Towards the analysis of coral skeletal density-banding using deep learning

X-ray micro–computed tomography (µCT) is increasingly used to record the skeletal growth banding of corals. However, the wealth of data generated is time consuming to analyse for growth rates and colony age. Here we test an artificial intelligence (AI) approach to assist the expert identification of annual density boundaries in small colonies of massive Porites spanning decades. A convolutional neural network (CNN) was trained with µCT images combined with manually labelled ground truths to learn banding-related features. The CNN successfully predicted the position of density boundaries in independent images not used in training. Linear extension rates derived from CNN-based outputs and the traditional method were consistent. In the future, well-resolved 2D density boundaries from AI can be used to reconstruct density surfaces and enable studies focused on variations in rugosity and growth gradients across colony 3D space. We recommend the development of a community platform to share annotated images for AI.

Four-Year Field Survey of Black Band Disease and Skeletal Growth Anomalies in Encrusting Montipora spp. Corals around Sesoko Island, Okinawa

The Indo-Pacific zooxanthellate scleractinian coral genus Montipora is the host of many coral diseases. Among these are cyanobacterial Black Band Disease (BBD) and Skeletal Growth Anomalies (GAs), but in general data on both diseases are lacking from many regions of the Indo-Pacific, including from Okinawa, southern Japan. In this study, we collected annual prevalence data of Black Band Disease (BBD) and Skeletal Growth Anomalies (GAs) affecting the encrusting form of genus Montipora within the shallow reefs of the subtropical Sesoko Island (off the central west coast of Okinawajima Island) from summer to autumn for four years (2017 to 2020). In 2020 Montipora percent coverage and colony count were also assessed. Generalized Linear Models (GLM) were used to understand the spatial and temporal variation of both BBD and GAs in the nearshore (NE) and reef edge (RE) sites, which revealed higher probability of BBD occurrence in RE sites. BBD prevalence was significantly higher in 2017 in some sites than all other years with site S12 having significant higher probability during all four surveyed years. In terms of GAs, certain sites in 2020 had higher probability of occurrence than during the other years. While the general trend of GAs increased from 2017 to 2020, it was observed to be non-fatal to colonies. In both diseases, the interaction between sites and years was significant. We also observed certain BBD-infected colonies escaping complete mortality. BBD progression rates were monitored in 2020 at site S4, and progression was related to seawater temperatures and was suppressed during periods of heavy rain and large strong typhoons. Our results suggest that higher BBD progression rates are linked with high sea water temperatures (SST > bleaching threshold SST) and higher light levels (> 1400 µmol m−2 s−1), indicating the need for further controlled laboratory experiments. The current research will help form the basis for continued future research into these diseases and their causes in Okinawa and the Indo-Pacific Ocean.

In situ Skeletal Growth Rates of the Solitary Cold-Water Coral Tethocyathus endesa From the Chilean Fjord Region

Cold-water corals (CWC) can be found throughout a wide range of latitudes (79°N–78°S). Since they lack the photosymbiosis known for most of their tropical counterparts, they may thrive below the euphotic zone. Consequently, their growth predominantly depends on the prevalent environmental conditions, such as general food availability, seawater chemistry, currents, and temperature. Most CWC communities live in regions that will face CaCO3 undersaturation by the end of the century and are thus predicted to be threatened by ocean acidification (OA). This scenario is especially true for species inhabiting the Chilean fjord system, where present-day carbonate water chemistry already reaches values predicted for the end of the century. To understand the effect of the prevailing environmental conditions on the biomineralization of the CWC Tethocyathus endesa, a solitary scleractinian widely distributed in the Chilean Comau Fjord, a 12-month in situ experiment was conducted. The in situ skeletal growth of the test corals was assessed at two sites using the buoyant weight method. Sites were chosen to cover the naturally present carbonate chemistry gradient, with pH levels ranging between 7.90 ± 0.01 (mean ± SD) and 7.70 ± 0.02, and an aragonite saturation (Ωarag) between 1.47 ± 0.03 and 0.98 ± 0.05. The findings of this study provide one of the first in situ growth assessments of a solitary CWC species, with a skeletal mass increase of 46 ± 28 mg per year and individual, at a rate of 0.03 ± 0.02% day. They also indicate that, although the local seawater chemistry can be assumed to be unfavorable for calcification, growth rates of T. endesa are comparable to other cold-water scleractinians in less corrosive waters (e.g., Lophelia pertusa in the Mediterranean Sea).

The Deleterious Effects of Impaired Fibrinolysis on Skeletal Development Are Dependent on Fibrin(ogen), but Independent of Interlukin-6

Chronic diseases in growing children, such as autoimmune disorders, obesity, and cancer, are hallmarked by musculoskeletal growth disturbances and osteoporosis. Many of the skeletal changes in these children are thought to be secondary to chronic inflammation. Recent studies have likewise suggested that changes in coagulation and fibrinolysis may contribute to musculoskeletal growth disturbances. In prior work, we demonstrated that mice deficient in plasminogen, the principal protease of degrading and clearing fibrin matrices, suffer from inflammation-driven systemic osteoporosis and that elimination of fibrinogen resulted in normalization of IL-6 levels and complete rescue of the skeletal phenotype. Given the intimate link between coagulation, fibrinolysis, and inflammation, here we determined if persistent fibrin deposition, elevated IL-6, or both contribute to early skeletal aging and physeal disruption in chronic inflammatory conditions. Skeletal growth as well as bone quality, physeal development, and vascularity were analyzed in C57BL6/J mice with plasminogen deficiency with and without deficiencies of either fibrinogen or IL-6. Elimination of fibrinogen, but not IL-6, rescued the skeletal phenotype and growth disturbances in this model of chronic disease. Furthermore, the skeletal phenotypes directly correlated with both systemic and local vascular changes in the skeletal environment. In conclusion, these results suggest that fibrinolysis through plasmin is essential for skeletal growth and maintenance, and is multifactorial by limiting inflammation and preserving vasculature.

Evidence of feedback regulation of C-type natriuretic peptide during Vosoritide therapy in Achondroplasia

Evidence from genetic disorders of CNP signalling suggests that plasma concentrations of CNP are subject to feedback regulation. In subjects with Achondroplasia (Ach), CNP intracellular activity is suppressed and plasma concentrations are raised but the therapeutic impact of exogenous CNP agonists on endogenous CNP is unknown. In this exploratory dose finding and extension study of 28 Ach children receiving Vosoritide over a 5 year period of treatment, endogenous CNP production was assessed using measurements of plasma aminoterminal proCNP (NTproCNP) adjusted for age and sex and normalised as standard deviation score (SDS), and then related to skeletal growth. Before treatment NTproCNP SDS was raised. Within the first 3 months of accelerating growth, levels were significantly reduced. Across the 5 years of sustained growth, levels varied widely and were markedly increased in some subjects during adolescence. Plasma NTproCNP was suppressed at 4 h post-injection in proportion to the prevailing level of hormone resistance as reflected by SDS before injection. We conclude CNP remains subject to regulation during growth promoting doses of Vosoritide. Fall in CNP during accelerating growth is consistent with an indirect feedback whereas the fall at 4 h is likely to be a direct effect from removal of intra cellular CNP resistance.

Disability and Difference on the New Zealand Frontier

The mid-nineteenth century saw extensive diaspora from Europe to the antipodes. New Zealand in particular was marketed to the poor and middle classes of the United Kingdom (UK) as a “Better Britain”; a pastoral utopia of abundant resources and easy living. These campaigns actively targeted young, able-bodied persons with the aim of creating a thriving and productive colony. The rural community of Milton, Otago, in the South Island, was a farming settlement established predominantly by immigrants from the UK. The University of Otago undertook an excavation at St. John’s Anglican burial ground (SJM) in 2016 with the aim of reconstructing some aspects of the lives of these nineteenth-century European (Pākehā) settlers. One of the 27 individuals recovered, burial 29, was an adult female with a striking thoracic deformity and several other features suggestive of a skeletal growth disorder. Here, we combine multiple lines of bioarchaeological evidence to create an osteobiographyof this individual and discuss the implications of our findings for conceptions of disability, status, personhood, and social value in Victorian frontier society. Tuhinga whakarāpopoto: Ko te puku o ngā tau o te rau tau 1800 te wā i matua heke ai ngā tāngata nō Ūropi ki te tuakoi tonga o te ao. Ko Niu Tīreni tonu i whakatairangahia ki te tūtūā o Peretānia hei Piritana hōu, he “Piritana Pai Ake ”; he whenua haumako, he huhua rauemi, he oranga ngāwari. Ko ēnei whakatairanga hei whaka- poapoa i te hunga rangatahi, i te hunga kua pakari tonu te tīnana hei tuarā hāpai i te koroni hōu, i te koroni tōnui i pīrangitia. Ko te taiwhenua o Milton i Ōtākou, i Te Waipounamu, tētehi hapori pāmu i whakatūria e ngā manene, ko te nuinga nō Peretānia. Nā Te Whare Wānanga o Ōtākou ngā rua kōiwi i te urupā Mihinare o Hato Hone (SJM) i keri ake i te tau 2016, ko te whainga matua ko te kimi kōrero mō ngā rā o ngā ao o ēnei tāngata whai nō Ūropi (Pākehā) i te rau tau 1800. Ko tētehi o te 27 tāngata i hahua, arā ko “nehunga 29”, he wahine pa- keke kua hauā rawa ōna kōiwi o te haurua o te tinana ō runga i tōna pito, ā, he tohu anō i kitea e hanga rite ana ki tētehi mate whakahauā kōiwi. I konei whakatōpūhia ai ngā taunakitanga maha kua puta i ngā whakamātautau kōiwi tangata hei waihanga anō i ngā rā o te ao o te wahine nei, ā, ka matapakina ā mātou whakapae mō ngā whakaaro o ngāi koroni wikitōria mō te hauā; mō tōna tūnga, mō tōna mana me tōna noho hei tangata i aua wā.

Evolution and future of growth plate therapeutics

Background: Longitudinal bone growth is regulated by multiple endocrine signals (e.g. growth hormone, insulin-like growth factor I, estrogen, androgen) and local factors (e.g. fibroblast growth factors and their receptors and the C-natriuretic peptide/NPR-2 pathway). Summary: Abnormalities in both endocrine and local regulation of growth plate physiology cause many disorders of human skeletal growth. Knowledge of these pathways creates therapeutic potential for sustaining or even augmenting linear growth. Key message: During the past four decades, advances in understanding growth plate physiology have been accompanied by development and implementation of growth-promoting treatments that have progressed in both efficacy and specificity of action. This paper reviews the history and continuing evolution of growth plate therapeutics.