in the mice for either one week, two weeks or four weeks, and found that one week was enough to cause the formation of aggressive T cell lymphomas. Whole genome sequencing of the mouse tumors revealed an increased recurrence of a particular chromosome pattern early in the tumor formation process. This “aneuploid profile” involved triple occurrences of chromosomes 4, 5, 14 and 15 (cells normally contain only two copies of each chromosome).

Scientists have long known that certain cancer types are associated with specific chromosome gains—for example, breast cancer often involves a gain of chromosome 1. “What our work potentially shows is that when you induce a transient pulse of chromosome instability, you accelerate the formation of such a recurrent aneuploidy profile,” said Shoshani. “We identify the profile originating very early in the formation of cancer, either at, or very close to, the formation of the cell that generates the tumor.”

Moreover, the researchers found that transient CIN events can drive tumorigenesis regardless of whether p53—a major tumor suppressor gene and the most commonly mutated gene in human cancer—is inactivated. “This tells you that transient CINs will enhance tumorigenesis independent of whether you have other genetic issues that might predispose you to cancer,” Cleveland said.

The findings could be especially relevant to cancer patients undergoing anti-cancer therapy, particularly those being treated with chemotherapeutic agents known as aneugens, which work by driving chromosome instability and aneuploidy.

“Our work suggests that cancer patients who undergo therapy using aneugenic drugs might develop secondary cancers down the road,” said Shoshani. “Of course, this would need to be further investigated, in both human patients and by using experimental models in the lab.”

This study was supported by Ludwig Cancer Research, the US National Institute of Health, the Dutch Cancer Society, and the Nora Baar, K.F. Hein and Jo Kolk Foundations.

In addition to his Ludwig post, Don Cleveland chairs the Department of Cellular and Molecular Medicine and is a professor of Medicine, Neurosciences and Cellular and Molecular Medicine at UC San Diego.


Provided by Ludwig Cancer Research

New Theory Suggests Blood Immune and Clotting Components Could Contribute To Psychosis (Psychiatry)

A scientific review has found evidence that a disruption in blood clotting and the first line immune system could be contributing factors in the development of psychosis.

The article, a joint collaborative effort by researchers at RCSI University of Medicine and Health Sciences, Cardiff University and the UCD Conway Institute, is published in Molecular Psychiatry.

Recent studies have identified blood proteins involved in the innate immune system and blood clotting networks as key players implicated in psychosis.

The researchers analysed these studies and developed a new theory that proposes the imbalance of both of these systems leads to inflammation, which in turn contributes to the development of psychosis.

The work proposes that alterations in immune defense mechanisms – including blood clotting – lead to an increased risk of inflammation, which is thought to contribute to the development of psychosis.

The new theory further refines the prevailing ‘two-hit’ hypothesis, where early genetic and/or environmental factors disrupt the developing central nervous system (the “first-hit”) and increases the vulnerability of the individual to subsequent, late environmental disruptions (the “second-hit”).

“Early identification and treatment significantly improves clinical outcomes of psychotic disorders. Our theory may provide a further step to biomarkers of psychosis and allow the identification of therapeutic targets for early and more effective treatment,” said Dr Melanie Föcking, joint first author on the paper and Lecturer in Psychiatric Neuroscience at RCSI Department of Psychiatry.

“While the idea of psychosis resulting from some form of inflammation and immune activation is not new, our data suggest a new understanding and change of focus towards a combined function of the innate immune complement system and coagulation pathways to the progression to psychotic disorder,” said Dr Meike Heurich, joint first author on the paper and lecturer at School of Pharmacy and Pharmaceutical Sciences, Cardiff University.

“The works builds on our recent studies which increasingly implicate dysregulation of the complement and coagulation pathways both in and preceding psychotic disorder,” said Professor David Cotter, senior author of the paper and Professor of Molecular Psychiatry at RCSI Department of Psychiatry.

The research was funded by the Health Research Board (HRB) in Ireland and Wellcome Trust.


Reference: Heurich, M., Föcking, M., Mongan, D. et al. Dysregulation of complement and coagulation pathways: emerging mechanisms in the development of psychosis. Mol Psychiatry (2021). https://doi.org/10.1038/s41380-021-01197-9


Provided by RCSI

Researchers Have Described A Novel Primary Immunodeficiency Due To A Mutation in AIOLOS (Medicine)

Researchers from Tokyo Medical and Dental University (TMDU) identify a new primary immunodeficiency resulting from a mutation that impedes proper protein function

Primary immunodeficiencies, such as severe combined immunodeficiency disease (SCID), occur when the immune system does not work properly, leading to increased susceptibility to various infections, autoimmunity, and cancers. Most of these are inherited and have an underlying genetic causes. A team at TMDU has identified a novel disorder resulting from a mutation in a protein called AIOLOS, which functions through a previously unknown pathogenic mechanism called heterodimeric interference.

The gene family known as IKAROS zinc finger proteins (IKZFs) is associated with the development of lymphocyte, a type of white blood cell involved in the immune response—meaning that mutations in this family can be involved in immune system deficiencies. Most research so far has focused on IKAROS protein, encoded by the gene IKZF1, although the underlying mechanism by which IKAROS mutations cause the deficiencies is not yet fully understood. A mutation in AIOLOS—another member of the IKZF family that is encoded by the gene IKZF3—has now also been revealed to cause a hereditary immune deficiency. In addition to not functioning properly itself, the resultant mutant protein interferes with the functioning of IKAROS protein.

TMDU researchers uncovered this new mechanism while investigating the cause of a previously undescribed inherited B cell deficiency observed in a family of patients. After sequencing all of the protein-coding genes, the team focused their research on AIOLOS as IKAROS is known to be the cause of B cell deficiency. They showed that the mutant form of AIOLOS that was present in this family did not just fail to function, but actively bound to a different DNA sequence than the normal version of the protein.

They went on to use a mouse model that harbors equivalent AIOLOS mutation identified in the patients to outline the underlying pathogenic mechanism. AIOLOS and IKAROS bind together to form a “heterodimer”. The mutant form of AIOLOS retained the ability to bind IKAROS but then interfered with the normal function of IKAROS, and led to the heterodimer being recruited to the incorrect regions of the genome. 

“This is a novel pathogenic mechanism that we termed heterodimeric interference,” says lead author Motoi Yamashita, “where a mutant protein in a heterodimer hijacks the function of the normal partner protein.”

The team were then able to rescue some of the immune function in the mouse model by deleting the dimerization domain of the mutant AIOLOS.

“The fact we could rescue the phenotype in our mouse model indicates a potential therapeutic approach,” says Tomohiro Morio, senior author. “The deletion of the domain responsible for binding IKAROS in the mutant AIOLOS protein could ameliorate the immunodeficiency observed in the patients.”

The discovery of this new pathogenic mechanism, heterodimeric interference, may well help to shed light on many other disease processes such as autoimmunity and cancer development where mutant proteins act in the same way. 

Figure 1. Fallen IKAROS blown by AIOLOS. The transcription factors IKAROS and AIOLOS (named after Greek mythology characters) regulate lymphocyte development. According to Greek mythology, Ikaros had wings that were made of feathers and wax; one day, he flew too close to the sun and his wings melted which resulted in his fall and subsequent death. Aiolos, on the other hand, was a god of wind and, upon the command of the higher-ranking gods, he brought violent stormy winds to bring devastation and despair. In this artwork, the mutant Aiolos loses his control and power over stormy winds and going berserk. The artwork illustrates the fallen Ikaros not due to being very close to the sun, but instead as a result of being blown away by the mutant Aiolos. © TMDU
Figure 2. Mutant AIOLOS interfere with IKAROS via heterodimers —Heteromeric interference. AIOLOS forms heterodimer with its partner IKAROS. They comprise transcription factor complex which regulates genes involved in lymphocyte development. In the patients and the patient-mimic mouse model, mutant AIOLOS forms heterodimer with IKAROS and interferes with its function by blocking AIOLOS-IKAROS bindings to their physiological binding sites and sequestrating IKAROS to non-physiological binding regions in the form of heterodimers. © TMDU

The article, “A Variant in Human AIOLOS Impairs Adaptive Immunity by Interfering with IKAROS”, was published in Nature Immunology at DOI: 10.1038/s41590-021-00951-z.

Summary

Researchers from TMDU have described a novel primary immunodeficiency due to a mutation in AIOLOS. This acts through a novel pathogenic mechanism termed “heterodimeric interference”, whereby when two different proteins bind together in a heterodimer, the mutant protein hijacks the function of the normal protein. In a mouse model, they were able to restore some of the lost functions by interfering with the mutated protein, suggesting a possible therapeutic approach to disorders of this nature.

Journal Article


Provided by TMDU

Study Identifies Monoclonal Antibodies That May Neutralize Many Norovirus Variants (Medicine)

Researchers at Vanderbilt University Medical Center (VUMC) and the Baylor College of Medicine in Houston, Texas, have taken a big step toward developing targeted treatments and vaccines against a family of viruses that attacks the gastrointestinal tract.

Each year in the United States circulating strains of the human norovirus are responsible for approximately 20 million cases of acute gastroenteritis. Hallmark symptoms include severe abdominal cramping, diarrhea and vomiting.

Several vaccine candidates are in clinical trials, but it is unclear how effective they will be, given the periodic emergence of novel norovirus variants. Developing broadly effective vaccines will require an understanding of the genetic diversity of the virus and the mechanisms by which the immune system can neutralize it.

Reporting this week in the journal Nature Communications, the researchers isolated a panel of human monoclonal antibodies from subjects with a history of acute gastroenteritis that are cross-reactive and which neutralize a broad range of norovirus variants in laboratory tests.

They describe a conserved, antigenic site on the norovirus that could be used to reformulate vaccine candidates so that they are broadly effective against circulating viral strains. The monoclonal antibodies also could be used to treat or prevent norovirus infection directly or as diagnostic reagents, they added.

Leading the research were the paper’s corresponding authors, James Crowe Jr., MD, director of the Vanderbilt Vaccine Center, and B.V. Venkataram Prasad, PhD, the Alvin Romansky Chair in Biochemistry, in collaboration with Mary Estes, PhD, the Cullen Chair and professor of virology at Baylor College of Medicine.

First authors of the paper were Gabriela Alvarado, PhD, formerly of Crowe’s lab, now at the National Institute of Allergy and Infectious Diseases, and Wilhelm Salmen, a graduate student in the Prasad lab.

“We were surprised to find naturally occurring antibodies that recognized so many different noroviruses,” said Crowe, the Ann Scott Carell Chair and professor of Pediatrics and Pathology, Microbiology & Immunology at VUMC.

“Previously, many experts thought that this would not be possible because of the extreme sequence diversity in the various groups and types of noroviruses in circulation,” he said. “The human immune system continues to surprise us in its capacity to recognize diverse virus variants.”

“One of the fascinating aspects of this study was the unexpected finding of where the human antibody attacks the virus for neutralization,” Prasad said.

“It is exciting to now have human monoclonal antibodies that neutralize many norovirus variants,” added Estes.

Also contributing to the work were Khalil Ettayebi and Liya Hu, PhD, assistant professor, Baylor College of Medicine, and Banumathi Sankaran, PhD, from the Lawrence Berkeley National Laboratory in Berkeley, California.

The research was supported in part by the National Institutes of Health and the Welch Foundation of Houston, Texas.

Featured image: James Crowe Jr., MD, director of the Vanderbilt Vaccine Center © Vanderbilt University Medical Center


Reference: Alvarado, G., Salmen, W., Ettayebi, K. et al. Broadly cross-reactive human antibodies that inhibit genogroup I and II noroviruses. Nat Commun 12, 4320 (2021). https://doi.org/10.1038/s41467-021-24649-w


Provided by VUMC

Researchers Reveal Solvatomorphism Influence of Porous Organic Cage on C2H2/CO2 Separation (Chemistry)

Porous organic cages (POCs) are discrete, covalently linked molecules with intrinsic cavities. The porous nature of POCs enables them to be nanoscale reaction vessels for catalysis, hosts for different guest molecules, and adsorbents for gas storage and separation. 

POCs materials exhibit solvatomorphs via altering their crystallographic packing in the solid state, but the investigation of real gas mixture separation by porous materials with such a behavior is still very rare. 

In a study published in ACS Appl. Mater. Interfaces, the group led by Prof. YUAN Daqiang from Fujian Institute of Research on the Structure of Matter of the Chinese Academy of Sciences reported that a lantern-shaped calix[4]resorcinarene-based porous organic cage (POC, namely, CPOC-101) can exhibit eight distinct solid-state solvatomorphs via crystallization in different solvents, and this POC solvatomorphism strongly influences their gas sorption capacities and separation abilities. 

The researchers found that the apparent Brunauer-Emmett-Teller (BET) surface area determined by nitrogen gas sorption at 77 K for CPOC-101α crystallized from toluene/chloroform is up to 406 m2 g-1, which is much larger than that of the rest of CPOC-101 solvatomorphs with BET values less than 40 m2 g-1.  

They also found that C2H2 and CO2 adsorbed capacities, in addition to the C2H2/CO2 separation ability at room temperature for CPOC-101α, are superior to those of CPOC-101β crystalized from nitrobenzene, the representative of POC solvatomorphs with low BET surface areas.  

To understand the mechanism of the higher affinity toward C2H2 over CO2 within CPOC-101, the researchers computed the interaction energies between the optimized cage host and gas guests by the first-principles dispersion-corrected density functional theory (DFT-D) calculations.  

The hydrogen-bond number (6 for C2H2 and 5 for CO2), the average hydrogen-bond length (3.12 Å for C2H2 and 3.26 Å for CO2), and the calculated interaction enthalpies highly indicated that the host-guest interaction between the C2H2 molecule and CPOC-101 is much stronger than that of CO2

This study reveals the possibility of adjusting gas sorption and separation properties of POC materials by controlling their solvatomorphs. 

Featured image: CPOC-101 for C2H2/CO2 separation. (Image by Prof. YUAN’s group)  


Provided by Chinese Academy of Sciences

Three Phase Electro-catalysis: a Step Forward for Polymer-grade Ethylene Purification (Chemistry)

In a study published online in Nature Catalysis, Prof. ZHANG Tierui from the Technical Institute of Physics and Chemistry (TIPC) of the Chinese Academy of Sciences, Prof. WANG Haotian from Rice University, and the collaborators, achieved high performance electrochemical acetylene reduction at room temperature. Their strategy shows special advantages in energy and atomic economics when compared with conventional thermal hydrogenation strategy.  

Ethylene is crucial to petrochemistry industry. Industrial ethylene is from the cracking of hydrocarbons such as naphtha. Cracking products inevitably contain 0.5-2.0% acetylene impurities, which will poison Ziegler Natta catalyst used for ethylene polymerization and affect the quality of polymer products. Therefore, it is necessary to reduce the concentration of acetylene impurities to parts per million (ppm) before polymerization. 

The acetylene thermal hydrogenation is widely used to the acetylene selective conversion for the production of polymer-grade ethylene. However, it requires more than 100℃ of operational temperature and excessive hydrogen. Ethylene will be over-hydrogenated to ethane. 

The researchers in this study developed a ‘gas-solid-liquid’ three phase electro-catalytic acetylene reduction (EAR) system. Nanomaterial such as Cu/Cu2O derived from layered double hydroxides can be used as catalyst to realize the selective reduction of acetylene in ethylene rich feed gas at room temperature. 

The conversion rate of acetylene reached 99.9%, and the ethylene selectivity is over 90%. Acetylene concentration was reduced from 5000 ppm to less than 1 ppm. Core indexes (acetylene conversion, ethylene selectivity, hydrogen volume, reaction temperature and specific rate) of the EAR system outperform most of thermal hydrogenation investigations. 

The three phase electro-catalytic system only needs an electricity cost equals to 0.5% of the market price of ethylene. It is highly possible to become an alternative to existing acetylene conversion technologies for the production of polymer-grade ethylene.


Reference: Shi, R., Wang, Z., Zhao, Y. et al. Room-temperature electrochemical acetylene reduction to ethylene with high conversion and selectivity. Nat Catal (2021). https://doi.org/10.1038/s41929-021-00640-y


Provided by Chinese Academy of Sciences