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Compensatory growth has been observed in forests, and it also appears as a common phenomenon in biology. Though it sometimes takes different names, the essential meanings are the same, describing the accelerated growth of organisms when recovering from a period of unfavorable conditions such as tissue damage at the individual level and partial mortality at the population level. Diverse patterns of compensatory growth have been reported in the literature, ranging from under-, to compensation-induced-equality, and to over-compensation. In this review and synthesis, we provide examples of analogous compensatory growth from different fields, clarify different meanings of it, summarize its current understanding and modeling efforts, and argue that it is possible to develop a state-dependent model under the conceptual framework of compensatory growth, aimed at explaining and predicting diverse observations according to different disturbances and environmental conditions. When properly applied, compensatory growth can benefit different industries and human society in various forms.

The morphological transformation of the pectoral/shoulder girdle is fundamental to the water-to-land transition in vertebrate evolution. Although previous studies have resolved the embryonic origins of tetrapod shoulder girdles, those of fish pectoral girdles remain uncharacterized, creating a gap in the understanding of girdle transformation mechanisms from fish to tetrapods. Here, we identify the embryonic origins of the zebrafish pectoral girdle, including the cleithrum as an ancestral girdle element lost in extant tetrapods. Our combinatorial approach of photoconversion and genetic lineage tracing demonstrates that cleithrum development combines four adjoining embryonic populations. A comparison of these pectoral girdle progenitors with extinct and extant vertebrates highlights that cleithrum loss, indispensable for neck evolution, is associated with the disappearance of its unique developmental environment at the head/trunk interface. Overall, our study establishes an embryological framework for pectoral/shoulder girdle formation and provides evolutionary trajectories from their origin in water to diversification on land. The embryonic origins of the pectoral girdle in fish remain unexplored. Here they show that the zebrafish pectoral girdle develops as an amalgam of four distinct cell populations.

The evolution of the tetrapod limb involved an expansion and elaboration of the endoskeletal elements, while the fish fin rays were lost. Loss of fin-specific genes, and regulatory changes in key appendicular patterning genes have been identified as mechanisms of limb evolution, however their contributions to cellular organization and tissue differences between fins and limbs remains poorly understood. During early larval fin development, hoxa13a/hoxd13a-expressing fin fold mesenchyme migrate through the median and pectoral fin along actinotrichia fibrils, non-calcified skeletal elements crucial for supporting the fin fold. Fin fold mesenchyme migration defects have previously been proposed as a mechanism of fin dermal bone loss during tetrapod evolution as it has been shown they contribute directly to the fin ray osteoblast population. Using the nitroreductase/metronidazole system, we genetically ablated a subset of hoxa13a/hoxd13a-expressing fin fold mesenchyme to assess its contributions to fin development. Following the ablation of fin fold mesenchyme in larvae, the actinotrichia are unable to remain rigid and the median and pectoral fin folds collapse, resulting in a reduced fin fold size. The remaining cells following ablation are unable to migrate and show decreased actinodin1 mesenchymal reporter activity. Actinodin proteins are crucial structural component of the actinotrichia. Additionally, we show a decrease in hoxa13a, hoxd13a, fgf10a and altered shha, and ptch2 expression during larval fin development. A continuous treatment of metronidazole leads to fin ray defects at 30dpf. Fewer rays are present compared to stage-matched control larvae, and these rays are shorter and less defined. These results suggest the targeted hoxa13a/hoxd13a-expressing mesenchyme contribute to their own successful migration through their contributions to actinotrichia. Furthermore, due to their fate as fin ray osteoblasts, we propose their initial ablation, and subsequent disorganization produces truncated fin dermal bone elements during late larval stages.

Actinotrichia are the first exoskeletal elements formed during zebrafish fin development. These rigid fibrils serve as skeletal support for the fin fold and as substrates for mesenchymal cell migration. In the adult intact fins, actinotrichia are restricted to the distal domain of the fin. Following fin amputation, actinotrichia also reform during regeneration. The actinodin gene family codes for structural proteins of actinotrichia. We have previously identified cis-acting regulatory elements in a 2kb genomic region upstream of the first exon of actinodin1, termed 2P, required for tissue-specific expression in the fin fold ectoderm and mesenchyme during embryonic development. Indeed, 2P contains an ectodermal enhancer in a 150bp region named epi. Deletion of epi from 2P results in loss of ectodermal-specific activity. In the present study, we sought to further characterize the activity of these regulatory sequences throughout fin development and during adult fin regeneration. Using a reporter transgenic approach, we show that a site within the epi region, termed epi3, contains an early mesenchymal-specific repressor. We also show that the larval fin fold ectodermal enhancer within epi3 remains functional in the basal epithelial layer during fin regeneration. We show that the first non-coding exon and first intron of actinodin1 contains a transcriptional enhancer and an alternative promoter that are necessary for the persistence of reporter expression reminiscent of actinodin1 expression during adulthood. Altogether, we have identified cis-acting regulatory elements that are required for tissue-specific expression as well as full recapitulation of actinodin1 expression during adulthood. Furthermore, the characterization of these elements provides us with useful molecular tools for the enhancement of transgene expression in adulthood.

This review and synthesis article attempts to integrate observations from forestry to contemporary development in related biological research fields to explore the issue of forest productivity enhancement and its contributions in mitigating the wood supply shortage now facing the forest sector. Compensatory growth has been clearly demonstrated in the long-term precommercial thinning and fertilization trial near the Shawnigan Lake, British Columbia, Canada. This phenomenon appears similar to many observations from other biological fields. The concept of compensatory growth can be applied to forest productivity enhancement through overcompensation, by taking advantage of theories and methods developed in other compensatory growth research. Modeling technology provides an alternative approach in elucidating the mechanisms of overcompensation, which could reveal whether the Shawnigan Lake case could be generalized to other tree species and regions. A new mitigation strategy for dealing with issues related to wood supply shortage could be formed through searching for and creating conditions promoting overcompensation. A forest growth model that is state dependent could provide a way of investigating the effect of partial harvest on forest growth trajectories and stand dynamics. Results from such a study could provide cost-effective decision support tools to practitioners.

Understanding stand dynamics is essential for predicting future wood supply and associated ecosystem services for sustainable forest management. The dynamics of natural stands can be characterized by age-dependent growth and yield models. However, dynamics in managed stands appear somewhat different from that of natural stands, especially with difficulties in explaining the phenomenon of post-thinning overcompensation, based upon some long-term observations. Though overcompensation is an ideal outcome for the forest sector, it had been largely treated as an outlier and thus ignored or dismissed as \"out-of-the-ordinary\". We developed a life history theory-based, state-dependent model of Tree Adaptive Growth (TAG) to investigate this phenomenon and verified that overcompensation should be a common outcome in post-thinning forest stands when the stand growth over time is sigmoid shaped. TAG posits that individual trees will invest proportionately more into growth following thinning because it is evolutionarily adaptive to do so. Our investigation of the model's behavior unearthed diverse stand growth patterns similar to that which is observed in the empirical datasets and predicted by a statistics-based Tree's Compensatory Growth (TreeCG) model. A simple, theory-driven, analytical model, TAG, can reproduce the diverse growth patterns in post-thinning stands and thus assist addressing silviculture-related issues. The model can be applied to various jurisdictions even without detailed regional growth and yield relationships and is capable of incorporating the effects of other time sensitive factors like fertilization, pruning, and climate change.

Syndromic birth defects are rare diseases that can present with seemingly pleiotropic comorbidities. Prime examples are rare congenital heart and cardiovascular anomalies that can be accompanied by forelimb defects, kidney disorders and more. Whether such multi-organ defects share a developmental link remains a key question with relevance to the diagnosis, therapeutic intervention and long-term care of affected patients. The heart, endothelial and blood lineages develop together from the lateral plate mesoderm (LPM), which also harbors the progenitor cells for limb connective tissue, kidneys, mesothelia and smooth muscle. This developmental plasticity of the LPM, which founds on multi-lineage progenitor cells and shared transcription factor expression across different descendant lineages, has the potential to explain the seemingly disparate syndromic defects in rare congenital diseases. Combining patient genome-sequencing data with model organism studies has already provided a wealth of insights into complex LPM-associated birth defects, such as heart-hand syndromes. Here, we summarize developmental and known disease-causing mechanisms in early LPM patterning, address how defects in these processes drive multi-organ comorbidities, and outline how several cardiovascular and hematopoietic birth defects with complex comorbidities may be LPM-associated diseases. We also discuss strategies to integrate patient sequencing, data-aggregating resources and model organism studies to mechanistically decode congenital defects, including potentially LPM-associated orphan diseases. Eventually, linking complex congenital phenotypes to a common LPM origin provides a framework to discover developmental mechanisms and to anticipate comorbidities in congenital diseases affecting the cardiovascular system and beyond.

The mutually exclusive expression of the Hoxa11 and Hoxa13 genes is required for pentadactyl (five-digit) limbs and is proposed to have contributed to the transition from several digits polydactyl (several-digit) limbs in the earliest tetrapods. Genetic control of digital (r)evolution In mice carrying the Prx1Cre; Rosa Hoxa11/Hoxa11 mutation, the Hoxa11 gene is expressed in distal limb buds, reminiscent of the expression in fin buds, and triggers the formation of extra-digits. Most living tetrapods—the four-legged land vertebrates—have five digits per limb. If this number varies through mutation, it is always a reduction from the canonical five. But this state, called pentadactyly, was not always so hardwired. The earliest tetrapods had six, seven or even eight digits per limb—polydactyly is only seen nowadays in rare mutations. How did pentadactyly become established? Marie Kmita and colleagues show that mutually exclusive expression of Hoxa11 and Hoxa13 is required for five-digit limbs, that a transcriptional enhancer has evolved in the intron of the Hoxa11 gene, and its function is required to maintain the pentadactyl state. The authors propose that the evolution of Hoxa11 regulation has contributed to the transition from polydactyly in stem-group (extinct) tetrapods to pentadactyly in extant tetrapods. The fin-to-limb transition represents one of the major vertebrate morphological innovations associated with the transition from aquatic to terrestrial life and is an attractive model for gaining insights into the mechanisms of morphological diversity between species 1 . One of the characteristic features of limbs is the presence of digits at their extremities. Although most tetrapods have limbs with five digits (pentadactyl limbs), palaeontological data indicate that digits emerged in lobed fins of early tetrapods, which were polydactylous 2 . How the transition to pentadactyl limbs occurred remains unclear. Here we show that the mutually exclusive expression of the mouse genes Hoxa11 and Hoxa13 , which were previously proposed to be involved in the origin of the tetrapod limb 1 , 2 , 3 , 4 , 5 , 6 , is required for the pentadactyl state. We further demonstrate that the exclusion of Hoxa11 from the Hoxa13 domain relies on an enhancer that drives antisense transcription at the Hoxa11 locus after activation by HOXA13 and HOXD13. Finally, we show that the enhancer that drives antisense transcription of the mouse Hoxa11 gene is absent in zebrafish, which, together with the largely overlapping expression of hoxa11 and hoxa13 genes reported in fish 3 , 4 , 5 , 6 , 7 , suggests that this enhancer emerged in the course of the fin-to-limb transition. On the basis of the polydactyly that we observed after expression of Hoxa11 in distal limbs, we propose that the evolution of Hoxa11 regulation contributed to the transition from polydactyl limbs in stem-group tetrapods to pentadactyl limbs in extant tetrapods.

This article compares labor market outcomes from two different approaches to a work release program in Illinois: direct provision by a government and a purchase-of-service (POS) contract between government and a public charity. Significantly better employment and earnings outcomes were associated with the POS contract. To better understand the reasons for the success of the POS contract, the authors further examined the specific terms of the contract, organizational expertise, and the political context of POS contracts. The results are organized according to the main theoretical assertions. Findings add to the weight of evidence that contractors, like public charities, can be valuable government partners for addressing challenging social policies and programs.

In a previous clinical study, a probiotic formulation (PF) consisting of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 (PF) decreased stress-induced gastrointestinal discomfort. Emerging evidence of a role for gut microbiota on central nervous system functions therefore suggests that oral intake of probiotics may have beneficial consequences on mood and psychological distress. The aim of the present study was to investigate the anxiolytic-like activity of PF in rats, and its possible effects on anxiety, depression, stress and coping strategies in healthy human volunteers. In the preclinical study, rats were daily administered PF for 2 weeks and subsequently tested in the conditioned defensive burying test, a screening model for anti-anxiety agents. In the clinical trial, volunteers participated in a double-blind, placebo-controlled, randomised parallel group study with PF administered for 30 d and assessed with the Hopkins Symptom Checklist (HSCL-90), the Hospital Anxiety and Depression Scale (HADS), the Perceived Stress Scale, the Coping Checklist (CCL) and 24 h urinary free cortisol (UFC). Daily subchronic administration of PF significantly reduced anxiety-like behaviour in rats (P < 0·05) and alleviated psychological distress in volunteers, as measured particularly by the HSCL-90 scale (global severity index, P < 0·05; somatisation, P < 0·05; depression, P < 0·05; and anger–hostility, P < 0·05), the HADS (HADS global score, P < 0·05; and HADS-anxiety, P < 0·06), and by the CCL (problem solving, P < 0·05) and the UFC level (P < 0·05). L. helveticus R0052 and B. longum R0175 taken in combination display anxiolytic-like activity in rats and beneficial psychological effects in healthy human volunteers.