Climate Mitigation through Biological Conservation: Extensive and Valuable Blue Carbon Natural Capital in Tristan da Cunha’s Giant Marine Protected Zone

Carbon-rich habitats can provide powerful climate mitigation if meaningful protection is put in place. We attempted to quantify this around the Tristan da Cunha archipelago Marine Protected Area. Its shallows (<1000 m depth) are varied and productive. The 5.4 km2 of kelp stores ~60 tonnes of carbon (tC) and may export ~240 tC into surrounding depths. In deep-waters we analysed seabed data collected from three research cruises, including seabed mapping, camera imagery, seabed oceanography and benthic samples from mini-Agassiz trawl. Rich biological assemblages on seamounts significantly differed to the islands and carbon storage had complex drivers. We estimate ~2.3 million tC are stored in benthic biodiversity of waters <1000 m, which includes >0.22 million tC that can be sequestered (the proportion of the carbon captured that is expected to become buried in sediment or locked away in skeletal tissue for at least 100 years). Much of this carbon is captured by cold-water coral reefs as a mixture of inorganic (largely calcium carbonate) and organic compounds. As part of its 2020 Marine Protection Strategy, these deep-water reef systems are now protected by a full bottom-trawling ban throughout Tristan da Cunha and representative no take areas on its seamounts. This small United Kingdom Overseas Territory’s reef systems represent approximately 0.8 Mt CO2 equivalent sequestered carbon; valued at >£24 Million GBP (at the UN shadow price of carbon). Annual productivity of this protected standing stock generates an estimated £3 million worth of sequestered carbon a year, making it an unrecognized and potentially major component of the economy of small island nations like Tristan da Cunha. Conservation of near intact habitats are expected to provide strong climate and biodiversity returns, which are exemplified by this MPA.

Post Mortem Analysis of Opioids and Metabolites in Skeletal Tissue

Every year, thousands of suspicious deaths are accounted for by an overdose of opioids. Occasionally all traditional matrices are unavailable due to decomposition. Skeletal tissue may pose a valid alternative. However, reference data on post-mortem concentrations in bone tissue and bone marrow is sparse. Therefore, a liquid chromatography tandem mass spectrometry method was developed and fully validated for the analysis of 4 opioids and 2 metabolites (tramadol, O-desmethyltramadol, morphine, fentanyl, norfentanyl, codeine) in bone tissue and bone marrow. Sample preparation was performed using solid phase extraction (bone marrow), methanolic extraction (bone) and a protein precipitation (whole blood). All validation parameters were successfully fulfilled. This method was applied to analyze 22 forensic cases involving opioids. All 6 opioids were proven to be detectable and quantifiable in all specimens sampled. When tramadol blood concentrations were correlated with bone concentrations, a linear trend could be detected. The same was seen between tramadol blood and bone marrow concentration. A similar linear trend was seen when correlating codeine blood concentration with bone and bone marrow concentration. Although some variability was detected, the same linear trend was seen for morphine. For fentanyl and norfentanyl, the sample size was too small to draw conclusions, regarding correlation. As far as the authors know this is the first-time fentanyl and norfentanyl are quantified in skeletal tissue. In conclusion, due to the absence of reference data for drugs in skeletal tissue, these findings are a step forward towards a more thorough understanding of drug concentration found in post-mortem skeletal tissue.

Piezoelectric Microvibration Mitigates Estrogen Loss-Induced Osteoporosis and Promotes Piezo1, MicroRNA-29a and Wnt3a Signaling in Osteoblasts

Biophysical stimulation alters bone-forming cell activity, bone formation and remodeling. The effect of piezoelectric microvibration stimulation (PMVS) intervention on osteoporosis development remains uncertain. We investigated whether 60 Hz, 120 Hz, and 180 Hz PMVS (0.05 g, 20 min/stimulation, 3 stimulations/week for 4 consecutive weeks) intervention affected bone integrity in ovariectomized (OVX) mice or osteoblastic activity. PMVS (120 Hz)-treated OVX mice developed fewer osteoporosis conditions, including bone mineral density loss and trabecular microstructure deterioration together with decreased serum resorption marker CTX-1 levels, as compared to control OVX animals. The biomechanical strength of skeletal tissue was improved upon 120 Hz PMVS intervention. This intervention compromised OVX-induced sparse trabecular bone morphology, osteoblast loss, osteoclast overburden, and osteoclast-promoting cytokine RANKL immunostaining and reversed osteoclast inhibitor OPG immunoreactivity. Osteoblasts in OVX mice upon PMVS intervention showed strong Wnt3a immunoreaction and weak Wnt inhibitor Dkk1 immunostaining. In vitro, PMVS reversed OVX-induced loss in von Kossa-stained mineralized nodule formation, Runx2, and osteocalcin expression in primary bone-marrow stromal cells. PMVS also promoted mechanoreceptor Piezo1 expression together with increased microRNA-29a and Wnt3a expression, whereas Dkk1 rather than SOST expression was repressed in MC3T3-E1 osteoblasts. Taken together, PMVS intervention promoted Piezo1, miR-29a, and Wnt signaling to upregulate osteogenic activity and repressed osteoclastic bone resorption, delaying estrogen deficiency-induced loss in bone mass and microstructure. This study highlights a new biophysical remedy for osteoporosis.

HIGH INTENSITY SPORTS PROMOTE THE DEVELOPMENT OF HEALTHY BONE TISSUE

ABSTRACT Introduction: Physical exercise can promote the growth and development of bones and delay bone loss; it is more effective when started young. Objective: This paper analyzes the impact of human exercise on human bone health. Methods: A questionnaire survey was conducted on elementary school students, and basic physical fitness monitoring was conducted. The physical fitness monitoring indicators covered ten items such as height and weight. Results: After the questionnaire survey and physical examination, it was found that there are differences in various physiological indicators between students who exercise frequently compared with students who exercise less frequently. Conclusion: Physical exercise can promote skeletal tissue development, therefore, young people should increase the practice of physical exercise. Level of evidence II; Therapeutic studies - investigation of treatment results.

Histopathological Study of Soft Tissue Lesions with Cytology Correlation

Soft tissue can be defined as non-epithelial extra skeletal tissue of the body, exclusive of the reticuloendothelial system, glia and supporting tissu e of various parenchymal organs. FNAC is a useful tool in distinguishing accurately between neoplastic and non-neoplastic lesions. To study the utility of fine needle aspiration cytology (FNAC) in the diagnosis of soft tissue tumours. To correlate FNAC with histopathological examination of soft tissue tumours with immunohistochemistry and / or histochemistry wherever required and assess the overall sensitivity and specificity of FNAC in diagnosing soft tissue tumours.

Ubiquitin-protein ligase Ubr5 cooperates with hedgehog signalling to promote skeletal tissue homeostasis

Mammalian Hedgehog (HH) signalling pathway plays an essential role in tissue homeostasis and its deregulation is linked to rheumatological disorders. UBR5 is the mammalian homologue of the E3 ubiquitin-protein ligase Hyd, a negative regulator of the Hh-pathway in Drosophila. To investigate a possible role of UBR5 in regulation of the musculoskeletal system through modulation of mammalian HH signaling, we created a mouse model for specific loss of Ubr5 function in limb bud mesenchyme. Our findings revealed a role for UBR5 in maintaining cartilage homeostasis and suppressing metaplasia. Ubr5 loss of function resulted in progressive and dramatic articular cartilage degradation, enlarged, abnormally shaped sesamoid bones and extensive heterotopic tissue metaplasia linked to calcification of tendons and ossification of synovium. Genetic suppression of smoothened (Smo), a key mediator of HH signalling, dramatically enhanced the Ubr5 mutant phenotype. Analysis of HH signalling in both mouse and cell model systems revealed that loss of Ubr5 stimulated canonical HH-signalling while also increasing PKA activity. In addition, human osteoarthritic samples revealed similar correlations between UBR5 expression, canonical HH signalling and PKA activity markers. Our studies identified a crucial function for the Ubr5 gene in the maintenance of skeletal tissue homeostasis and an unexpected mode of regulation of the HH signalling pathway.

Mechanobiological Behavior of a Pathological Bone

Bone density and bone microarchitecture are two principle parameters needed for the evaluation of mechanical bone performance and consequently the detection of bone diseases. The mechanobiological behavior of the skeletal tissue has been described through several mathematical models. Generally, these models fingerboard different length scale processes, such as the mechanical, the biological, and the chemical ones. By means of the mechanical stimulus and the biological factors involved in tissue regeneration, bone cells’ behavior and bone volume changes are determined. The emergence of bone diseases leads to disrupt the bone remodeling process and thus, induces bone mechanical properties’ alteration. In the present chapter, an overview of bone diseases and their relationship with bone density alteration will be presented. Besides, several studies treating bone diseases’ effect on bone remodeling will be discussed. Finally, the mechanobiological models proposed to treat bone healing and drugs’ effect on bone, are going to be reviewed. For this sake, the chapter is subdivided into three main sequences: (i) Bone remodeling, (ii) Bone deterioration causes, (iii) Mathematical models of a pathological bone, and (iv) Mechanobiological models treating bone healing and drugs effect.