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Wild felids are one of the most vulnerable species due to habitat loss caused by fragmentation of ecosystems. We analyzed the effect of a structural corridor, defined as a strip of vegetation connecting two habitat patches, on the richness and habitat occupancy of felids on three sites in Marqués de Comillas, Chiapas, one with two isolated forest patches, the second with a structural corridor, and the third inside the Montes Azules Biosphere Reserve. We found only two species (L. pardalis and H. yagouaroundi) in the isolated forest patches, five species in the structural corridor, and four species inside the Reserve. The corridor did not significantly affect occupancy, but due to the low detection rates, further investigation is needed to rule out differences. Our results highlight the need to manage habitat connectivity in the remaining forests in order to preserve the felid community of Marqués de Comillas, Chiapas, México.

Specialized proresolving mediators and, in particular, 5(S), (6)R, 7-trihydroxyheptanoic acid methyl ester (BML-111) emerge as new therapeutic tools to prevent cardiac dysfunction and deleterious cardiac damage associated with myocarditis progression. The cardioprotective role of BML-111 is mainly caused by the prevention of increased oxidative stress and nuclear factor erythroid-derived 2-like 2 (NRF2) down-regulation induced by myocarditis. At the molecular level, BML-111 activates NRF2 signaling, which prevents sarcoplasmic reticulum-adenosine triphosphatase 2A down-regulation and Ca 2+ mishandling, and attenuates the cardiac dysfunction and tissue damage induced by myocarditis., Competing Interests: This work was supported by the Spanish Ministry of Economy and Competitiveness and the European Regional Development Fund (SAF-2017-84777R), Instituto de Salud Carlos III (ISCIII) (PI17/01093, PI17/01344, and PI20/01482), Sociedad Española de Cardiología, Proyecto Traslacional 2019 and Asociación del Ritmo Cardiaco (SEC, España), Proyecto Asociación Insuficiencia Cardiaca (Trasplante Cardiaco) 2020, Fondo Europeo de Desarrollo Regional, Fondo Social Europeo, and CIBERCV, a network funded by ISCIII, Spanish Ministry of Science, Innovation and Universities (PGC2018-097019-B-I00), Ministerio de Economía, Industria y Competitividad/Agencia Estatal de Investigación 10.13039/501100011033 PID2020-113238RB-I00, PID2019-105600RB-I00, the Instituto de Salud Carlos III (Fondo de Investigación Sanitaria grant PRB3 [PT17/0019/0003-ISCIII-SGEFI/ERDF, ProteoRed]), and “la Caixa” Foundation (project code HR17-00247). The Centro Nacional de Investigaciones Cardiovasculares is supported by the ISCIII, the Ministerio de Ciencia, Innovación y Universidades. Dr Ruiz-Hurtado is Miguel Servet I researcher of ISCIII (CP15/00129 Carlos III Health Institute). Dr Tamayo and R.I. Jaén, and M. Gil-Fernández were or currently are PhD students funded by the Formación de Profesorado Universitario program of the Spanish Ministry of Science, Innovation and Universities (FPU17/06135; FPU16/00827, FPU1901973). The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2022 The Authors.)

Adverse ventricular remodeling is the heart's response to damaging stimuli and is linked to heart failure and poor prognosis. Formyl-indolo [3,2-b] carbazole (FICZ) is an endogenous ligand for the aryl hydrocarbon receptor (AhR), through which it exerts pleiotropic effects including protection against inflammation, fibrosis, and oxidative stress. We evaluated the effect of AhR activation by FICZ on the adverse ventricular remodeling that occurs in the early phase of pressure overload in the murine heart induced by transverse aortic constriction (TAC). Cardiac structure and function were evaluated by cardiac magnetic resonance imaging (CMRI) before and 3 days after Sham or TAC surgery in mice treated with FICZ or with vehicle, and cardiac tissue was used for biochemical studies. CMRI analysis revealed that FICZ improved cardiac function and attenuated cardiac hypertrophy. These beneficial effects involved the inhibition of the hypertrophic calcineurin/NFAT pathway, transcriptional reduction in pro-fibrotic genes, and antioxidant effects mediated by the NRF2/NQO1 pathway. Overall, our findings provide new insight into the role of cardiac AhR signaling in the injured heart.

Ca 2+ mishandling is a common feature in several cardiovascular diseases such as heart failure (HF). In many cases, impairment of key players in intracellular Ca 2+ homeostasis has been identified as the underlying mechanism of cardiac dysfunction and cardiac arrhythmias associated with HF. In this review, we summarize primary novel findings related to Ca 2+ mishandling in HF progression. HF research has increasingly focused on the identification of new targets and the contribution of their role in Ca 2+ handling to the progression of the disease. Recent research studies have identified potential targets in three major emerging areas implicated in regulation of Ca 2+ handling: the innate immune system, bone metabolism factors and post-translational modification of key proteins involved in regulation of Ca 2+ handling. Here, we describe their possible contributions to the progression of HF., (© 2021 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)

Risk of cardiovascular disease (CVD) increases considerably as renal function declines in chronic kidney disease (CKD). Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) has emerged as a novel innate immune receptor involved in both CVD and CKD. Following activation, NOD1 undergoes a conformational change that allows the activation of the receptor-interacting serine/threonine protein kinase 2 (RIP2), promoting an inflammatory response. We evaluated whether the genetic deficiency of Nod1 or Rip2 in mice could prevent cardiac Ca 2+ mishandling induced by sixth nephrectomy (Nx), a model of CKD. We examined intracellular Ca 2+ dynamics in cardiomyocytes from Wild-type ( Wt ), Nod1 -/- and Rip2 -/- sham-operated or nephrectomized mice. Compared with Wt cardiomyocytes, Wt -Nx cells showed an impairment in the properties and kinetics of the intracellular Ca 2+ transients, a reduction in both cell shortening and sarcoplasmic reticulum Ca 2+ load, together with an increase in diastolic Ca 2+ leak. Cardiomyocytes from Nod1 -/- -Nx and Rip2 -/- -Nx mice showed a significant amelioration in Ca 2+ mishandling without modifying the kidney impairment induced by Nx. In conclusion, Nod1 and Rip2 deficiency prevents the intracellular Ca 2+ mishandling induced by experimental CKD, unveiling new innate immune targets for the development of innovative therapeutic strategies to reduce cardiac complications in patients with CKD.

Cardiovascular diseases (CVDs) are the leading cause of death in the industrialized world. Most CVDs are associated with increased inflammation that arises mainly from innate immune system activation related to cardiac damage. Sustained activation of the innate immune system frequently results in maladaptive inflammatory responses that promote cardiovascular dysfunction and remodeling. Much research has focused on determining whether some mediators of the innate immune system are potential targets for CVD therapy. The innate immune system has specific receptors-termed pattern recognition receptors (PRRs)-that not only recognize pathogen-associated molecular patterns, but also sense danger-associated molecular signals. Activation of PRRs triggers the inflammatory response in different physiological systems, including the cardiovascular system. The classic PRRs, toll-like receptors (TLRs), and the more recently discovered nucleotide-binding oligomerization domain-like receptors (NLRs), have been recently proposed as key partners in the progression of several CVDs (e.g., atherosclerosis and heart failure). The present review discusses the key findings related to the involvement of TLRs and NLRs in the progression of several vascular and cardiac diseases, with a focus on whether some NLR subtypes (nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing receptor 3 and nucleotide-binding oligomerization domain-containing protein 1) can be candidates for the development of new therapeutic strategies for several CVDs., (© 2020 The Authors.)

Heart failure (HF) is a complex syndrome characterized by cardiac dysfunction, Ca 2+ mishandling, and chronic activation of the innate immune system. Reduced cardiac output in HF leads to compensatory mechanisms via activation of the adrenergic nervous system. In turn, chronic adrenergic overstimulation induces pro-arrhythmic events, increasing the rate of sudden death in failing patients. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is an innate immune modulator that plays a key role in HF progression. NOD1 deficiency in mice prevents Ca 2+ mishandling in HF under basal conditions, but its role during β-adrenergic stimulation remains unknown. Here, we evaluated whether NOD1 regulates the β-adrenergic modulation of Ca 2+ signaling in HF. Ca 2+ dynamics were examined before and after isoproterenol perfusion in cardiomyocytes isolated from healthy and from post-myocardial infarction (PMI) wild-type (WT) and Nod1 -/- mice. Isoproterenol administration induced similar effects on intracellular [Ca 2+ ] i transients, cell contraction, and sarcoplasmic reticulum (SR)-Ca 2+ load in healthy WT and Nod1 -/- cells. However, compared with WT-PMI cells, isoproterenol exposure induced a significant increase in the [Ca 2+ ] i transients and cell contraction parameters in Nod1 -/- -PMI cells, which mainly due to an increase in SR-Ca 2+ load. NOD1 deficiency also prevented the increase in diastolic Ca 2+ leak (Ca 2+ waves) induced by isoproterenol in PMI cells. mRNA levels of β1 and β2 adrenergic receptors were significantly higher in Nod1 -/- -PMI hearts vs WT-PMI hearts. Healthy cardiomyocytes pre-treated with the selective agonist of NOD1, iE-DAP, and perfused with isoproterenol showed diminished [Ca 2+ ] i transients amplitude, cell contraction, and SR-Ca 2+ load compared with vehicle-treated cells. iE-DAP-treated cells also presented increased diastolic Ca 2+ leak under β-adrenergic stimulation. The selectivity of iE-DAP on Ca 2+ handling was validated by pre-treatment with the inactive analog of NOD1, iE-Lys. Overall, our data establish that NOD1 deficiency improves the β-adrenergic modulation of Ca 2+ handling in failing hearts.

An 18-year-old woman pregnant at 37 weeks gestation and with a history of recurrent urinary tract infection was admitted with a clinical picture of pyelonephritis that responded favorably to antibiotic treatment. After 2 days, cervical ripening was induced with prostaglandin E2 gel and labor was induced with oxytocin. The patient requested epidural analgesia. Six hours after induction, cesarean delivery was indicated owing to risk of fetal distress. The operation was carried out under epidural anesthesia with 10 mL of 0.5% bupivacaine without a vasoconstrictor. After delivery, uterine atony was treated unsuccessfully with oxytocin and methylergometrine maleate; the obstetrician then gave an intramyometrial injection of 0.25 mg of 15-methyl-prostaglandin F2alpha (PGF2alpha). After 5 minutes, SpO2 fell to 89%, accompanied by dyspnea and sinus tachycardia of 130-140 beats/min, with normal cardiorespiratory sounds. The patient was transferred to the postoperative recovery unit, where a chest radiograph led to a diagnosis of acute pulmonary edema. Treatment to reduce edema was successful. PGF2alpha and its analogs are useful for treating uterine atony that does not respond to other drugs, but side effects are not unknown. Caution in prescribing PGF2alpha and care in monitoring the patient's reaction are therefore recommended during and after anesthesia. Unnecessary overhydration should be avoided.

We study the effects of low concentrations of mercury vapour on the nervous system of a group of eleven workers of a chloroalkali plant exposed to it. Twenty-three non-exposed workers in the same factory were used as control group. We used clinical and analytic explorations, psychometric tests and evoked potentials to evaluate the subjects. The average Hg in urine of the exposed group was 41.74 micrograms/gr creatinine and the average of the non-exposed group as 9.71 mu/yr. In the exposed group the evoked potentials have found a slowing-down of conduction in all the nervous paths studied (optical, auditive and somatosensory) and in the latency of P300 wave, although this was not statistically significant compared to the control group. Of the psychometric test used, only Rey's Complex Figure Test showed deterioration in the visual memory subtest of the exposed group (p < 0.05) compared to the control group, although in Wechsler's digit span test lower scores were obtained which were close to being statistically significant comparing the averages of the two groups (0.05 < p < 0.051). Bearing in mind these results we think that the amounts of Hg in urine and TLV-TWA (50 micrograms/gr creatinine and 50 micrograms/m3 respectively) accepted by most authors as innocuous should be reduced.