Question

1-What is the evolutionary process behind sleep?

2-If a similar environmental pressure was applied to apes that led to the early evolution of humans, could they eventually evolve like early humans did give enough time?

3-How do historical constraints effect variation?

Answer 1

Question 1-What is the evolutionary process behind sleep?

Answer: Sleep is nearly ubiquitous throughout the animal kingdom, yet little is known about how ecological factors or perturbations to the environment shape the duration and timing of sleep. In diverse animal taxa, poor sleep negatively impacts development, cognitive abilities and longevity. In addition to mammals, sleep has been characterized in genetic model organisms, ranging from the nematode worm to zebrafish, and, more recently, in emergent models with simplified nervous systems such as Aplysia and jellyfish. In addition, evolutionary models ranging from fruit flies to cavefish have leveraged natural genetic variation to investigate the relationship between ecology and sleep.

Sleep appears to be fundamental to animal life, yet little is known about how sleep has evolved throughout the animal kingdom. In diverse animal taxa, poor sleep can have detrimental effects on development, cognitive abilities and life span, and it is now appreciated that normal sleep is fundamental to healthy physiology and bodily function. While the function of sleep remains unknown, studies have identified relationships between sleep and anatomical, physiological or ecological traits. For example, in mammals, parameters such as diet, brain size, social hierarchy and body mass index all affect total sleep times. A great deal of variation exists in sleep duration and timing among different animal phyla, with animals such as the African Elephant sleeping only 3–4 h a day while many animals spend the majority of their time sleeping, including the armadillo, which sleeps over 18 h per day. Even among humans, sleep times vary widely, ranging from less than 5 h to 10 h or more. Despite a widespread appreciation for the diversity in sleep duration between and within species, surprisingly little is known about the relationship between sleep and an animal's ecological and evolutionary history.

Large differences in sleep duration and timing among humans suggests that existing genetic variation among individuals potently affects sleep. While many laboratory studies investigating the molecular mechanisms of sleep regulation have relied on highly inbred model systems including mice, zebrafish and fruit flies, the study of sleep in outbred populations has revealed that geographical location, evolutionary history and naturally occurring genetic variation contribute to robust sleep differences within animals of the same species. Even though sleep has been characterized in surprisingly few evolutionary systems, small, non-mammalian model organisms with a well-defined evolutionary history provide opportunities to identify novel mechanisms underlying sleep regulation.

Achieving a full understanding of sleep function requires detailed characterization of the genetic, molecular and neuronal properties associated with sleep and wakefulness. Over the past few decades, non-mammalian genetic model systems including the nematode worm Caenorhabditis elegans, the fruit fly Drosophila melanogaster and the zebrafish Danio rerio (have been particularly advantageous in elucidating genetic and molecular components underlying sleep. Many forward-genetic screens have highlighted the conservation of molecular and neural principles underlying sleep–wake regulation, and initial studies in zebrafish, Drosophila and C. elegans have identified novel and conserved regulators of sleep. Although a mechanistic understanding of sleep regulation is far from complete, these studies provide a framework for interpreting how inter- and intra-species variation may account for naturally occurring differences in sleep.

Classical approaches to characterizing sleep

Sleep is characterized in different ways, depending on the available methods in the organism of study. The two hallmarks classically have been (i) electrophysiological or (ii) behavioral changes associated with sleep-like states. Importantly, there is a strong correlation between sleep-like states defined by electrophysiological and behavioral criteria in animals ranging from invertebrates to mammal. Electrophysiologically, sleep is characterized by changes in brain wave activity, as measured by the electroencephalogram (EEG) in mammals, or local field potential recordings in invertebrates. The EEG has established its place in sleep research, and provides the ability to compartmentalize sleep into three different stages based on unique patterns of brain wave activity: (i) waking periods, (ii) non-rapid eye movement (NREM), slow-wave sleep, and (iii) REM (see Glossary) or paradoxical sleep . Nevertheless, a number of limitations to electrophysiological recordings, including difficulty of recording in small animals and impracticality of recording in a natural setting, highlight the need for behavioral observations that can be used to define sleep.

Animals in a sleep-like state, as measured by an EEG, typically assume stereotypical behaviors, and, by carefully correlating behavior with changes in EEG patterns, behavioral identifiers have been established. Behaviorally, sleep can be characterized by five criteria: (i) prolonged behavioral quiescence, (ii) which is reversible upon stimulation (to differentiate from torpor or coma), (iii) a species-specific posture, (iv) increased arousal threshold (see Glossary) to respond to external stimuli, and (v) rebound (see Glossary) following sleep deprivation. The establishment of behavioral definitions of sleep has opened the door to investigating sleep in small model systems that are not amenable to EEG analysis. Although EEG measurements are typically restricted to a limited subset of taxonomic groups, behavioral definitions are largely generalizable to all animals in the animal kingdom, and permit the investigation of sleep from a comparative perspective, as well as in small genetically amenable animal models.

Landmark papers over the past 20 years have defined sleep in classic genetic systems including C. elegans, Drosophila and zebrafish. Each model has unique and shared characteristics that are particularly useful for sleep analysis. In all three model systems, sleep state is associated with prolonged periods of behavioral quiescence, which are readily reversible and correspond to an increase in arousal threshold; reviewed in. Of the classic genetic model systems, worms contain the fewest neurons. The adult hermaphrodite worm has 302 neurons, all of which have been mapped out with sufficient detail, while the larval zebrafish brain and adult fruit fly brain contain 100,000 and 250,000 neurons, respectively. The simple nervous system and powerful genetics of these models has led to the identification of neural circuits, up to single-neuron resolution, that modulate sleep. The unique application of sophisticated genetic tools and high-throughput genetic screens have paved the way for mechanistic investigation of sleep regulation that has revealed robust conservation across the animal kingdom.

Physiological approaches to characterizing sleep

Although studies in invertebrates and fish have typically relied on behavioral metrics of sleep, there is growing evidence that physiological metrics often used to characterize sleep in mammals are present in small non-mammalian models. Sleep-associated brain activity has been convincingly demonstrated in the fruit fly, where five minutes of inactivity was initially used to define sleep based on the standardized behavioral characteristics, and standardized behavioral systems have been developed to measure sleep.The detailed behavioral characterization of sleep opened the door to genetic interrogation of sleep in invertebrates and fish models; they lack the precision of EEG or other physiological read-outs of sleep and come with a number of limitations including difficulty of identifying awake animals engaged in torpor.

Later, elegant experimental designs demonstrated that definitions of sleep based on behavior and those based on electrophysiology largely corresponded with one another. A system was devised to record the neural properties of the fly brain in an adult tethered to a tracking ball, providing the opportunity to simultaneously observe neural and behavioral correlates of sleep. Simultaneous recordings of brain local field potentials (see Glossary) and locomotor activity (see Glossary) on a rotating ball revealed reduced neuronal activity (11–40 Hz oscillations) when flies are immobile, which also correlates with elevated arousal threshold. In agreement with these findings, dynamic changes in metabolic rate were observed in sleeping flies, supporting the notion that flies, like mammals, suppress metabolic rate when starved of food. It is possible that these physiological metrics of sleep will reveal physiological changes akin to sleep stages in animals with more complex brains and can be applied to additional invertebrate and fish models. For example, a study in crayfish identified sleep using all the behavioral correlates, and electrophysiological recordings revealed synchronized activity similar to slow-wave sleep. Together, these findings highlight the strength of model organisms in genetic research to identify brain states associated with sleep that are conserved throughout the animal kingdom

Screen-based identification of sleep regulators using classic model systems

A significant strength of small, genetically amenable model organisms is the ability to screen large numbers of animals for mutations or drugs that affect behavior. In the case of sleep studies, this has been supported by the development of behavioral monitoring systems in C. elegans, Drosophila and zebrafish that allow for high-throughput analysis of locomotor activity. The combination of defined methodology for measuring sleep, and a vast array of genetic mutants and tools provide the capability to identify genetic and pharmacological regulators of sleep.

Classic genetics were first used to investigate circadian rhythms (see Glossary) in fruit flies, and more recently applied to identify novel sleep genes. Large-scale forward-genetic screens in fruit flies have used mutagenesis or transgenic expression of interfering RNA (RNAi) to identify sleep-regulating genes including the K+ channel Shaker, the regulator of cell-cycle modulator Cyclin A, and transmembrane protein Sleepless. Similar endeavors in C. elegans and zebrafish have identified additional regulators of sleep, many of which appear to be conserved in mammals. For example, a prominent role for the worm homologue of mammalian Neuropeptide Y receptor NPR-1 is required for sleep homeostasis in C. elegans, and genome-wide screening identified striking overlap between sleep genes in worms and mammalian systems. Similarly, screens in zebrafish have implicated the prominent regulators of mammalian sleep Hypocretin/Orexin and melatonin, as well as a number of novel genes required for integration of sleep and sensory systems that detect light. The diversity of genes identified in these forward-genetic screens highlights the strength of model systems to identify novel genetic architecture contributing to sleep circuits.

The strength of invertebrate and fish models extend beyond genetic applications. Zebrafish, Drosophila and C. elegans are well suited for drug screening, where the quantity of available compounds is often a limiting factor, and pharmacological targets can be validated genetically. In a landmark study, over 5000 compounds were assayed in larval zebrafish for their effect on sleep latency (see Glossary), duration and bout number. This study identified a number of sleep- or activity-regulating drugs including inhibitors of ether-a-go-go-related K+ channel, which promote waking activity. Similar approaches have been used in fruit flies, where a sleep screen testing 1280 small molecules identified numerous novel regulators of sleep including the vesicular monoamine transporter VMAT. Although these approaches have yet to be applied to study sleep in C. elegans, the use of small-molecule screens to study other processes and availability of high-throughput behavioral monitoring systems suggest that this approach is feasible. These approaches highlight the potential for drug discovery using small-molecule-based screens and sleep itself providing a behavioral read-out of drug efficacy.

Use of emergent systems to study how evolution and ecology shape sleep

Investigating the origins of sleep

Genetic variation has been selected against in many laboratory strains of genetic model organisms, often obscuring the ecological relevance of different genetic or neuronal perturbations. Moreover, the small number of genetically amenable models, typically limited to inbred populations of C. elegans, Drosophila, zebrafish and mice, represent a narrow subset of species that sleep. The identification of sleep in C. elegans revealed that sleep exists even in animals with relatively simple nervous systems, suggesting that sleep is an ancient behavior that is probably present throughout the animal kingdom . The potentially ancient ancestral origins of sleep has led to a prominent question in the field of whether sleep is a property of neural circuits, or rather a property of individual cells . Although this is difficult to address in animals with complex brains, organisms with simplified nervous systems provide the ability to ask questions about the fundamental cellular function of sleep.

As stated above, characterizing sleep in novel animal models requires defining sleep based upon behavioral criteria including the period of behavioral quiescence that is associated with changes in arousal threshold. Recently, these metrics have been applied to marine species with simplified nervous systems, called nerve nets, including the Cnidarian jellyfish, as well as multiple different species of molluscs. Each of these organisms has nervous systems that may be useful in dissecting the basic neural principles and functions of sleep regulation, although it is noted that the duration, circadian timing and characteristics of sleep vary dramatically between species.

The nerve net in jellyfish consists of rings of neurons along the axial length of the organism. Sleep has been investigated in different species of the ‘upside-down’ jellyfish, Casseopea, a genus typically found in the shallow coastal waters surrounding Florida and the Caribbean islands. When active, they display contractions of the nerve net, which in turn causes pulsing behavior that facilitates feeding and flow of nutrients throughout the organism. Pulsing behavior and their sensitivity to external stimuli is reduced during night-time periods, suggesting that night-time behavioral quiescence is a sleep-like state. Lastly, when sleep deprived by mechanical stimulation (intermittent water flow during the night), jellyfish exhibit increased immobility the following day that is indicative of a homeostatic rebound in sleep. Therefore, jellyfish possess many of the behavioral hallmarks of sleep and provide a new model for studying the origins of sleep.

Similarly, sleep has been characterized in several species of molluscs, including the gastropods Aplysia californica, pond snail (Lymnaea stagnalis), the octopus (Octopus vulgaris) and at least one cephalopod, the cuttlefish (Sepia officinalis). All of these organisms show periods of behavioral quiescence that correspond to a sleep-like state. Interestingly, circadian modulation of sleep–wake cycles varies among molluscs: Aplysia and cuttlefish display robust diurnal (see Glossary) waking rhythms, whereas the octopus is nocturnal (see Glossary) and the pond snail exhibits infrequent sleep states that occur without influence of time of day. Thus, even between these cephalopod and gastropod species, sleep structure is highly variable, and may provide insight into ecological- and niche-dependent interactions between sleep and circadian rhythms.

Natural variation in sleep regulation

The naturally occurring variation in human sleep duration or timing appears to be genetically encoded, although little is known about the specific genes that contribute to differences in sleep need between individuals. Although single genes have been identified that contribute to naturally occurring variation in sleep, most variability undoubtedly comes from a complex genetic architecture. Recent genome-wide association studies (GWAS) have typically relied on self-reported sleep duration, latency and chronotype, while other studies have used actigraphy. A significant impediment to these studies has been validating the function of GWAS alleles and investigating their mechanistic role in sleep regulation. One GWAS study that used self-reported sleep data from over 4000 individuals estimated that a locus containing the KATP channel ABCC9 accounted for approximately 5% of variation in human sleep. Genetic knock-down of the ABCC9 fruit fly ortholog sufonurea receptor 2 (dsur2) in neurons selectively reduced night sleep without affecting daytime sleep. These findings validate a role for ABCC9/dsur2 and the utility of reverse-genetic approaches to functionally validate genes identified through human GWAS studies.

Naturally occurring variation and its effects on sleep can be leveraged in a laboratory setting, and as such, the contributions of naturally occurring genetic variation to sleep regulation can also be directly investigated in model systems. While laboratory studies of D. melanogaster typically rely on inbred strains that have been housed in the laboratory for decades, this species is found in diverse climates all over the world.. Drosophila melanogaster from different geographical regions are genetically distinguishable at genetic and behavioral levels Multiple studies have found that increased sleep duration is associated with proximity to the equator, suggesting that flies from warmer climates with reduced seasonal variation in temperature sleep longer than flies from northern latitude clines. A transcriptome comparison between flies from high and low latitudes revealed enrichment of differentially expressed genes related to circadian clock function. These findings, combined with short-sleeping phenotypes of circadian mutants, and a known wake-promoting role for circadian neurons, suggest that selection on latitude-associated changes in the circadian genes may contribute to sleep difference in naturally occurring populations of Drosophila. Investigating the relationship between sleep and circadian function in flies from geographically diverse regions may uncover novel interactions between the circadian and sleep–wake rhythms

Additional ecologically relevant factors that modulate sleep

While sleep research has predominantly focused on measuring sleep under standardized and stable laboratory conditions, the responses to environmental perturbations are understudied, and are likely to be under strong evolutionary selection (Tourgeron and Abram, 2017). Many environmental factors, including food availability, social interactions and temperature, potently impact sleep in diverse phyla. For example, sleep is reduced in flies reared in isolation, and exposure of male flies to females suppresses sleep, revealing robust modulation of sleep by social stimuli. These important modulators of sleep are likely to be missed in behavioral assays used in most animal systems that measure each animal in an independent arena, and highlight the need for investigating sleep in an ecologically relevant context.

In addition to social experience, nutrient availability is a crucial modulator of sleep, and animals weigh the cost–benefit of energy savings from sleep against the benefits of wakefulness. Animals ranging from flies to humans sleep more following a meal, and sleep is disrupted during starvation. Although it has long been presumed that these acute responses to nutrient availability represent a mechanism of maintaining metabolic homeostasis, this hypothesis has been difficult to test experimentally. A number of studies in fruit flies have investigated neural circuits regulating starvation-induced changes in sleep. These studies have found that both sensory perception of taste and signalling molecules that promote food consumption inhibit sleep, supporting the notion that shared pathways regulate both sleep and feeding. A genetic screen identified pathways that appear to modulate starvation-induced changes in sleep that do not affect energy stores, metabolic function or feeding behavior. While the relationship between sleep and food availability has not been tested in many models, including zebrafish, it is possible that different species have unique adaptations to food availability. For example, prolonged starvation increases sleep in cavefish, similar to what is observed in birds, perhaps representing an energy-saving mechanism to account for long periods with limited food during the dry season. Broader systematic analysis of species-specific responses to changes in food availability and improved understanding of the neural basis for these changes will determine how sleep is modulated by environmental perturbations.

In an ethologically relevant context, many additional factors will have a potent impact on sleep. For example, increased sleep during early development has been documented in flies and humans, and it appears to be crucial for normal brain development. Sleep is affected by many environmental variables, and the small model systems are likely to be amenable to investigation of how sleep is affected by diverse social processes. It is possible that the drive to identify sleep genes and standardization of approaches has obscured many key regulators of sleep that are related to the response to stress, food availability, social behavior or other factors. Investigating the relationship between ecology and these factors is necessary to understand the evolutionary features regulating sleep, and the short lifespan of many models allows for tracing sleep differences throughout development

The development of behavioral assays to measure sleep in fruit flies, C. elegans and zebrafish has led to the rapid discovery of genetic and neural processes regulating sleep. These findings pave the way for investigating the function of sleep, and how it is altered by an animal's ecological environment and evolutionary history. In recent years, progress using behavioral criteria to define sleep in a number of novel model organisms including the jellyfish, Aplysia and cavefish have potential to provide new insight into the biological and functional basis of sleep regulation. Many animals are uniquely suited for studying specific functions of sleep, including the use of Aplysia to study the relationship between sleep and memory formation, and the honeybee to examine interactions between sleep and social experience. We propose that by characterizing sleep in additional animal models of evolution ranging from organisms with simplified nervous systems such as the starlet sea anemone Nematostella to the three-spined stickleback, a model of microevolution, we will gain a better understanding of how ecology and life history traits regulate sleep. The emergence of sleep studies in organisms with simplified nervous systems or defined evolutionary history, combined with the development of gene-editing technology, provide novel avenues to investigate the evolution of function of sleep. Together, these integrative approaches in diverse models will help define the relevance of genetic and neural principles regulating sleep to the broader animal kingdom.

Question 2-If a similar environmental pressure was applied to apes that led to the early evolution of humans, could they eventually evolve like early humans did give enough time?

Answer:  

In the approximately 3.8 billion years since life originated on Earth, evolution has resulted in many complex organisms and structures. The human brain and stereoscopic eyes are just two examples. At the same time, simpler organisms like algae, bacteria, yeast, and fungi, which arose several billion years ago, not only persist but thrive. The presence of single-celled organisms alongside complex organisms like humans testifies to the fact that evolution within a given lineage does not necessarily advance toward increasing complexity. When more complex organs are advantageous, complex organs have arisen. Single-celled organisms, however, fill many roles, or niches, much better than any multicellular organism could, and so they remain in a relatively stable state of adaptation.

Extinction is often caused by a change in environmental conditions. When conditions change, some species possess adaptations that allow them to survive and reproduce, while others do not. If the environment changes slowly enough, species will sometimes evolve the necessary adaptations, over many generations. If conditions change more quickly than a species can evolve, however, and if members of that species lack the traits they need to survive in the new environment, the likely result will be extinction.

It is possible that in many millions of years present day apes could evolve into some other humanlike species. It is, however, very improbable. First of all, humans did not evolve from any of the species we know as apes today. At some point 5 to 8 million years ago, the common ancestor of humans and modern apes diverged to form the two separate lineages we know today. The species at the end of these lineages are a result of a very specific combination of selection pressures and genetic mutations over millions of years. This same combination is highly unlikely to occur ever again.

Evolution isn't a progression. It's about how well organisms fit into their current environments. In the eyes of scientists who study evolution, humans aren't "more evolved" than other primates, and we certainly haven't won the so-called evolutionary game. While extreme adaptability lets humans manipulate very different environments to meet our needs, that ability isn't enough to put humans at the top of the evolutionary ladder. We have this idea of the fittest being the strongest or the fastest, but all you really have to do to win the evolutionary game is survive and reproduce.

Even our earliest ancestors that diverged from our common ancestor with chimpanzees would have been adept at both climbing in trees and walking on the ground. It was more recently — maybe 3 million years ago — that these ancestors' legs began to grow longer and their big toes turned forward, allowing them to become mostly full-time walkers.

Humans did not evolve from present-day apes. Rather, humans and apes share a common ancestor that gave rise to both. This common ancestor, although not identical to modern apes, was almost certainly more apelike than humanlike in appearance and behavior. At some point -- scientists estimate that between 5 and 8 million years ago -- this species diverged into two distinct lineages, one of which were the hominids, or humanlike species, and the other ultimately evolved into the African great ape species living today.

Most scientists would agree unequivocally that humans have greatly affected the process of evolution, from the rise of antibiotic and pesticide resistance to the largely human-caused increase in the extinction rate. Our effect on the process of evolution even extends to our own species' evolution. Technology and culture have protected us to a great extent from the selective pressures that drive evolution, allowing many people -- especially those in developed nations who, without medical intervention, would not live to reproductive age -- to pass their genes on to the next generation. Other scientists note that technology and culture have changed but not eliminated the role of natural selection on our species. We now adapt to crowding, pollution, and new disease rather than the necessity to escape from large predators. Humans will change in the future, but are unlikely to evolve into a new, separate species because no human group is truly isolated anymore, given our transportation systems. Without genetic isolation, there is no further opportunity for speciation among humans.

Question 3-How do historical constraints effect variation?

Answer: Evolutionary constraints are restrictions, limitations, or biases on the course or outcome of adaptive evolution. The term usually describes factors that limit or channel the action of natural selection. It is not equivalent to evolutionary stasis (absence of change) or even to factors that cause stasis. Evolutionary stasis may be caused by stabilizing selection, but stabilizing selection caused by the external environment is not usually considered a constraint. In a general sense all evolution is constrained. There are no Darwinian demons, immortal organisms that can reproduce infinitely fast, and the concept of constraint is most useful in relation to specific traits, selective agents or ecological contexts. Constraints occur when a trait is precluded from reaching, shifted away from, or slowed down in its approach to a (defined) selective optimum. Interest in the interplay between selection and constraints goes back to Darwin, and specifically to his concept of correlation of growth, which he used to explain how traits may change as side effects of selection on other traits. The fundamental idea is that selection acts on variation so that the structure and availability of variation may constrain what selection can do. Constraint thinking also has links to orthogenesis, the notion that evolution is driven in particular directions by some internal lineage-specific force rather than by external selection caused by interactions with the environment. Orthogenesis was rejected during the modern synthesis due to a lack of plausible mechanism, accumulating evidence for local adaptations, and an emerging understanding of macroevolution as a messy historical process rather than a rectilinear march toward perfection. The modern synthesis saw increasing emphasis on functional explanations based on external natural selection while structural explanations based on development became marginalized. This was influenced first by the realization that selection can act efficiently on minute differences, and later by the empirical findings of large amounts of genetic variation both on molecular and organismal levels. Hence, mainstream evolutionary biology increasingly took it as given that the necessary variation for selection to act was available. After a nadir in the 60s, a structuralist perspective with an emphasis on developmental constraints started to reemerge. This was manifest first in the revival of concepts such as heterochrony and allometry, which may be seen as specific constraints on evolution, and later in the emerging field of evolutionary developmental biology, or evodevo, where the study of developmental constraints is central. An important element in the modern treatment of constraints is that constraints are not just seen as limitations and explanations of last resort, but are also assigned positive explanatory roles based on channeling variation in directions that may facilitate and explain adaptation.

Few concepts in biology are as manifold and lacking in consensus as that of constraints. On the top level are genetic constraints, which are reasonably well operationalized in terms of standing genetic variation. Levels of genetic variation may limit evolution if they are absent or too low, or if variation in different traits are bound up with each other by genetic correlations. The underlying cause of genetic constraints is developmental constraints, which control the input of new genetic variation through mutation, and thus determine genetic constraints in interaction with selection. Selective and functional constraints refer to effects of selection on other traits or for other functions than the focal adaptation, and thus explain how genetic correlations constrain evolution. They also help explain patterns of genetic variation that stem from fundamental trade-offs and physical limitations that no biological system can circumvent. Phylogenetic and historical constraints are orthogonal to this scheme. Here the emphasis is on the role of ancestry in determining the subsequent course of evolution. This is both because the species may inherit particular traits or developmental systems that constrain the possible variation that forms the basis for new adaptations, and because the ancestral position in a complex adaptive landscape can influence which local adaptive peak is eventually reached. Schwenk 1995 and Richardson and Chipman 2003 provide other classifications of constraint terminology. Futuyma 2010 is a recent review of explanations for stasis in evolution showing that maladaptation is common and that there is room for constraints as an explanatory factor alongside adaptation. Gould 2002 and Amundson 2005 provide historical overviews of structuralist positions in evolutionary biology in which developmental and historical constraint concepts are central.

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