Size-Mediated Sea Turtle Behavioral Responses at Artificial Habitats in the Northern Gulf of Mexico.

Our understanding of size-specific sea turtle behavior has lagged due to methodological limitations. However, stereo-video cameras (SVC) are an in-water approach that can link body-size and allow for relatively undisturbed behavioral observations. In this study, we conducted SVC dive surveys at local artificial reefs, piers, and jetties in the northern Gulf of Mexico (nGOM) from May 2019 to August 2021. Using SVCs, we measured sea turtle straight carapace length, documented behaviors, and quantified wariness by assessing minimum approach distance (MAD). In green sea turtles (Chelonia mydas), the observed MAD ranged from 0.72 to 5.99 m (mean 2.10 m ± 1.10 standard deviation (SD), n = 73). For loggerhead sea turtles (Caretta caretta), the MAD ranged between 0.93 and 3.80 m (mean 2.12 m ± 0.99 SD, n = 16). Kemp's ridley sea turtles (Lepidochelys kempii) were similar to loggerheads, and MAD ranged from 0.78 to 3.63 m (mean 2.35 m ± 0.99 SD, n = 8). We then evaluated what biological factors could impact the MAD observed by species, but we excluded Kemp's ridleys as the sample size was small. Using a linear mixed model and model selection based on AICc, the top ranked model for both green and loggerhead sea turtles included SCL as the most important factor influencing MAD. MAD did not vary with habitat type for either species. Our results showed that larger individuals, regardless of species, have a greater wariness response, becoming startled at greater distances than smaller individuals. The findings of our study support the use of SVC as an accessible, non-invasive tool to conduct ecologically relevant in-water surveys of sea turtles to link behavioral observations to body size.

Stochastic force dynamics of the model microswimmer Chlamydomonas reinhardtii: Active forces and energetics.

We study the stochastic force dynamics of a model microswimmer (Chlamydomonas reinhardtii), using a combined experimental, theoretical, and numerical approach. While swimming dynamics have been extensively studied using hydrodynamic approaches, which infer forces from the viscous flow field, we directly measure the stochastic forces generated by the microswimmer using an optical trap via the photon momentum method. We analyze the force dynamics by modeling the microswimmer as a self-propelled particle, à la active matter, and analyze its energetics using methods from stochastic thermodynamics. We find complex oscillatory force dynamics and power dissipation on the order of 10^{6}k_{B}T/s(∼fW).

El corazón en los tiempos del COVID-19 / The heart in the times of COVID-19

SarsCov2 infection produces a clinical syndrome known as COVID-19, which presents mainly respiratory manifestations and various conditions are associated with a higher rate of complications of this pathology, with acute cardiovascular syndrome by COVID-19 being a relatively common complication. In this article we will review the most frequent manifestations, the prognosis, the diagnostic and therapeutic approach of these.

Quantifying the non-equilibrium activity of an active colloid.

Active matter systems exhibit rich emergent behavior due to constant injection and dissipation of energy at the level of individual agents. Since these systems are far from equilibrium, their dynamics and energetics cannot be understood using the framework of equilibrium statistical mechanics. Recent developments in stochastic thermodynamics extend classical concepts of work, heat, and energy dissipation to fluctuating non-equilibrium systems. We use recent advances in experiment and theory to study the non-thermal dissipation of individual light-activated self-propelled colloidal particles. We focus on characterizing the transition from thermal to non-thermal fluctuations and show that energy dissipation rates on the order of ∼kBT s-1 are measurable from finite time series data.

Deep proteomic analysis of Dnmt1 mutant/hypomorphic colorectal cancer cells reveals dysregulation of epithelial-mesenchymal transition and subcellular re-localization of Beta-Catenin.

DNA methyltransferase I plays the central role in maintenance of CpG DNA methylation patterns across the genome and alteration of CpG methylation patterns is a frequent and significant occurrence across many cancers. Cancer cells carrying hypomorphic alleles of Dnmt1 have become important tools for understanding Dnmt1 function and CpG methylation. In this study, we analyse colorectal cancer cells with a homozygous deletion of exons 3 to 5 of Dnmt1, resulting in reduced Dnmt1 activity. Although this cell model has been widely used to study the epigenome, the effects of the Dnmt1 hypomorph on cell signalling pathways and the wider proteome are largely unknown. In this study, we perform the first quantitative proteomic analysis of this important cell model and identify multiple signalling pathways and processes that are significantly dysregulated in the hypomorph cells. In Dnmt1 hypomorph cells, we observed a clear and unexpected signature of increased Epithelial-to-Mesenchymal transition (EMT) markers as well as reduced expression and sub-cellular re-localization of Beta-Catenin. Expression of wild-type Dnmt1 in hypomorph cells or knock-down of wild-type Dnmt1 did not recapitulate or rescue the observed protein profiles in Dnmt1 hypomorph cells suggesting that hypomorphic Dnmt1 causes changes not solely attributable to Dnmt1 protein levels. In summary, we present the first comprehensive proteomic analysis of the widely studied Dnmt1 hypomorph colorectal cancer cells and identify redistribution of Dnmt1 and its interaction partner Beta-Catenin.

Permanent pacemaker-associated actinomycetemcomitans endocarditis: A case report.

Aggregatibacter actinomycetemcomitans is a Gram-negative bacillus, member of the HACEK group of bacteria, and it is a very rare cause of endocarditis. It is also an extremely rare cause of device-associated infection of the heart. We describe the case of a 25 year-old man who presented with pacemaker-associated endocarditis due to Aggregatibacter actinomycetemcomitans and also discuss the implications and treatment of this organism.

The surface electrocardiogram predicts risk of heart block during right heart catheterization in patients with preexisting left bundle branch block: implications for the definition of complete left bundle branch block.

BACKGROUND: Patients with left bundle branch block (LBBB) undergoing right heart catheterization can develop complete heart block (CHB) or right bundle branch block (RBBB) in response to right bundle branch (RBB) trauma. We hypothesized that LBBB patients with an initial r wave (>or=1 mm) in lead V1 have intact left to right ventricular septal (VS) activation suggesting persistent conduction over the left bundle branch. Trauma to the RBB should result in RBBB pattern rather than CHB in such patients. METHODS: Between January 2002 and February 2007, we prospectively evaluated 27 consecutive patients with LBBB developing either CHB or RBBB during right heart catheterization. The prevalence of an r wave >or=1 mm in lead V1 was determined using 118 serial LBBB electrocardiographs (ECGs) from our hospital database. RESULTS: Catheter trauma to the RBB resulted in CHB in 18 patients and RBBB in 9 patients. All 6 patients with >or=1 mm r wave in V1 developed RBBB. Among these 6 patients q wave in lead I, V5, or V6 were present in 3. Four patients (3 in CHB group and 1 in RBBB group) developed spontaneous CHB during a median follow-up of 61 months. V1 q wave >or=1 mm was present in 28% of hospitalized complete LBBB patients. CONCLUSIONS: An initial r wave of >or=1 mm in lead V1 suggests intact left to right VS activation and identifies LBBB patients at low risk of CHB during right heart catheterization. These preliminary findings indicate that an initial r wave of >or=1 mm in lead V1, present in approximately 28% of ECGs with classically defined LBBB, may constitute a new exclusion criterion when defining complete LBBB.

Zinc dyshomeostasis in rats with aldosteronism. Response to spironolactone.

Zinc is a structural constituent of many proteins, including Cu/Zn superoxide dismutase (SOD), an endogenous antioxidant enzyme. Hypozincemia has been found in patients hospitalized with congestive heart failure, where neurohormonal activation, including the renin-angiotensin-aldosterone system (RAAS), is expected and oxidative stress is present. This study was undertaken to elucidate potential pathophysiological mechanisms involved in Zn dyshomeostasis in aldosteronism. In rats receiving aldosterone/salt treatment (ALDOST) alone for 1 and 4 wk or in combination with spironolactone (Spiro), an ALDO receptor antagonist, we monitored 24-h urinary and fecal Zn excretion and tissue Zn levels in heart, liver, and skeletal muscle, together with tissue metallothionein (MT)-I, a Zn(2+)-binding protein, and Cu/Zn-SOD activities in plasma and tissues. When compared with unoperated, untreated, age-/sex-matched controls, urinary and, in particular, fecal Zn losses were markedly increased (P < 0.05) at days 7 and 28 of ALDOST, leading to hypozincemia and a fall (P < 0.05) in plasma Cu/Zn-SOD activity. Microscopic scars and perivascular fibrosis of intramural coronary arteries first appeared in the right and left ventricles at week 4 of ALDOST and were accompanied by increased (P < 0.05) tissue Zn, MT-I, and Cu/Zn-SOD activity, which were not found in uninjured liver or skeletal muscle. Spiro cotreatment prevented cardiac injury and Zn redistribution to the heart. Thus increased urinary and fecal Zn losses, together with their preferential translocation to sites of cardiac injury, where MT-I overexpression and increased Cu/Zn-SOD activity appeared, contribute to Zn dyshomeostasis in rats with aldosteronism, which were each prevented by Spiro. These findings may shed light on Zn dyshomeostasis found in patients with decompensated heart failure.

Calcium paradox of aldosteronism and the role of the parathyroid glands.

The hypercalciuria and hypermagnesuria that accompany aldosteronism contribute to a fall in plasma ionized extracellular Ca2+ and Mg2+ concentrations ([Ca2+]o and [Mg2+]o). Despite these losses and the decline in extracellular levels of these cations, total intracellular and cytosolic free Ca2+ concentration ([Ca2+]i) is increased and oxidative stress is induced. This involves diverse tissues, including peripheral blood mononuclear cells (PBMC) and plasma. The accompanying elevation in plasma parathyroid hormone (PTH) and reduction in bone mineral density caused by aldosterone (Aldo)-1% NaCl treatment (AldoST) led us to hypothesize that Ca2+ loading and altered redox state are due to secondary hyperparathyroidism (SHPT). Therefore, we studied the effects of total parathyroidectomy (PTx). In rats receiving AldoST, without or with a Ca2+-supplemented diet and/or PTx, we monitored urinary Ca2+ and Mg2+ excretion; plasma [Ca2+]o, [Mg2+]o, and PTH; PBMC [Ca2+]i and H2O2 production; plasma alpha1-antiproteinase activity; total Ca2+ and Mg2+ in bone, myocardium, and rectus femoris; and gp91(phox) labeling in the heart. We found that 1) the hypercalciuria and hypermagnesuria and decline (P < 0.05) in plasma [Ca2+]o and [Mg2+]o that occur with AldoST were not altered by the Ca2+-supplemented diet alone or with PTx; 2) the rise (P < 0.05) in plasma PTH with AldoST, with or without the Ca2+-supplemented diet, was prevented by PTx; 3) increased (P < 0.05) PBMC [Ca2+]i and H2O2 production, increased total Ca2+ in heart and skeletal muscle, and fall in bone Ca2+ and Mg2+ and plasma alpha1-antiproteinase activity with AldoST were abrogated (P < 0.05) by PTx; and 4) gp91(phox) activation in right and left ventricles at 4 wk of AldoST was attenuated by PTx. AldoST is accompanied by SHPT, with parathyroid gland-derived calcitropic hormones being responsible for Ca2+ overload in diverse tissues and induction of oxidative stress. SHPT plays a permissive role in the proinflammatory vascular phenotype.