Islands jutting up from the world’s oceans provided environmental conditions necessary for early life to flourish, a new study co-authored by a Yale scientist suggests.
Significantly, the finding offers important evidence supporting one of the most popular ideas about the origins of life on Earth — Charles Darwin’s notion of “warm little ponds.”
Earth scientists Jun Korenaga of Yale University and Juan Carlos Rosas of the Ensenada Center for Scientific Research and Higher Education in Mexico describe their new theory in the Jan. 4 online edition of the journal Nature Geoscience.
In his writings, Darwin hypothesized that life began when shallow, warm ponds of water allowed essential biomolecules to concentrate and undergo polymerization reactions. Many scientists believe that if such ponds existed in abundance, or if they existed over a long period of time, it is possible that life emerged from a series of these chemical reactions.
Yet there was a problem when applying this theory. The early Earth was a “water world,” covered by deep oceans long before the first continents poked their way to the surface. In such a world, Darwin’s shallow, warm ponds simply didn’t exist.
Korenaga and Rosas say they may have the answer.
The researchers developed a theoretical model for the likely topography of Earth’s sea floor during the Archean eon, which lasted from 4,000 million years ago until 2,500 million years ago.
Their model found that a higher amount of internal heating in the Earth’s mantle than what exists today may have halted certain ongoing geophysical processes — creating a shallowing of ocean basins in some parts of the world. In this scenario, the researchers said, volcanic island chains and oceanic plateaus may have remained above sea level for hundreds of millions of years.
“This is a very exciting finding for solid Earth science as well as prebiotic chemistry,” said Korenaga, a professor of earth and planetary sciences at Yale.
Earth’s internal heating comes from the decay of radioactive elements such as uranium. Because these elements disappear over time, there would have been more of them during the Archeon eon. Korenaga said this would mean there was greater internal heating in the past.
“My earlier collaboration with Jeffrey Bada, a world expert on prebiotic chemistry at the Scripps Institution of Oceanography, tempted me to look into the influence of this well-known fact of sea-floor topography in the past, which had never been explored before,” Korenaga said. “Juan and I were surprised when we first saw our results, but in hindsight, it actually makes sense.”
Korenaga said he hopes the study will motivate further investigations into the dynamic nature of Earth’s early landscape and its implications for the origin and evolution of life.
Grants from NASA and the National Science Foundation supported the research.
New study shows targeting arterial stiffening earlier in a person’s lifespan could provide cognitive benefits in older age and may help to delay the onset of dementia.
Researchers at the University of Oxford and University College London investigated 542 older adults who received two measurements of aortic stiffness, at 64 years old and 68 years old. Subsequent cognitive tests and brain magnetic resonance imaging (MRI) scans assessed the size, connections and blood supply of different brain regions.
The body’s largest artery (the aorta) gets stiffer with age, and the study found that faster aortic stiffening in mid-life to older age was linked to markers of poorer brain health, for example:
Lower brain blood supply
Reduced structural connectivity between different brain regions
Medical interventions and changes of lifestyle made earlier in the lifespan could help to slow down arterial stiffening. In an ageing society where we expect a near tripling in the number of people living with dementia by 2050, identifying ways to prevent or delay its onset could have significant societal and economic impact.
Dr Sana Suri, Alzheimer’s Society Research Fellow at the Department of Psychiatry, University of Oxford, said, ‘Our study links heart health with brain health, and gives us insights into the potential of reducing aortic stiffening to help maintain brain health in older ages. Reduced connectivity between different brain regions is an early marker of neurodegenerative diseases such as Alzheimer’s disease, and preventing these changes by reducing or slowing down the stiffening of our body’s large blood vessels may be one way to maintain brain health and memory as we grow older.’
This study shows the importance of interdisciplinary work in this field and stresses the benefits of studying the brain in conjunction with other organ systems. Arteries stiffen faster if someone has pre-existing heart diseases, high blood pressure, diabetes and other vascular diseases. Arterial stiffening is also progressively faster with long-term exposure to poor health behaviours and lifestyle risk factors, such as smoking or poor diets. It is possible to reduce arterial stiffening by medical treatments or lifestyle interventions, such as modifying the diet and exercising.
Dr Scott Chiesa, Research Associate at the UCL Institute of Cardiovascular Science, said, ‘With no cure for dementia, there is an increased focus on understanding how to prevent or delay its onset. Importantly, our study helps us understand when in the lifespan it will be best to target and improve cardiovascular health to benefit the brain.’
Dr Richard Oakley, Head of Research at Alzheimer’s Society, which funded the study, said, ‘Dementia devastates lives, and with the number of people with dementia set to rise to 1 million by 2025 and more families affected than ever before, reducing our risk has never been more important. This Alzheimer’s Society funded study didn’t look for a link between heart health and dementia directly, but it has shed important light on a connection between the health of our blood vessels and changes in the brain that indicate brain health.
‘We know that what’s good for your heart is good for your head, and it’s exciting to see research that explores this link in more detail. But we need even more research to understand the impact of heart health on brain health as we age, and how that affects our own dementia risk. Alzheimer’s Society is committed to funding research into dementia prevention as well as research into a cure. But coronavirus has hit us hard, so it’s vital the Government honours its commitment to double dementia research spending to continue research like this.’
Participants in this study were part of the Imaging subset of the Whitehall II Study, a cohort of British civil service members who have received clinical follow-ups for over 30 years. Participants were predominantly white males and were selected if they had no clinical diagnosis of dementia. Further research in diverse samples and people with more advanced cognitive deficits will be needed to confirm these findings in a wider population.
The Whitehall II Study and the Whitehall II Imaging Sub-study are funded by grants from the UK Medical Research Council, British Heart Foundation, and US National Institute on Aging.
A research team at the Department of Paediatrics and Adolescent Medicine, LKS Faculty of Medicine, The University of Hong Kong (HKUMed) discovered a novel gene CC2D1A that is associated with human heterotaxy, a spectrum of congenital disease that disrupts the arrangement of internal organs. It is the first time that CC2D1A is reported to be associated with heterotaxy in the literature. The ground-breaking findings have been published in the leading academic journal, Circulation: Genomic and Precision Medicine. [Link to the publication]
In human bodies, the left side and right side are not symmetrical. For example, heart and spleen are on the left side of the body, whereas most of the liver is on the right side. Heterotaxy, also known as situs ambiguous, is a class of human congenital disorders that are characterised by the failure to establish normal left-right asymmetry, resulting in the abnormal arrangement of internal organs on the wrong side of the body. Patients with heterotaxy have congenital birth defects that multiple organs can be affected, including the heart, lungs, liver, spleen, stomach and intestines. The estimated incidence at birth is around 1 in 10,000, and is more common in Asians than in Caucasians. Approximately 90% of heterotaxy patients have complex congenital heart defects. Patients with heterotaxy have poor prognosis, with overall survival of less than 50% in 10 years.
With the advancement of sequencing, more than 20 genes have been reported to cause heterotaxy. Some of these genes are related to the formation of cilia, which are hair-like projections that stick out from the cells surfaces. Cilia defects may cause abnormal flow of signals that guide the left-right axis formation at the embryonic development, resulting in heterotaxy. The Division of Paediatric Cardiology, Department of Paediatrics and Adolescent Medicine, HKUMed, has been taking care of this group of patients in Hong Kong for a long time. However, the genetic causes of these patients remained unknown.
Herein, the team utilised whole exome sequencing technology to identify the disease-causing mutations in 26 patients with heterotaxy. Whole exome sequencing refers to the sequencing of all the coding regions of all genes (approximately 20,000 genes) in the human genome. The whole exome sequencing results showed that no pathogenic mutations can be identified in known genes associated with heterotaxy. Therefore, the team tried to identify new genes that have not been associated with heterotaxy. By comparing the mutations identified in patients with controls, there was a significant enrichment of CC2D1A damaging variants in patients.
The CC2D1A gene is located on chromosome 19. It produces a protein with 951 amino acids, and has been reported to be involved in regulating signalling pathway, immune response and synapse maturation. CC2D1A has been reported to be associated with intellectual disability in human1 2, but not heterotaxy. In collaboration with Dr Alvin Ma Chun-hang, Assistant Professor, Department of Health Technology and Informatics, The Hong Kong Polytechnic University, the function of this gene was further examined by the zebrafish model. Zebrafish was chosen because the zebrafish heart and human heart undergo similar morphogenetic processes.
Gene editing tool was used to edit the cc2d1a gene in the zebrafish, creating an abnormal protein that lost its functions. Zebrafish with cc2d1a mutation showed disarrangements in heart and digestive systems, suggesting that the normal left-right asymmetry was disrupted. In addition, defective ciliary was also observed, resulting in fewer and shorter cilia. More importantly, injections of wild type cc2d1a (i.e. cc2d1a without any mutation) to the edited fertilised egg can rescue the abnormal organ arrangement and ciliary defects. The result demonstrated that mutations in cc2d1a disrupt the establishment of left-right axis formation, and the disease mechanism of heterotaxy has resulted from abnormal function of cilia.
“Research for heterotaxy in Hong Kong is important as the clinical management continues to be challenging, and we are excited to understand more about the underlying cause,” said Professor Cheung Yiu-fai, Bryan Lin Professor in Paediatric Cardiology, Clinical Professor, Department of Paediatrics and Adolescent Medicine, HKUMed.
“Surprisingly, mutations in Caucasian patients with heterotaxy cannot be found in our local patients. It shows that we have to perform the genetic study at our own capacity to discover the unique disease-causing mutations in Chinese or Asians. Our study provides the first evidence on the association of the CC2D1A gene with human heterotaxy, which will facilitate the genetic diagnosis of heterotaxy patients more precisely in Hong Kong,” said Dr Brian Chung Hon-yin, Clinical Associate Professor, Department of Paediatrics and Adolescent Medicine, HKUMed.
Significance of the study
The findings of the study have significant implications in the understanding of the genetics of heterotaxy in Hong Kong. It is the first time that CC2D1A is reported to be associated with heterotaxy in the literature. With the identification of the genetic cause, preimplantation genetic diagnosis of CC2D1A in families with family history is possible.
About the research team
The research was led by Professor Cheung Yiu-fai, Bryan Lin Professor in Paediatric Cardiology, Clinical Professor; Dr Brian Chung Hon-yin, Clinical Associate Professor, Department of Paediatrics and Adolescent Medicine, HKUMed. Dr Alvin Ma Chun-hang, Assistant Professor, Department of Health Technology and Informatics, The Hong Kong Polytechnic University; and Dr Christopher Mak Chun-yu, Assistant Lecturer, Department of Paediatrics and Adolescent Medicine, HKUMed are the co-first authors.
Other researchers include Dr Yeung Kit-san, post-doctoral fellow; Dr Steven Pei Lim-cho, Senior Research Assistant; Dr Ying Dingge, Research Officer; Mr Mullin Yu Ho-chung, PhD candidate, Department of Paediatrics and Adolescent Medicine, HKUMed; Mr Kazi Md Mahmudul Hasan and Mr Chen Xiangke, PhD candidates, Department of Health Technology and Informatics, The Hong Kong Polytechnic University; Dr Chow Pak-cheong, Paediatric Consultant Cardiologist in Department of Paediatrics and Adolescent Medicine, Hong Kong Children’s Hospital and Honorary Clinical Associate Professor, Department of Paediatrics and Adolescent Medicine, HKUMed.
This work was supported in part by Seed Fund for Basic Research (No. 201711159132) of The University of Hong Kong, and the Society for the Relief of Disabled Children.
New treatments to cut the global death rate from dengue, Zika and West Nile viruses could result from research led by The University of Queensland.
Associate Professor Daniel Watterson from UQ’s School of Chemistry and Molecular Biosciences said the team identified an antibody that improved survival rates in laboratory trials and reduced the presence of virus in the blood.
“We made a discovery in 2015 in the wake of the Zika outbreak that identified a new target for flavivirus treatments, a viral protein called NS1,” Dr Watterson said.
“Now we’ve shown for the first time that a single NS1 antibody can be protective against multiple flaviviruses including dengue, Zika and West Nile.
“No other antibody reported has shown such a broad range of protection.
“The improved protection we saw compared to existing treatments was really unexpected.”
An estimated 390 million people are infected with dengue globally each year, particularly in tropical and sub-tropical areas.
Of those cases, about half a million people develop a more severe form of the disease, which can be fatal.
Dr Watterson said the discovery was important, as the development of a vaccine for viruses like dengue is an unmet global challenge.
“Creating vaccines and therapies has been greatly hindered because antibodies that target the main viral envelope protein can also enhance disease.
“This phenomenon is called antibody dependent enhancement (ADE), and contributed to the complications arising from large-scale roll-out of the first licensed dengue vaccine.
“But because NS1 antibodies don’t drive ADE, our findings provide the blueprint for new and safe broad-spectrum vaccines against multiple flaviviruses, including dengue.”
Lead author UQ’s Dr Naphak Modhiran said the antibody could also provide the first line of defence in future viral outbreaks across the world.
“The antibody binds to a wide range of flaviviruses including Usuto virus in Europe, and Rocio and Ilheus viruses in South America,” Dr Modhiran said.
“These viruses have already caused local outbreaks in the past and have the potential to be the next Zika.”
Co-author Professor Paul Young said the antibodies were first developed in his group more than 30 years ago.
“Since then, they have provided numerous insights into the biology of the dengue viruses and have been employed in the development of new diagnostics,” Professor Young said.
“It’s great to see them now progressing as potential templates for therapeutics.
“This highlights the critical nature of discovery research in providing the foundation for translation into clinical practice.”
The UQ team worked in collaboration with Professor George Gao, Professor Yi Shi and Dr Hao Song at the Institute of Microbiology, Chinese Academy of Sciences.
The work was supported by the Australian Government National Health and Medical Research Council (NHMRC).
The research has been published in Science (DOI: 10.1126/science.abb9425).
Computer models efficiently and accurately simulate the magnetic responses of ferrofluids by considering only the fluid’s surface.
The spiky structure that erupts from the smooth surface of a ferrofluid when a magnet is brought close can be predicted more accurately than previously thought. KAUST researchers have shown that computational algorithms can calculate the ferrofluid’s bristling response to a magnet by simulating only the liquid’s surface layer.
Ferrofluids are liquid suspensions of iron-based particles that behave like a regular fluid, but once a magnet is present, the ferrofluid rapidly shape-shifts to form spikes that align with the magnetic field. Originally developed by NASA, ferrofluids have numerous uses ranging from advanced electronics to nanomedicine and have the potential for even broader use, if their magnetic responses could be predicted more accurately.
Dominik Michels and his team are applying computer simulations to model ferrofluid behavior. “Our aim is to develop an efficient and accurate algorithm to simulate the macroscopic shapes and dynamic movement of ferrofluids,” says Libo Huang, a Ph.D. student in Michels’ team.
Recently, looking at the wider field of fluid simulation, the team has shown that the concept of simulating fluid motion by considering only the liquid’s surface can be adapted to ferrofluids.
Video: KAUST researchers are applying computer simulations to model ferrofluid behavior with the goal of developing an efficient and accurate algorithm to simulate the macroscopic shapes and dynamic movement of ferrofluids. 2021 KAUST; Anastasia Serin.
“While the surface-only liquid simulation provides a platform for fluid simulation, its extension to ferrofluids is significant,” Huang says. To model a fluid’s behavior based only on its surface, the liquid must respond to inputs in a simple linear fashion. Most ferrofluids have a complex non-linear response to a magnetic field.
“Our aim is to develop an efficient and accurate algorithm to simulate the macroscopic shapes and dynamic movement of ferrofluids,” said Huang.
However, the team showed that as long as the magnetic field is not too strong, the response is close to linear, enabling them to perform a surface-only calculation of the magnetic field response.
In the simulation, the researchers represented the liquid surface as a series of triangles, Huang explains. “The representation of ferrofluids as surface triangles allowed us to accurately estimate the curvature of the liquid interface as well as the interface position,” he says. The spike structure can be simulated by calculating the interplay between the magnetic force and the liquid’s surface tension.
Considering only the fluid’s surface, rather than its entire volume, made the simulation far more computationally efficient, enabling more accurate simulation of the complex ferrofluid behavior. “We were able to reproduce the distance between spikes of the real fluid’s spike pattern in an accurate quantitative fashion,” Michels says. “We could simulate much more complex dynamic motion.”
The next step could be to extend the work to include nonlinear magnetic relationships, Huang says.
A study led by researchers at the UCLA Jonsson Comprehensive Cancer Center has found that magnetic resonance imaging, or MRI, frequently underestimates the size of prostate tumors, potentially leading to undertreatment.
The study authors found that such underestimation occurs most often when the MRI-measured tumor size is small and the PI-RADS score, which is used to classify lesions in prostate MRI analysis, is low.
For prostate tumor treatments to be successful, both the MRI size measurement and PI-RADS score must be accurate because they allow physicians to determine precisely where tumors end and where the normal, healthy tissue surrounding them begins.
MRI is frequently used to diagnose and manage prostate cancer. It is also increasingly used as a means to map and guide delivery of new, highly focused therapies that use freezing (cryotherapy), ultrasound (HIFU) and heat (laser ablation) to destroy cancerous tissue in the prostate gland while sparing healthy tissue.
Researchers compared MRI-measured tumor size with actual tumor size after prostate removal in 441 men treated for prostate cancer.
Improving the ability to better predict ablation margins will allow for more successful treatments for men with prostate cancer and can help reduce the morbidity of prostate cancer treatment.
The senior author is Dr. Robert Reiter, professor of urology at the David Geffen School of Medicine at UCLA and director of UCLA’s prostate cancer program. The lead author is Dr. Aydin Pooli, clinical instructor of urology at UCLA. Other authors are David Johnson, Dr. Joseph Shirk, Daniela Markovic, Dr. Taylor Sadun, Dr. Anthony Sisk, Amirhossein Bajgiran, Dr. Sohrab Mirak, Dr. Ely Felker, Alexa Hughes and Dr. Steven Raman, all of UCLA.
Research led by scientists from UCLA and Harvard University has uncovered details about how the bacterium Clostridioides difficile causes excessive inflammation in the gut that can lead to potentially deadly colitis. Studying C. difficile toxin A, one of two toxins released by the bacterium, the researchers produced two key findings.
They pinpointed which part of the toxic protein can permeate cell membranes to gain entry to cellular structures called endosomes, demonstrating that even fragments of the protein that contain that key segment are capable of accessing endosomes.
In addition, they revealed how the toxin molecule causes inflammation, which has been a long-standing mystery because such molecules are generally quickly digested in the gut. The scientists found that toxin A — and surprisingly even fragments of the toxin — can organize DNA into ordered crystalline particles that amplify an immune response by binding to multiple TLR9 receptors, which are normally part of the body’s early detection system for microbial DNA. The findings demonstrate that this mechanism causes the body’s natural defenses to produce excessive inflammation.
Infection from C. difficile in the gut can cause life-threatening colitis, with nearly 500,000 cases and 29,000 deaths in the U.S. alone each year, according to the Centers for Disease Control and Prevention.
Older patients who have been treated with antibiotics are at particular risk from C. difficile, which is resistant to a number of antibiotics. The bacterium is usually harmless when it is kept in check by symbiotic microbes normally found in the human gut. However, when the gut microbiome is suppressed by antibiotics, C. difficile can take over: Its toxins can spur a severe autoimmune response that causes symptoms such as diarrhea, cramping, fever and nausea.
The research combined machine learning, experiments with a technique called small-angle X-ray scattering at the Stanford Synchrotron Radiation Lightsource (a Department of Energy laboratory), and experiments using human cell lines, mouse cell lines and mice.
Understanding the mechanisms by which C. difficile’s toxins trigger intestinal inflammation is an important step toward developing methods for treating or preventing infection by the bacterium.
Jaime de Anda, a graduate student in bioengineering at UCLA, is the study’s co-first author, along with Xinhua Chen and Xiaotong Yang of Harvard Medical School. Corresponding authors are Gerard Wong, a UCLA professor of bioengineering and member of the California NanoSystems Institute at UCLA, and Chen. Other authors are Jun Huang, Dan Li, Hua Xu, Kelsey Shields, Joshua Hansen, Marianne Grant and Ciarán Kelly of Harvard; Mária Dzunková of the Lawrence Berkeley National Laboratory; Ishan Patel of Stony Brook University Hospital in New York; Eric Yee of the University of Arkansas; and Douglas Golenbock of the University of Massachusetts.
The study was funded by the National Institutes of Health, the National Science Foundation, the DOE, the Irving W. and Charlotte F. Rabb Award, and the Crohn’s and Colitis Foundation of America.
Reference: Xinhua Chen, Xiaotong Yang, Jaime de Anda, Marianne A. Grant, Gerard C.L. Wong, Ciarán P. Kelly et al., “Clostridioides difficile Toxin A Remodels Membranes and Mediates DNA Entry Into Cells to Activate Toll-Like Receptor 9 Signaling”, Gastroenterology, 159(6), pp. 2181-2192, Dec 1, 2021 https://doi.org/10.1053/j.gastro.2020.08.038
Ali Ovgun and colleagues studied the evolving wormhole, using dark matter and dark energy. They have obtained the evolving dark wormhole with interesting results.
A wormhole in spacetime is a gravitational quantum fluctuation or bridge, connecting different points and creating a short-cut. Einstein and Rosen first elaborate on wormhole in 1935 using the theory of general relativity. Then, main contributions on traversable wormholes are done by Morris, Thorne and Yurtsever in 1980s. However, since then, no one has discovered a wormhole to date, it is pure theoretical research area. To understand the nature of the Universe with its mysterious is an one of the puzzle of the human’s life.
Now, Ali Ovgun and colleagues have obtained the evolving dark wormhole with interesting results. Their solutions of the dark wormhole showed that it is located in the early universe and it decays during the inflation. On the other hand, evolving dark wormhole is inflated and continues to accelerated expansion.
The importance of their work is that the matter has two components: cosmological part (only time dependent) and wormhole part (only space dependent). To do so, they used the Chaplygin gas as an equation of state for cosmic part,
and Navarro-Frenk-White dark matter density profile to form dark wormhole.
They revealed more interesting results that evolving dark wormhole is located between the Big Bang and inflation. During inflation, it decays, and then there is no dark wormhole i.e. it vanished. It showed that wormhole behaves similarly to the inflation.
Moreover, in the Fig. (1-5), they plot the scale factor R(t) versus time t, scale factor R(t) versus α with different configurations to show behavior of the evolving wormhole in the inflation era. The figures showed that, first evolving wormhole begun with negative α till inflation, then it was periodically expanding at an accelerating rate and then decelerating rate. The α has a role of fine tuning.
“We have also addressed some open questions to the Kim’s arguments that one might raise. For example, the scale factor of the universe has two components complex and real. We wonder that how it is possible, and how we can explain it. Another issue is that wormhole shall be small as a scale of the Planck length at the Big bang, but then expands too much greater and decays smaller than the Planck length. One may wonder whether wormholes make phase transition to black hole in fact contribute significantly to inflation. On the other hand, if it is correct, this proposal renew in basis our aspiration of understanding how Nature works as parallel of evolving wormhole in universe.”, concluded authors of the study.
Amendola and colleagues presented a novel framework for primordial black hole (BH) formation which does not rely on a particular feature in the spectrum of primordial density fluctuations generated during inflation. They proposed that the primordial black holes can be produced by a long range attractive fifth force stronger than gravity, mediated by a light scalar field interacting with nonrelativistic “heavy” particles.
In spite of the many observations leading to the establishment of dark matter as an essential ingredient of modern cosmology, its fundamental nature remains an open question. Among the many dark matter candidates, primordial black holes (BH) are interesting since they could account for the gravitational wave signals observed by the Laser Interferometer Gravitational Wave Observatory (LIGO) and the VIRGO observatory or seed the formation of supermassive black holes. The existence of primordial BHs could be a natural consequence of inflation. In particular, if the inflationary potential contains a nontrivial feature along the inflaton trajectory, the spectrum of primordial perturbations might develop a peak at intermediate scales. If the amplitude of this peak is large enough, the nonlinear perturbations will collapse into BHs after horizon reentry. Alternatively, the formation of primordial BHs could take place at phase transitions or be associated with the fragmentation of a scalar condensate into Q-balls.
Now, Amendola and colleagues in their paper presented a novel framework for primordial BH formation which does not rely on a particular feature in the spectrum of primordial density fluctuations generated during inflation. The main assumption of their scenario is the presence in the early Universe of a long-range interaction stronger than gravity. They associate this fifth force to a light scalar field interacting with some heavy degrees of freedom beyond the Standard Model particle content. More precisely, they assume that during some epoch in cosmology the Hubble parameter, which they designate as ‘H’, is larger than the mass of a scalar field ‘φ’. If this scalar field couples to some “heavy particles” ψ with masses larger than Hubble parameter ‘H’, it mediates an attractive fifth force which is effectively long range, similar to gravity. This attraction can be, however, substantially stronger than the gravitational attraction. As a result, the fluctuations in the energy density of the heavy fields can grow rapidly and eventually become nonlinear. If the range and strength of the fifth force is large enough, it seems likely that a substantial part of the ψ fluid will collapse into BHs or similar screened objects.
“As soon as the energy fraction of heavy particles reaches a threshold, the fluctuations rapidly become nonlinear. The overdensities collapse into black holes or similar screened objects, without the need for any particular feature in the spectrum of primordial density fluctuations generated during inflation.”, said Amendola.
So, the question is whether such primordial black holes can constitute the total dark matter component in the Universe?
Well friends, existence of long-range attractive forces stronger than gravity is a natural expectation in particle physics models containing scalar fields. The simplest example is the attractive interaction among Standard Model fermions via Higgs particle exchange. In early cosmology it is much stronger than the gravitational attraction. If not countered by electromagnetic interactions, even the Standard Model Higgs would have induced gravitational collapse at early times. Alternatively, the scalar field i.e. φ and heavy particle ‘ψ’ fields could be associated with grand unified frameworks involving, for instance, a scalar triplet interacting with heavy neutrinos. In this case, the BH formation process could occur very early in cosmology, for example nearly after the end of inflation. For different properties of the participating particles it could also take place rather late in the cosmological history, say after nucleosynthesis.
The heavy particles remaining outside primordial BHs might decay after the formation epoch and be unobservable today. The scalar field could relax after BH formation to a minimum of its effective potential with mass eventually exceeding the decreasing Hubble parameter. In this case, the scalar field φ would not be observable at the present time either. Alternatively, φ could be an additional dark matter candidate, or have a runaway behavior and be associated with dynamical dark energy. The BH formation process is not affected by what happens to the participating fields or particles at later times. Once BHs are formed, they behave as nonrelativistic matter. If the total energy density of BHs is large enough, they could constitute the dark matter component of our Universe.
Their work got support from the DFG through the project TRR33, “The Dark Universe”.