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Background Although surveillance systems used to mitigate disasters serve essential public health functions, communities of color have experienced disproportionate harms (eg, criminalization) as a result of historic and enhanced surveillance. Methods To address this, we developed and piloted a novel, equity-based scoring system to evaluate surveillance systems regarding their potential and actual risk of adverse effects on communities made vulnerable through increased exposure to policing, detention/incarceration, deportation, and disruption of access to social services or public resources. To develop the scoring system, we reviewed the literature and surveyed an expert panel on surveillance to identify specific harms (eg, increased policing) that occur through surveillance approaches. Results Scores were based on type of information collected (individual and/or neighborhood level) and evidence of sharing information with law enforcement. Scores were 0 (no risk of harm identified), 1 (potential for risk), 2 (evidence of risk), and U (data not publicly accessible). To pilot the scoring system, 44 surveillance systems were identified between June 2020 and October 2020 through an environmental scan of systems directly related to COVID-19 (n=21), behavioral and health-related services (n=11), and racism and racism-related factors (n=12). A score of 0-2 was assigned to 91% (n=40) of the systems; 9% were scored U; 30% (n=13) scored a 0. Half scored a 1 (n=22), indicating a “potential for the types of harm of concern in this analysis.” “Evidence of harm,” a score of 2, was found for 12% (n=5). Conclusions The potential for surveillance systems to compromise the health and well-being of racialized and/or vulnerable populations has been understudied. This project developed and piloted a scoring system to accomplish this equity-based imperative. The nobler pursuits of public health to improve the health for all must be reconciled with these potential harms.

Objectives Exergame training is a promising method for delivering evidence-based fall prevention exercise as it can facilitate exercise adherence and can be tailored to address cognitive and motor risk factors for falls. This study examined the effectiveness of two home-based computer game interventions (seated brain training and step training; smart±step) in preventing falls in community-dwelling older people, compared to a minimal-intervention control group. Design Assessor-blinded, randomised controlled trial. Setting Research institute and homes of older people living in the community of Sydney, Australia. Participants 769 people aged 65+ years living independently in the community and free of cognitive impairment, progressive neurological disease, or any other unstable or acute medical condition that precludes exercise. Interventions Participants were randomised to one of three arms: brain training using a computerised touch pad while seated; exergame step training on a computerised mat; or control. The intervention groups were provided with a home-based training system and were asked to train for at least two hours per week over the 12-month trial. Main outcome measures The primary outcome was the rate of falls reported monthly over 12 months. Results Between October 2016 and May 2019, 769 participants were randomised (seated brain training =262, exergame step training=252, control=255) and all were included in the intention-to-treat analyses. The rate of falls over 12 months was significantly reduced in the exergame step training group compared to control (IRR=0.74, 95%CI=0.56 to 0.98) and was not statistically different between the seated brain training and control groups (IRR=0.86, 95%CI=0.65 to 1.12). No serious intervention-related adverse events were reported. Conclusions A home-based exergame step training program provides a safe and effective means for preventing falls in older people living in the community. As this intervention can be conducted at home and requires only minimal equipment, it has the potential for scalability as a public health intervention to address the increasing problem of falls and fall-related injuries. Trial registration Australian and New Zealand Clinical Trial Registry ACTRN12616001325493, registered 22 September 2016.

Bioactive lipids initiate inflammatory reactions leading to pathogenesis of atherosclerosis. Evidence shows that they also contribute to bone loss by inhibiting parathyroid hormone receptor (PTH1R) expression and differentiation of osteoblasts. We previously demonstrated that bone anabolic effects of PTH(1-34) are blunted in hyperlipidemic mice and that these PTH effects are restored by antioxidants. However, it is not clear which osteoblastic cell developmental stage is targeted by bioactive lipids. To investigate the effects of hyperlipidemia at the cellular level, hyperlipidemic Ldlr(-/-) mice were bred with Col3.6GFPtpz mice, in which preosteoblasts/osteoblasts carry a topaz fluorescent label, and with Col2.3GFPcyan mice, in which more mature osteoblasts/osteocytes carry a cyan fluorescent label. Histological analyses of trabecular bone surfaces in femoral as well as calvarial bones showed that intermittent PTH(1-34) increased fluorescence intensity in WT-Tpz mice, but not in Tpz-Ldlr(-/-) mice. In contrast, PTH(1-34) did not alter fluorescence intensity in femoral cortical envelopes of either WT-Cyan or Ldlr(-/-)-Cyan mice. To test the mechanism of PTH1R downregulation, preosteoblastic MC3T3-E1 cells were treated with bioactive lipids and the antioxidant Trolox. Results showed that inhibitory effects of PTH1R levels by bioactive lipids were rescued by pretreatment with Trolox. The inhibitory effects on expression of PTH1R as well as on PTH-induced osteoblastic genes were mimicked by xanthine/xanthine oxidase, a known generator of reactive oxygen species. These findings suggest an important role of the preosteoblastic development stage as the target and downregulation of PTH receptor expression mediated by intracellular oxidant stress as a mechanism in hyperlipidemia-induced PTH resistance.

Cell migration is essential for morphogenesis, for organ formation and homeostasis, with relevance for clinical conditions. The migration of primordial germ cells (PGCs) is a useful model to study this process in the context of the developing embryo. Zebrafish PGC migration depends on the formation of cellular protrusions in form of blebs, a type of protrusion found in various cell types. Here we report on the mechanisms allowing the inflation of the membrane during bleb formation. We show that the rapid expansion of the protrusion depends on membrane invaginations that are localized preferentially at the cell front. The formation of these invaginations requires the function of Cdc42, and their unfolding allows bleb inflation and dynamic cell-shape changes performed by migrating cells. Inhibiting the formation and release of the invaginations strongly interfered with bleb formation, cell motility and with the ability of the cells to reach their target.

Summary The notochord, a conserved axial structure required for embryonic axis elongation and spine development, consists of giant vacuolated cells surrounded by an epithelial sheath [1–3]. During morphogenesis, vacuolated cells maintain their structural integrity despite being under constant mechanical stress [4]. We hypothesized that the high density of caveolae present in vacuolated cells [5, 6] could buffer mechanical tension. Caveolae are 50- to 80-nm membrane invaginations lined by cage-like polygonal structures [7, 8] formed by caveolin 1 (Cav1) or Cav3 and one of the cavin proteins [6, 9–11]. Recent in vitro work has shown that plasma membrane caveolae constitute a membrane reservoir that can buffer mechanical stresses such as stretching or osmotic swelling [12]. Moreover, mechanical integrity of vascular and muscle cells is partly dependent on caveolae [13–15]. However, the in vivo mechano-protective roles of caveolae have only begun to be explored. Using zebrafish mutants for cav1 , cav3 , and cavin1b , we show that caveolae are essential for notochord integrity. Upon loss of caveola function, vacuolated cells collapse at discrete positions under the mechanical strain of locomotion. Then, sheath cells invade the inner notochord and differentiate into vacuolated cells, thereby restoring notochord function and allowing normal spine development. Our data further indicate that nucleotides released by dying vacuolated cells promote sheath cell vacuolization and trans-differentiation. This work reveals a novel structural role for caveolae in vertebrates and provides unique insights into the mechanisms that safeguard notochord and spine development.

An unusual expression of a putative squamous cell marker, small proline-rich protein (spr1), in mucociliary epithelial cells of conducting airways was demonstrated in a serum-free culture system. A cDNA clone was isolated from the cDNA library of monkey tracheobronchial epithelial (TBE) cells by differential hybridization. This cDNA clone, MT5, exhibited 98% homology to a DNA sequence obtained from human keratinocytes treated with either UV light or phorbol esters (T. Kartasova et al., 1988, Mol. Cell. Biol. 8:2195-2230). The predicted peptide of MT5 is unusual for its high content of proline (29%), glutamine (18%), and cysteine (9%) and its repeated PKVPEPC units. The level of spr1 mRNA in cultured cells was inhibited more than 90% by vitamin A. In contrast, phorbol 12-myristate 13-acetate (PMA) stimulated the level of spr1 mRNA by 3- to 8-fold. This differential regulation coincided with the effects of these chemicals on the cornification of cultured TBE cells. Using MT5 as a probe, we have localized the tracheal spr1 gene on the human chromosome 1 by a Southern blot analysis using a panel of human-rodent somatic cell hybrid DNAs. The gene was further sublocalized to bands q22-23 by in situ hybridization.

The complete manuscript of this communication appears in: Angew. Chem. Suppl. 1982, 785. DOI:10.1002/anie.198207850