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\"A smart philosophical look at the cult hit television show, Arrested Development. Arrested Development earned six Emmy awards, a Golden Globe award, critical acclaim, and a loyal cult following-and then it was canceled. Fortunately, this book steps into the void left by the show's premature demise by exploring the fascinating philosophical issues at the heart of the quirky Bluths and their comic exploits. Whether it's reflecting on Gob's self-deception or digging into Tobias's double entendres, you'll watch your favorite scenes and episodes of the show in a whole new way. Takes an entertaining look at the philosophical ideas and tensions in the show's plots and themes. Gives you new insights about the Bluth family and other characters: Is George Michael's crush on his cousin unnatural? Is it immoral for Lindsay to lie about stealing clothes to hide the fact that she has a job? Are the pictures really of bunkers or balls? Lets you sound super-smart as you rattle off the names of great philosophers like Sartre and Aristotle to explain key characters and episodes of the show. Packed with thought-provoking insights, Arrested Development and Philosophy is essential reading for anyone who wants to know more about their late, lamented TV show. And it'll keep you entertained until the long-awaited Arrested Development movie finally comes out. (Whenever that is.)\"-- Provided by publisher.

Developmental arrest of the preimplantation embryo is a multifactorial condition, characterized by lack of cellular division for at least 24 hours, hindering the in vitro fertilization cycle outcome. This systematic review aims to present the molecular drivers of developmental arrest, focusing on embryonic and parental factors. A systematic search in PubMed/Medline, Embase and Cochrane-Central-Database was performed in January 2021. A total of 76 studies were included. The identified embryonic factors associated with arrest included gene variations, mitochondrial DNA copy number, methylation patterns, chromosomal abnormalities, metabolic profile and morphological features. Parental factors included, gene variation, protein expression levels and infertility etiology. A valuable conclusion emerging through critical analysis indicated that genetic origins of developmental arrest analyzed from the perspective of parental infertility etiology and the embryo itself, share common ground. This is a unique and long-overdue contribution to literature that for the first time presents an all-inclusive methodological report on the molecular drivers leading to preimplantation embryos’ arrested development. The variety and heterogeneity of developmental arrest drivers, along with their inevitable intertwining relationships does not allow for prioritization on the factors playing a more definitive role in arrested development. This systematic review provides the basis for further research in the field.

Turtle embryos enter a state of arrested development in the oviduct, allowing the mother greater flexibility in her reproductive schedule. Development recommences once eggs transition from the hypoxic oviduct to the normoxic nest. Significant mortality can occur if turtle eggs are moved between 12 h and 20 d after oviposition, and this is linked to the recommencement of embryonic development. To better understand the timing of developmental arrest and to determine how movement-induced mortality might be avoided, we determined the latency (i.e., time elapsed since oviposition) to recommencement of development following oviposition by exposing the eggs of green turtles (Chelonia mydas) to hypoxia (oxygen tension <8 mmHg) for 3 d, commencing 30 min to 48 h after oviposition. Embryonic development—including development of the characteristic opaque white spot on the eggshell—was halted by hypoxic incubation. When the delay before hypoxic incubation was 12 h or less, hatching success did not differ from a control group. If the hypoxic treatment began after 16 h or more in normoxia, then all embryos died. Thus, by returning eggs to a hypoxic environment before they have broken from arrest (i.e., within 12 h of oviposition), it is possible to extend embryonic arrest for at least 3 d, with no apparent detriment to hatching success. Therefore, hypoxic incubation may provide a new approach for avoidance of movement-induced mortality when conservation or research efforts require the relocation of eggs. Our findings also suggest that movement-induced mortality may have constrained the evolution of viviparity in turtles.

Arrested embryonic development involves the downregulation or cessation of active cell division and metabolic activity, and the capability of an animal to arrest embryonic development results in temporal plasticity of the duration of embryonic period. Arrested embryonic development is an important reproductive strategy for egg-laying animals that provide no parental care after oviposition. In this review, we discuss each type of embryonic developmental arrest used by oviparous reptiles. Environmental pressures that might have directed the evolution of arrest are addressed and we present previously undiscussed environmentally dependent physiological processes that may occur in the egg to bring about arrest. Areas for future research are proposed to clarify how ecology affects the phenotype of developing embryos. We hypothesize that oviparous reptilian mothers are capable of providing their embryos with a level of phenotypic adaptation to local environmental conditions by incorporating maternal factors into the internal environment of the egg that result in different levels of developmental sensitivity to environmental conditions after they are laid.

A case report of an incidental finding of bilateral fourth and fifth metacarpal fusions with fifth metacarpal hypoplasia in a 36 year old male. No evidence of any other skeletal abnormality. No evidence of endocrine pathology. An X –linked recessive inheritance is postulated.

Although viviparity (live birth) has evolved from oviparity (egg laying) at least 140 times in vertebrates, nearly 120 of these independent events occurred within a single reptile taxon. Surprisingly, only squamate reptiles (lizards and snakes) are capable of facilitating embryonic development to increasingly advanced stages inside the mother during extended periods of oviducal egg retention. Viviparity has never evolved in turtle lineages, presumably because embryos enter and remain in an arrested state until after eggs are laid, regardless of the duration of egg retention. Until now, the limiting factor that initiates and maintains developmental arrest has remained elusive. Here, we show that oviducal hypoxia arrests embryonic development. We demonstrate that hypoxia can maintain developmental arrest after oviposition and that subsequent exposure of arrested embryos to normoxia triggers resumption of their development. We discovered remarkably low oxygen partial pressure in the oviducts of gravid turtles and found that secretions produced by the oviduct retard oxygen diffusion. Our results suggest that an extremely hypoxic environment in the oviduct arrests embryonic development and may constrain the evolution of viviparity in turtles, with the reduced diffusive capacity of oviducal secretions possibly creating or contributing to this hypoxia. We anticipate that these findings will allow us to better understand the mechanisms underlying the evolutionary transition between reproductive modes.

Skillful El Niño–Southern Oscillation (ENSO) prediction is one of the most important problems in climate science due to its substantial global impacts. There have been many successful examples of predicting ENSO using dynamical climate models since the mid-1980s. It was therefore unexpected that many operational climate models significantly overestimated the likelihood of La Niña conditions in 2024. In this report, we examine the physical processes associated with the arrested development of La Niña conditions in 2024/25, and the possible reasons for overestimated predictions of its strength. Despite favorable subsurface cooling conditions following a strong 2023/24 El Niño, we argue that arrested development of La Niña conditions in 2024/25 resulted from weak episodic easterly wind anomalies and associated weak upwelling Kelvin wave activity, which failed to shoal the thermocline sufficiently to initiate basin-wide air-sea coupling. Furthermore, we find that weaker Kelvin wave activity and ENSO amplitude reduction were linked to the ENSO regime shift with strengthened mean zonal sea surface temperature contrast and enhanced mean trade winds in the tropical Pacific around 2000. Model limitations in capturing atmospheric variability and interdecadal shift contributed to the overestimated strength of the La Niña predictions in 2024/25, underscoring the importance of properly simulating atmospheric variability and the interdecadal regime shift in dynamical models used for predicting ENSO.

Piagetian cross-cultural psychology indicated that humans living in preindustrial nations do not develop the adolescent stage of formal operations but stay in the preoperational or concrete operational stage. The stage of formal operations originated among intellectual elites of early modern times and became a mass phenomenon in the 20th century, many empirical indicators suggest. Racial-biological approaches cannot explain these phenomena, but those that combine developmental psychology with socialization theory can. The culture of modern, industrial nations, with their systems of primary and secondary socialization and their systems of occupation and media, stimulate young brains and psyches to use open developmental windows so strongly that they can reach the formal operational stage successfully. Conversely, premodern cultures, across times and regions, do not stimulate humans to develop beyond the childhood stages. Accordingly, unused developmental windows in youth lead to early arrested development there. Both ethnographic data and Piagetian training studies indicate that premodern adults cannot skip stages, being stuck in the childhood stages throughout their lives. However, children born in premodern cultures can develop the formal operational stage when they move to modern cultures in their early years. Only the theory of (open or closed) developmental windows can explain these remarkable phenomena. Data indicate that every stage or substage described by developmental psychology was once the “developmental age” certain nations or social milieus had actually reached.

Many marine animals produce numerous larvae, few of which survive to adulthood. While larval mortality is generally attributed to environmental causes such as predation and transport to unsuitable habitats, mortality deriving from the process of ontogeny has rarely been investigated. This study examines 2 hypotheses (Acquisition of Robustness Hypothesis and Transitional Timing Hypothesis) that relate ontogenescence (high mortality early in life that declines with age) to the biological process of development. We conducted 2 experiments with larvae of the barnacle Amphibalanus improvisus to test these hypotheses. In Expt 1, where the survival and duration-in-stage of hundreds of individual larvae were tracked under low stress conditions, half of the developing individuals died. Deaths were concentrated in the larval stages immediately adjacent to the 2 major transitions (nauplius-to-cyprid and cyprid-to-juvenile). 89% of deaths occurred in individuals that had delayed their transition to the next stage. In almost every stage, delays were associated with increased risk of death before reaching the next stage. In Expt 2, which examined stage-based tolerance of temperature and salinity stress, the cyprid stage was most susceptible to ecological stressors. Results of both experiments closely follow the predictions of the Transitional Timing Hypothesis, while neither support an Acquisition of Robustness across development. Stages adjacent to major transitions have reduced physiological tolerance to stressors. Simultaneously, these individuals must achieve competence for the next transition or remain in the current stage until death. The resulting suppression of adult recruitment likely plays an important and under-appreciated role in the population ecology of marine animals.

Background Toxocara canis is quite closely related to Ascaris suum but its biology is more complex, involving a phase of arrested development (diapause or hypobiosis) in tissues as well as transplacental and transmammary transmission routes. In the present study, we explored and compared dauer-like signalling pathways of T. canis and A. suum to infer which components in these pathways might associate with, or regulate, this added complexity in T. canis . Methods Guided by information for Caenorhabditis elegans , we bioinformatically inferred and compared components of dauer-like signalling pathways in T. canis and A. suum using genomic and transcriptomic data sets. In these two ascaridoids, we also explored endogenous dafachronic acids (DAs), which are known to be critical in regulating larval developmental processes in C. elegans and other nematodes, by liquid chromatography-mass spectrometry (LC-MS). Results Orthologues of C. elegans dauer signalling genes were identified in T. canis ( n = 55) and A. suum ( n = 51), inferring the presence of a dauer-like signalling pathway in both species. Comparisons showed clear differences between C. elegans and these ascaridoids as well as between T. canis and A. suum , particularly in the transforming growth factor-β (TGF-β) and insulin-like signalling pathways. Specifically, in both A. suum and T. canis , there was a paucity of genes encoding SMAD transcription factor-related protein ( daf-3 , daf-5 , daf-8 and daf-14 ) and insulin/insulin-like peptide ( daf-28 , ins-4 , ins-6 and ins-7 ) homologues, suggesting an evolution and adaptation of the signalling pathway in these parasites. In T. canis , there were more orthologues coding for homologues of antagonist insulin-like peptides ( Tc-ins-1 and Tc-ins-18 ), an insulin receptor substrate ( Tc-ist-1 ) and a serine/threonine kinase ( Tc-akt-1 ) than in A. suum , suggesting potentiated functional roles for these molecules in regulating larval diapause and reactivation. A relatively conserved machinery was proposed for DA synthesis in the two ascaridoids, and endogenous Δ4- and Δ7-DAs were detected in them by LC-MS analysis. Differential transcription analysis between T. canis and A. suum suggests that ins-17 and ins-18 homologues are specifically involved in regulating development and migration in T. canis larvae in host tissues. Conclusion The findings of this study provide a basis for functional explorations of insulin-like peptides, signalling hormones (i.e. DAs) and related nuclear receptors, proposed to link to development and/or parasite-host interactions in T. canis . Elucidating the functional roles of these molecules might contribute to the discovery of novel anthelmintic targets in ascaridoids.