The dynamics of pattern matching in camouflaging cuttlefish.

Many cephalopods escape detection using camouflage1. This behaviour relies on a visual assessment of the surroundings, on an interpretation of visual-texture statistics2-4 and on matching these statistics using millions of skin chromatophores that are controlled by motoneurons located in the brain5-7. Analysis of cuttlefish images proposed that camouflage patterns are low dimensional and categorizable into three pattern classes, built from a small repertoire of components8-11. Behavioural experiments also indicated that, although camouflage requires vision, its execution does not require feedback5,12,13, suggesting that motion within skin-pattern space is stereotyped and lacks the possibility of correction. Here, using quantitative methods14, we studied camouflage in the cuttlefish Sepia officinalis as behavioural motion towards background matching in skin-pattern space. An analysis of hundreds of thousands of images over natural and artificial backgrounds revealed that the space of skin patterns is high-dimensional and that pattern matching is not stereotyped-each search meanders through skin-pattern space, decelerating and accelerating repeatedly before stabilizing. Chromatophores could be grouped into pattern components on the basis of their covariation during camouflaging. These components varied in shapes and sizes, and overlay one another. However, their identities varied even across transitions between identical skin-pattern pairs, indicating flexibility of implementation and absence of stereotypy. Components could also be differentiated by their sensitivity to spatial frequency. Finally, we compared camouflage to blanching, a skin-lightening reaction to threatening stimuli. Pattern motion during blanching was direct and fast, consistent with open-loop motion in low-dimensional pattern space, in contrast to that observed during camouflage.

Disparities in Hypoxemia Detection by Pulse Oximetry Across Self-Identified Racial Groups and Associations With Clinical Outcomes.

OBJECTIVES: To assess disparities in hypoxemia detection by pulse oximetry across self-identified racial groups and associations with clinical outcomes. DESIGN: Observational cohort study from May 5, 2018, to December 31, 2020. SETTING: Three academic medical centers in the United States. PATIENTS: Adults greater than or equal to 18 years who self-identified as White, Black, Asian, or American Indian admitted to the ICU or undergoing surgery during inpatient hospitalization with simultaneous measurements of pulse oximetry-estimated oxygen saturation and arterial blood gas-derived oxygen saturation. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Multivariable models were employed to assess the relationships between race, occult hypoxemia (i.e., arterial blood gas-derived oxygen saturation < 88% despite pulse oximetry-estimated oxygen saturation ≥ 92%), and clinical outcomes of hospital mortality and hospital-free days. One-hundred twenty-eight-thousand two-hundred eighty-five paired pulse oximetry-estimated oxygen saturation-arterial blood gas-derived oxygen saturation measurements were included from 26,603 patients. Pulse oximetry-estimated oxygen saturation on average overestimated arterial blood gas-derived oxygen saturation by 1.57% (1.54-1.61%). Black, Asian, and American Indian patients were more likely to experience occult hypoxemia during hospitalization (estimated probability 6.2% [5.1-7.6%], 6.6% [4.9-8.8%], and 6.6% [4.4-10.0%], respectively) compared with White patients (3.6% [3.4-3.8%]). Black patients had increased odds of occult hypoxemia compared with White patients after adjustment (odds ratio, 1.65; 1.28-2.14; p < 0.001). Differences in occult hypoxemia between Asian and American Indian patients compared with White patients were not significant after adjustment (odds ratio, 1.53; 0.95-2.47; p = 0.077 and odds ratio, 1.31; 0.80-2.16; p = 0.288, respectively). Occult hypoxemia was associated with increased odds of mortality in surgical (odds ratio, 2.96; 1.20-7.28; p = 0.019) and ICU patients (1.36; 1.03-1.80; p = 0.033). Occult hypoxemia was associated with fewer hospital-free days in surgical (-2.5 d [-3.9 to -1.2 d]; p < 0.001) but not ICU patients (0.4 d [-0.7 to 1.4 d]; p = 0.500). CONCLUSIONS: Occult hypoxemia is more common in Black patients compared with White patients and is associated with increased mortality, suggesting potentially important outcome implications for undetected hypoxemia. It is imperative to validate pulse oximetry with expanded racial inclusion.

Repigmentation by combined narrow­band ultraviolet B/adipose­derived stem cell transplantation in the mouse model: Role of Nrf2/HO­1­mediated Ca2+ homeostasis.

Vitiligo is a depigmentation disease commonly seen in clinical practice, mainly involving loss of functional epidermal pigment cells and hair follicle melanocytes. Narrow­band ultraviolet B (NB­UVB) has emerged as the first choice of treatment for vitiligo, but long­term exposure may have serious consequences. Recently, it was reported that adipose­derived stem cells (ADSCs) improve melanocyte growth and the efficacy of melanocyte transplantation. The present study aimed to examine the efficacy of NB­UVB/ADSC­transplantation combined therapy on a mouse vitiligo model and explore the underlying mechanisms by focusing on endoplasmic reticulum stress and cellular calcium (Ca2+) homeostasis. Vitiligo mice models were established by applying 40% monobenzone (MBZ) cream twice daily and treated with NB­UVB/ADSC combination therapy. Some treated mice were also given ML385, a nuclear factor erythroid 2 like 2 (Nr2) inhibitor. Histopathological changes were evaluated using a depigmentation evaluation score and observed with hematoxylin and eosin staining on skin tissues. ELISA was used to measure diagnostic markers in plasma. Flow cytometric assay was performed to quantify CD3+, CD4+ and CD8+ levels. Expression levels of associated proteins were detected with western blot and immunofluorescence. Treatment of mice with MBZ­induced depigmentation patches on the skin was accompanied with loss of redox balance and disruption of cellular Ca2+ homeostasis. Oxidative stress and Ca2+ unbalancing were improved after the mice were treated by NB­UVB/ADSCs transplantation combination therapy. ML385, strongly negated the protective effect of NB­UVB/ADSC transplantation combination therapy, indicating the critical role of Nr2 signaling. The findings improved the understanding of the pathogenesis of vitiligo and will guide future development of therapeutic strategies against it.

Initial Phylotranscriptomic Confirmation of Homoplastic Evolution of the Conspicuous Coloration and Bufoniform Morphology of Pumpkin-Toadlets in the Genus Brachycephalus.

The genus Brachycephalus is a fascinating group of miniaturized anurans from the Brazilian Atlantic Forest, comprising the conspicuous, brightly colored pumpkin-toadlets and the cryptic flea-toads. Pumpkin-toadlets are known to contain tetrodotoxins and therefore, their bright colors may perform an aposematic function. Previous studies based on a limited number of mitochondrial and nuclear-encoded markers supported the existence of two clades containing species of pumpkin-toadlet phenotype, but deep nodes remained largely unresolved or conflicting between data sets. We use new RNAseq data of 17 individuals from nine Brachycephalus species to infer their evolutionary relationships from a phylogenomic perspective. Analyses of almost 5300 nuclear-encoded ortholog protein-coding genes and full mitochondrial genomes confirmed the existence of two separate pumpkin-toadlet clades, suggesting the convergent evolution (or multiple reversals) of the bufoniform morphology, conspicuous coloration, and probably toxicity. In addition, the study of the mitochondrial gene order revealed that three species (B. hermogenesi, B. pitanga, and B. rotenbergae) display translocations of different tRNAs (NCY and CYA) from the WANCY tRNA cluster to a position between the genes ATP6 and COIII, showing a new mitochondrial gene order arrangement for vertebrates. The newly clarified phylogeny suggests that Brachycephalus has the potential to become a promising model taxon to understand the evolution of coloration, body plan and toxicity. Given that toxicity information is available for only few species of Brachycephalus, without data for any flea-toad species, we also emphasize the need for a wider screening of toxicity across species, together with more in-depth functional and ecological study of their phenotypes.

CRTC3, a sensor and key regulator for melanogenesis, as a tunable therapeutic target for pigmentary disorders.

Background: Although CREB phosphorylation is known to be essential in UVB/cAMP-stimulated melanogenesis, CREB null mice did not show identifiable pigmentation phenotypes. Here, we show that CREB-regulated transcription co-activator 3 (CRTC3) quantitatively regulates and orchestrates melanogenesis by directly targeting microphthalmia-associated transcription factor (MITF) and regulating the expression of most key melanogenesis-related genes. Methods: We analyzed CRTC3-null, KRT14-SCF transgenic, and their crossover mice. The molecular basis of CRTC3 effects on pigmentation was investigated by histology, melanin/tyrosinase assay, immunoblotting, shRNA, promoter assay, qRT-PCR, and subcellular localization. These analyses were carried out in primary cultured melanocytes, mouse cell lines, normal human cells, co-cultures, and ex vivo human skin. CRTC/CREB activity screening was performed to identify candidate agents for the regulation of melanogenesis. Results: The coat and skin color of CRTC3-null mice was paler due to a reduction in melanin deposition. Melanogenesis-related genes were reduced in CRTC3-deficient cultured melanocytes and tail skin of CRTC3-null mice. Notably, basal levels of MITF present in CRTC3-null mice were sufficient for melanocytic differentiation/survival. Thus CRTC3-null mice showed a comparable number of epidermal melanocytes compared to control mice. Stem cell factor (SCF) introduction by crossing with KRT14-SCF mice increased epidermal melanocytes and melanin deposition in control and CRTC3-null mice, but the skin color remained still light on the CRTC3-null background. Furthermore, we identified the therapeutic potential of altiratinib to inhibit melanogenesis in human melanocytes and human skin effectively and safely. Conclusion: CRTC3 appears to be a key sensor for melanogenesis and can be used as a reversible and tunable tool for selectively regulating melanogenesis without affecting melanocyte integrity. Thus, CRTC3 can also serve as a screening tool for the discovery of ideal melanogenesis-modulating small molecules.

Rapid phenotypic change in a polymorphic salamander over 43 years.

Color polymorphic animals offer a unique system for studying intraspecific phenotypic responses to climate change. Discrete color morphs are easy to identify, and correlated trait responses of morphs can indicate how climate warming may facilitate long-term maintenance of polymorphisms. We use a historical dataset spanning 43 years to examine temporal shifts in color morph frequency and body size in response to climate in the Eastern Red-backed Salamander, Plethodon cinereus, which contains a widespread striped/unstriped color polymorphism. We created a pipeline to extract high-throughput trait data from fluid-preserved museum specimens where we batch-photographed salamanders, de-aggregated individual specimens from photographs, and solicited help of community scientists to score color morphs. We used a linear modeling framework that includes information about spatial population structure to demonstrate that color morph frequency and body size vary in response to climate, elevation, and over time, with an overall trend of higher frequency and decreased body size of the striped morph, but increased size of the unstriped morph. These surprising results suggest that morphs may be responding to multiple climate and geographic drivers through co-adapted morphological changes. This work highlights new practices of extracting trait data from museum specimens to demonstrate species phenotypes response to climate change.

Melanin Produced by Bordetella parapertussis Confers a Survival Advantage to the Bacterium during Host Infection.

Bordetella parapertussis causes respiratory infection in humans, with a mild pertussis (whooping cough)-like disease. The organism produces a brown pigment, the nature and biological significance of which have not been elucidated. Here, by screening a transposon library, we demonstrate that the gene encoding 4-hydroxyphenylpyruvate dioxygenase (HppD) is responsible for production of this pigment. Our results also indicate that the brown pigment produced by the bacterium is melanin, because HppD is involved in the biosynthesis of a type of melanin called pyomelanin, and homogentisic acid, the monomeric precursor of pyomelanin, was detected by high-performance liquid chromatography-mass spectrometry analyses. In an infection assay using macrophages, the hppD-deficient mutant was internalized by THP-1 macrophage-like cells, similar to the wild-type strain, but was less able to survive within the cells, indicating that melanin protects B. parapertussis from intracellular killing in macrophages. Mouse infection experiments also showed that the hppD-deficient mutant was eliminated from the respiratory tract more rapidly than the wild-type strain, although the initial colonization levels were comparable between the two strains. In addition, melanin production by B. parapertussis was not regulated by the BvgAS two-component system, which is the master regulator for the expression of genes contributing to the bacterial infection. Taken together, our findings indicate that melanin produced by B. parapertussis in a BvgAS-independent manner confers a survival advantage to the bacterium during host infection. IMPORTANCE In addition to the Gram-negative bacterium Bordetella pertussis, the etiological agent of pertussis, Bordetella parapertussis also causes respiratory infection in humans, with a mild pertussis-like disease. These bacteria are genetically closely related and share many virulence factors, including adhesins and toxins. However, B. parapertussis is clearly distinguished from B. pertussis by its brown pigment production, the bacteriological significance of which remains unclear. Here, we demonstrate that this pigment is melanin, which is known to be produced by a wide range of organisms from prokaryotes to humans and helps the organisms to survive under various environmental stress conditions. Our results show that melanin confers a survival advantage to B. parapertussis within human macrophages through its protective effect against reactive oxygen species and eventually contributes to respiratory infection of the bacterium in mice. This study proposes melanin as a virulence factor involved in the increased survival of B. parapertussis during host infection.

UV-induced reduction in Polycomb repression promotes epidermal pigmentation.

Ultraviolet (UV) radiation is a prime environmental stressor that our epidermis is exposed to on a daily basis. To avert UV-induced damage, epidermal stem cells (EpSCs) become pigmented via a process of heterotypic interaction between melanocytes and EpSCs; however, the molecular mechanisms of this interaction are not well understood. In this study, we show that the function of a key chromatin regulator, the Polycomb complex, was reduced upon UV exposure in human and mouse epidermis. Genetic ablation of key Polycomb subunits in murine EpSCs, mimicking depletion upon UV exposure, results in an increased number of epidermal melanocytes and subsequent epidermal pigmentation. Genome-wide transcriptional and chromatin studies show that Polycomb regulates the expression of UV-responsive genes and identifies type II collagen (COL2A1) as a critical secreted regulator of melanogenesis and epidermal pigmentation. Together, our findings show how UV exposure induces Polycomb-mediated changes in EpSCs to affect melanocyte behavior and promote epidermal pigmentation.

Alterations of the pigmentation system in the aging process.

Human skin aging is a natural phenomenon that results from continuous exposure to intrinsic (time, genetic factors, hormones) as well as extrinsic factors (UV exposure, pollution, tobacco). In areas that are frequently exposed to the sun, photoaging blends with the process of intrinsic aging, resulting in an increased senescent cells number and consequently accelerating the aging process. The severity of photodamage depends on constitutional factors, including skin phototype (skin color, tanning capacity), intensity, and duration of sunlight/UV exposure. Aging affects nearly every aspect of cutaneous biology, including pigmentation. Clinically, the phenotype of age pigmented skin has a mottled, uneven color, primarily due to age spots, with or without hypopigmentation. Uneven pigmentation might be attributed to the hyperactivation of melanocytes, altered distribution of pigment, and turnover. In addition to direct damage to pigment-producing cells, photodamage alters the physiological crosstalk between keratinocytes, fibroblasts, endothelial cells, and melanocytes responsible for natural pigmentation homeostasis. Interestingly, age-independent diffuse expression of senescence-associated markers in the dermal and epidermal compartment is also associated with vitiligo, suggesting that premature senescence plays an important role in the pathology.

Thyroid hormones regulate the formation and environmental plasticity of white bars in clownfishes.

Determining how plasticity of developmental traits responds to environmental conditions is a challenge that must combine evolutionary sciences, ecology, and developmental biology. During metamorphosis, fish alter their morphology and color pattern according to environmental cues. We observed that juvenile clownfish (Amphiprion percula) modulate the developmental timing of their adult white bar formation during metamorphosis depending on the sea anemone species in which they are recruited. We observed an earlier formation of white bars when clownfish developed with Stichodactyla gigantea (Sg) than with Heteractis magnifica (Hm). As these bars, composed of iridophores, form during metamorphosis, we hypothesized that timing of their development may be thyroid hormone (TH) dependent. We treated clownfish larvae with TH and found that white bars developed earlier than in control fish. We further observed higher TH levels, associated with rapid white bar formation, in juveniles recruited in Sg than in Hm, explaining the faster white bar formation. Transcriptomic analysis of Sg recruits revealed higher expression of duox, a dual oxidase implicated in TH production as compared to Hm recruits. Finally, we showed that duox is an essential regulator of iridophore pattern timing in zebrafish. Taken together, our results suggest that TH controls the timing of adult color pattern formation and that shifts in duox expression and TH levels are associated with ecological differences resulting in divergent ontogenetic trajectories in color pattern development.

Influence of survival, promotion, and growth on pattern formation in zebrafish skin.

The coloring of zebrafish skin is often used as a model system to study biological pattern formation. However, the small number and lack of movement of chromatophores defies traditional Turing-type pattern generating mechanisms. Recent models invoke discrete short-range competition and long-range promotion between different pigment cells as an alternative to a reaction-diffusion scheme. In this work, we propose a lattice-based "Survival model," which is inspired by recent experimental findings on the nature of long-range chromatophore interactions. The Survival model produces stationary patterns with diffuse stripes and undergoes a Turing instability. We also examine the effect that domain growth, ubiquitous in biological systems, has on the patterns in both the Survival model and an earlier "Promotion" model. In both cases, domain growth alone is capable of orienting Turing patterns above a threshold wavelength and can reorient the stripes in ablated cells, though the wavelength for which the patterns orient is much larger for the Survival model. While the Survival model is a simplified representation of the multifaceted interactions between pigment cells, it reveals complex organizational behavior and may help to guide future studies.

Bioluminescent Tumor Signal Is Mouse Strain and Pelt Color Dependent: Experience in a Disseminated Lymphoma Model.

BACKGROUND: Many preclinical cancer studies use mice with varied phenotypes to monitor tumor treatment. We compared survival and optical imaging characteristics of strains with varied coat colors harboring luciferase-expressing disseminated lymphoma. RESULTS: Luciferase-expressing lymphoma cells (Raji-luc) were injected via tail vein into severe combined immunodeficient (SCID) and Rag2-IL2rg (R2G2) mice, and survival was tracked. Tumor signals were obtained by imaging ventral and dorsal aspects of mice. Signal attenuation by isolated mouse pelts was measured in vitro. R2G2 mice had decreased survival compared to SCID mice (17 vs. 32 days, p<0.001) despite similar bioluminescence signal when mice were imaged dorsally (p=0.37). However, signal was 17.3-fold higher in R2G2 mice compared to SCID (p<0.001) when imaged ventrally. Isolated dark R2G2 dorsal pelts attenuated signal more than ventral pelts when placed over cells in vitro. CONCLUSIONS: Mouse pelt color and imaging aspect are critical considerations for quantifying bioluminescent tumor signal, and the R2G2 mouse strain may prove useful for preclinical targeted therapy studies.

Skin Pigmentation Abnormalities and Their Possible Relationship with Skin Aging.

Skin disorders showing abnormal pigmentation are often difficult to manage because of their uncertain etiology or pathogenesis. Abnormal pigmentation is a common symptom accompanying aging skin. The association between skin aging and skin pigmentation abnormalities can be attributed to certain inherited disorders characterized by premature aging and abnormal pigmentation in the skin and some therapeutic modalities effective for both. Several molecular mechanisms, including oxidative stress, mitochondrial DNA mutations, DNA damage, telomere shortening, hormonal changes, and autophagy impairment, have been identified as involved in skin aging. Although each of these skin aging-related mechanisms are interconnected, this review examined the role of each mechanism in skin hyperpigmentation or hypopigmentation to propose the possible association between skin aging and pigmentation abnormalities.

Reaction-diffusion in a growing 3D domain of skin scales generates a discrete cellular automaton.

We previously showed that the adult ocellated lizard skin colour pattern is effectively generated by a stochastic cellular automaton (CA) of skin scales. We additionally suggested that the canonical continuous 2D reaction-diffusion (RD) process of colour pattern development is transformed into this discrete CA by reduced diffusion coefficients at the borders of scales (justified by the corresponding thinning of the skin). Here, we use RD numerical simulations in 3D on realistic lizard skin geometries and demonstrate that skin thickness variation on its own is sufficient to cause scale-by-scale coloration and CA dynamics during RD patterning. In addition, we show that this phenomenon is robust to RD model variation. Finally, using dimensionality-reduction approaches on large networks of skin scales, we show that animal growth affects the scale-colour flipping dynamics by causing a substantial decrease of the relative length scale of the labyrinthine colour pattern of the lizard skin.

The Vhl E3 ubiquitin ligase complex regulates melanisation via sima, cnc and the copper import protein Ctr1A.

VHL encodes a tumour suppressor, which possesses E3 ubiquitin ligase activity in complex with EloC and Cul2. In tumour cells or in response to hypoxia, VHL activity is lost, causing accumulation of the transcription factor HIF-1alpha. In this study, we demonstrated that in Drosophila, Rpn9, a regulatory component of the 26 s proteasome, participates in the Vhl-induced proteasomal degradation of sima, the Drosophila orthologue of HIF-1alpha. Knockdown of Vhl induces increased melanisation in the adult fly thorax and concurrent decrease in pigmentation in the abdomen. Both these defects are rescued by knockdown of sima and partially by knockdown of cnc, which encodes the fly orthologue of the transcription factor Nrf2, the master regulator of oxidative stress response. We further show that sima overexpression and Rpn9 knockdown both result in post-translational down-regulation of the copper uptake transporter Ctr1A in the fly eye and that Ctr1A expression exacerbates Vhl knockdown defects in the thorax and rescues these defects in the abdomen. We conclude that Vhl negatively regulates both sima and cnc and that in the absence of Vhl, these transcription factors interact to regulate Ctr1A, copper uptake and consequently melanin formation. We propose a model whereby the co-regulatory relationship between sima and cnc flips between thorax and abdomen: in the thorax, sima is favoured leading to upregulation of Ctr1A; in the abdomen, cnc dominates, resulting in the post-translational downregulation of Ctr1A.

Pharmacologic manipulation of skin pigmentation.

Skin complexion is among the most recognizable phenotypes between individuals and is mainly determined by the amount and type of melanin pigment deposited in the epidermis. Persons with dark skin complexion have more of a brown/black pigment known as eumelanin in their epidermis whereas those with fair skin complexions have less. Epidermal eumelanin acts as a natural sunblock by preventing incoming UV photons from penetrating into the skin and therefore protects against UV mutagenesis. By understanding the signaling pathways and regulation of pigmentation, strategies can be developed to manipulate skin pigmentation to improve UV resistance and to diminish skin cancer risk.

The constraints of racialization: How classification and valuation hinder scientific research on human variation.

Human biological variation has historically been studied through the lens of racialization. Despite a general shift away from the use of overt racial terminologies, the underlying racialized frameworks used to describe and understand human variation still remain. Even in relatively recent anthropological and biomedical work, we can observe clear manifestations of such racial thinking. This paper shows how classification and valuation are two specific processes which facilitate racialization and hinder attempts to move beyond such frameworks. The bias induced by classification distorts descriptions of phenotypic variation in a way that erroneously portrays European populations as more variable than others. Implicit valuation occurs in tandem with classification and produces narratives of superiority/inferiority for certain phenotypic variants without an objective biological basis. The bias of racialization is a persistent impediment stemming from the inheritance of scientific knowledge developed under explicitly racial paradigms. It is also an internalized cognitive distortion cultivated through socialization in a world where racialization is inescapable. Though undeniably challenging, this does not present an insurmountable barrier, and this bias can be mitigated through the critical evaluation of past work, the active inclusion of marginalized perspectives, and the direct confrontation of institutional structures enforcing racialized paradigms.

Clinical impact of a sub-epidermal moisture scanner: what is the real-world use?

OBJECTIVE: The presence of sub-epidermal moisture (SEM) over a bony prominence is indicative of incipient pressure ulcer (pressure injury/decubitus/bedsore) (PU). Early identification of patients at increased risk of PU can prompt interventions that reduce the incidence and severity of hospital (or community)-acquired PUs (HAPUs). This study evaluated the clinical utility of a SEM Scanner device in HAPU management. METHOD: The study used a pragmatic 'real-world' approach. HAPU data before and during SEM Scanner use were obtained through routine audit. Patients had regular visual and daily SEM Scanner skin assessments over the sacrum and heels. Nursing care otherwise followed standard of care according to the established protocols of individual participating sites. HAPU incidence rates were determined and feedback gathered from health professionals on how the device influenced HAPU-related clinical decision-making. RESULTS: There were 15 participating sites: 13 acute care, one palliative care and one community care setting. The sample size was 1478 patients. All sites reported a substantial reduction in mean HAPU incidence: 87.2% in acute care settings; 46.7% in the palliative care setting and 26.7% in the community care setting. A 100% incidence reduction was reported in 10 (66.7%) sites. In the palliative care setting, SEM Scanner results changed HAPU-related clinical decision-making for 40% of patients scanned. The community care site demonstrated a 82% change in clinical decision-making. CONCLUSION: In this study, SEM analysis fitted seamlessly into routine skin assessment and enabled early identification of increased risk of tissue damage, with clinically important reductions in the incidence of HAPU across all participating sites.

Bio-inspired photonics - marine hatchetfish camouflage strategies for RF steganography.

Camouflage is a strategy that animals utilize for concealment in their habitat, making themselves invisible to their predators and preys. In RF systems, steganography or stealth transmission is the camouflage of information - a technology of hiding and transmitting secret messages in public media. Steganography conceals the secret message in publicly available media such that the eavesdropper or attacker will not be able to tell if there is a secret message to look for. Marine hatchetfish have two effective camouflage skills to help them hide from their predators - silvering and counterillumination. Silvering in marine hatchetfish uses its microstructured skin on its sides to achieve destructive interference at colors that could indicate the presence of the fish, while they also emit light at their bottom part to match its color and intensity to its surrounding, making it invisible from below, referred to as counterillumination. In this work, we borrow the two underwater camouflage strategies from marine hatchetfish, mimic them with photonic phenomena, and apply the camouflage strategies for physical stealth transmission of a 200 MBaud/s 16QAM OFDM secret signal at 5 GHz over a 25-km of optical fiber. The proposed bio-inspired steganography strategies successfully hid the secret signal in plain sight in temporal, RF spectral, and optical spectral domains, by blending in using counterillumination and turning invisible using silvering techniques. The stealth signal can only be retrieved with the precise and correct parameter for constructive interference at the secret signal frequency to unmask the silvering.