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We explore the properties of Stepanov–Bogoliubov’s interacting fields in the framework of null-plane causal perturbation theory. Considering light-front quantum electrodynamics, that have been previously studied in this framework, and extending the results from there, we show that, contrary to what occurs in instant dynamics, in light-front dynamics the interacting equations of motion are satisfied only in the adiabatic limit for the fields whose Feynman’s propagators acquire an instantaneous term in the splitting of their (anti-)commutation distribution. The null-plane gauge condition, on the other hand, can be imposed on the interacting electromagnetic field for every switching function, at all orders of perturbation theory. We also show that the interacting fields satisfy finite Källén–Yang–Feldman’s equations that are formally independent of the normalization of the retarded distributions.

The radiation observed in quasars and active galactic nuclei is mainly produced by a relativistic plasma orbiting close to the black hole event horizon, where strong gravitational effects are relevant. The observational data of such systems can be compared with theoretical models to infer the black hole and plasma properties. In the comparison process, ray-tracing algorithms are essential to computing the trajectories followed by the photons from the source to our telescopes. In this paper, we present OSIRIS: a new stable FORTRAN code capable of efficiently computing null-geodesics around compact objects, including general relativistic effects such as gravitational lensing, redshift, and relativistic boosting. The algorithm is based on the Hamiltonian formulation and uses different integration schemes to evolve null-geodesics while tracking the error in the Hamiltonian constrain to ensure physical results. We found from an error analysis that the integration schemes are all stable, and the best one maintains an error below 10-11. Particularly, to test the robustness and ability of the code to evolve geodesics in curved space-time, we compute the shadow and Einstein rings of a Kerr black hole with different rotation parameters and obtain the image of a thin Keplerian accretion disk around a Schwarzschild black hole. Although OSIRIS is parallelized neither with MPI nor with CUDA, the computation times are of the same order as those reported by other codes with these types of parallel computing platforms.

Neonatal arterial ischemic stroke (NAIS) and neonatal hypoxic‐ischemic encephalopathy (HIE) are common causes of neurological impairments in infants, for which treatment options are very limited. NAIS and HIE induce an innate immune response that involves the recruitment of peripheral immune cells, including monocytes, into the brain. Monocytes and monocyte‐derived cells have the potential to contribute to both harmful and beneficial pathophysiological processes, such as neuroinflammation and brain repair, but their roles in NAIS and HIE remain poorly understood. Furthermore, recent evidence indicates that monocyte‐derived macrophages can persist in the brain for several months following NAIS and HIE in mice, with possible long‐lasting consequences that are still unknown. This review provides a comprehensive overview of the mechanisms of monocyte infiltration and their potential functions in the ischemic brain, focusing on HIE and NAIS. Therapeutic strategies targeting monocytes and the possibility of using monocytes for cell‐based therapies are also discussed. Monocytes and monocyte‐derived cells in hypoxic‐ischemic encephalopathy (HIE) and neonatal arterial ischemic stroke (NAIS). (A) The origin of monocytes infiltrating the brain in neonatal HIE and NAIS has yet to be investigated, including the possibility that they originate from various sources, such as the spleen and bone marrow. (B) Monocytes can infiltrate the brain through different routes, but it is not yet known whether they can migrate from the meninges to the brain parenchyma after HIE and NAIS. (C) Monocytes infiltrate the brain in the first hours and days following HIE and NAIS, and chronic monocyte infiltration has been observed in HIE models. Monocytes can differentiate into macrophages and microglia‐like cells, which can persist in the brain during the chronic phase of NAIS and HIE. Key points Monocytes are recruited to the brain within the first days following neonatal arterial ischemic stroke (NAIS) and hypoxic‐ischemic encephalopathy (HIE). More severe lesions or a combination of HIE and systemic inflammatory insults lead to more robust recruitment of monocytes to the brain. Monocytes differentiate into macrophages and microglia‐like cells, which can remain in the brain for several months following NAIS and HIE. CCR2 signaling is critical for monocyte infiltration and represents a potential therapeutic target. The outcomes of CCR2 inhibition or knockout vary depending on the HIE model used, highlighting the need for more studies in different models. Models of cerebral ischemia in neonates and adults indicate that monocytes may contribute to both brain damage, through their pro‐inflammatory activity and ability to modify perineuronal nets, and brain repair and functional recovery, through efferocytosis and their role in vascular repair. Umbilical cord blood monocytes and preconditioned monocytes could be used for the development of cell‐based therapies. Pharmacological interventions targeting monocyte infiltration or function require further testing in experimental models of HIE and NAIS.

Regulation of our water homeostasis is fine-tuned by dynamic translocation of Aquaporin-2 (AQP2)-bearing vesicles to and from the plasma membrane of renal principal cells. Whereas binding of vasopressin to its type-2 receptor initiates a cAMP-protein kinase A cascade and AQP2 translocation to the apical membrane, this is counteracted by protein kinase C-activating hormones, resulting in ubiquitination-dependent internalization of AQP2. The proteins targeting AQP2 for ubiquitin-mediated degradation are unknown. In collecting duct mpkCCD cells, siRNA knockdown of NEDD4 and NEDD4L E3 ligases yielded increased AQP2 abundance, but they did not bind AQP2. Membrane Yeast Two-Hybrid assays using full-length AQP2 as bait, identified NEDD4 family interacting protein 2 (NDFIP2) to bind AQP2. NDFIP2 and its homologue NDFIP1 have PY motifs by which they bind NEDD4 family members and bring them close to target proteins. In HEK293 cells, NDFIP1 and NDFIP2 bound AQP2 and were essential for NEDD4/NEDD4L-mediated ubiquitination and degradation of AQP2, an effect not observed with PY-lacking NDFIP1/2 proteins. In mpkCCD cells, downregulation of NDFIP1, NEDD4 and NEDD4L, but not NDFIP2, increased AQP2 abundance. In mouse kidney, Ndfip1 and Ndfip2 mRNA distribution was similar and high in proximal tubules and collecting ducts, which was also found for NDFIP1 proteins. Our results reveal that NEDD4/NEDD4L mediate ubiquitination and degradation of AQP2, but that NDFIP proteins are needed to connect NEDD4/NEDD4L to AQP2. As NDFIP1/2 bind many NEDD4 family E3 ligases, which are implicated in several cellular processes, NDFIP1/2 may be the missing link for AQP2 ubiquitination and degradation from different subcellular locations.

Bopp–Podolsky electrodynamics is generalized to curved space-times. The equations of motion are written for the case of static spherically symmetric black holes and their exterior solutions are analyzed using Bekenstein’s method. It is shown that the solutions split up into two parts, namely a non-homogeneous (asymptotically massless) regime and a homogeneous (asymptotically massive) sector which is null outside the event horizon. In addition, in the simplest approach to Bopp–Podolsky black holes, the non-homogeneous solutions are found to be Maxwell’s solutions leading to a Reissner–Nordström black hole. It is also demonstrated that the only exterior solution consistent with the weak and null energy conditions is the Maxwell one. Thus, in the light of the energy conditions, it is concluded that only Maxwell modes propagate outside the horizon and, therefore, the no-hair theorem is satisfied in the case of Bopp–Podolsky fields in spherically symmetric space-times.

A bstract Not all complete set of spinors can be used as expansion coefficients of a quantum field. In fact, Steven Weinberg established the uniqueness of Dirac spinors for this purpose provided: (a) one paid due attention to the multiplicative phases for each of the spinors, and (b) one paired these to creation and annihilation operators in a specific manner. This is implicit in his implementation of the rotational symmetry for the spin half quantum field. Among the numerous complete set of spinors that are available to a physicist, Elko occupies a unique status that allows it to enter as expansion coefficients of a quantum field without violating Weinberg’s no go theorem. How this paradigm changing claim arises is the primary subject of this communication. Weinberg’s no go theorem is evaded by exploiting a uniquely special feature of Elko that allows us to introduce a doubling of the particle-antiparticle degrees of freedom from four to eight. Weinberg had dismissed this degeneracy on the ground that, “no examples are known of particles that furnish unconventional representations of inversions.” Here we will find that this degeneracy, once envisioned by Eugene Wigner, in fact gives rise to a quantum field that has all the theoretical properties required of dark matter.

Neutrophil extracellular traps (NETs) evolved as a unique effector mechanism contributing to resistance against infection that can also promote tissue damage in inflammatory conditions. Malaria infection can trigger NET release, but the mechanisms and consequences of NET formation in this context remain poorly characterized. Here we show that patients suffering from severe malaria had increased amounts of circulating DNA and increased neutrophil elastase (NE) levels in plasma. We used cultured erythrocytes and isolated human neutrophils to show that Plasmodium-infected red blood cells release macrophage migration inhibitory factor (MIF), which in turn caused NET formation by neutrophils in a mechanism dependent on the C-X-C chemokine receptor type 4 (CXCR4). NET production was dependent on histone citrullination by peptidyl arginine deiminase-4 (PAD4) and independent of reactive oxygen species (ROS), myeloperoxidase (MPO) or NE. In vitro, NETs functioned to restrain parasite dissemination in a mechanism dependent on MPO and NE activities. Finally, C57/B6 mice infected with P. berghei ANKA, a well-established model of cerebral malaria, presented high amounts of circulating DNA, while treatment with DNAse increased parasitemia and accelerated mortality, indicating a role for NETs in resistance against Plasmodium infection.

Introduction: Very low-calorie diets with hospitalization have demonstrated promise as a viable therapeutic option for severe obesity and its associated comorbidities. However, large studies providing a comprehensive longitudinal observation of patients undergoing this therapy are lacking. We evaluated the effectiveness of treating severe obesity in hospitalized patients, using very low-calorie diets and clinical support to develop lifestyle changes. Methods: This study was a retrospective cohort comparing exposure variables in a secondary data analysis with a pre-post treatment design. Data were obtained from medical records of patients with severe obesity (grade II or III) treated in a Brazilian obesity specialist hospital from 2016 to 2022. The patients underwent a very low-calorie diet (500–800 kCal/day) and immersive changes in lifestyle habits, monitored by a multidisciplinary team. At 3 months, 777 patients presented complete data and 402 presented complete data at 6 months. The study compared changes in bioimpedance and laboratory tests, between men and women and age groups. Results: Three months of hospitalization yielded significant reductions in weight, body mass index (BMI), body fat, skeletal muscle mass, glucose, inflammatory, and lipid parameters. These reductions were more pronounced after 6 months, nearly doubling those observed at 3 months. In women, BMI and fat mass reduced by 10.4% and 15.2% at 3 months and 20.4% and 31.3% at 6 months, respectively. In men, BMI and fat mass decreased by 12.9% and 25.3 at 3 months and 23.6% and 45.3% at 6 months, respectively. Elderly individuals (aged ≥ 60 years) had smaller reductions in BMI and fat mass than non-elderly individuals (aged < 60 years) but still presented significant improvements. Conclusion: This study suggests the viability of treating severe obesity by hospitalization with low-calorie diets and immersive lifestyle changes. This treatment modality significantly improves anthropometric measurements, glucose, lipids, and inflammatory markers, thereby reducing cardiovascular risk.

Abstract The use of botanical insecticides has increased in recent years due to the demand for effective products, particularly against insects resistant to conventional insecticides. Among these is Aedes aegypti, a well-adapted mosquito to urban environments that opportunistically feeds on humans and animals, contributing to the spread of virus. We evaluated the potential of essential oils (EOs) extracted from Eucalyptus citriodora, Eucalyptus staigeriana, Eucalyptus caryophyllus, and Mentha arvensis in terms of their larvicidal activity against Ae. aegypti. EOs’ compounds were determined using gas chromatography-mass spectrometry (GC-MS). Bioassays were performed on third instar larvae of Ae. aegypti to evaluate the larvicidal effects of EO dilutions in dimethyl sulfoxide (DMSO) at different concentrations. Mortality rates were observed over a 72-hour period to determine the efficacy of the treatments. Citronellal (86.64) predominated in E. citriodora, limonene in E. staigeriana (41.68), eugenol in E. caryophyllus (87.76), and menthol in M. arvensis (51.53%). EOs exhibited larvicidal activity from 10 ppm, with notable efficacy at 85 ppm, in which those from E. staigeriana and M. arvensis caused maximum mortality to Ae. aegypti larvae. Results revealed distinct efficacy patterns among EOs, with E. staigeriana displaying high toxicity within 24 h, achieving LC50 and LC95 values of 47.04 ppm and 97.35 ppm, respectively. Larvicidal effects within 1 h were observed for E. citriodora and E. caryophyllus. This study underscores larvicidal efficacy against Ae. aegypti, notably E. staigeriana, which had the lowest LC50 value. The findings indicate that the tested samples have potential for use as bioinsecticides. Resumo O uso de inseticidas botânicos tem aumentado nos últimos anos devido à demanda por produtos eficazes, especialmente contra insetos resistentes aos inseticidas convencionais. Entre eles está o Aedes aegypti, um mosquito bem adaptado a ambientes urbanos que se alimenta oportunisticamente de humanos e animais, contribuindo para dispersão de vírus. Avaliamos o potencial de óleos essenciais (OEs) extraídos de Eucalyptus citriodora, Eucalyptus staigeriana, Eucalyptus caryophyllus e Mentha arvensis em relação à sua atividade larvicida contra Ae. aegypti. Os compostos dos OEs foram determinados usando cromatografia gasosa acoplada à espectrometria de massa (GC-MS). Os bioensaios foram realizados em larvas de terceiro instar de Ae. aegypti para avaliar os efeitos larvicidas das diluições de OE em dimetil sulfóxido (DMSO) em diferentes concentrações. As taxas de mortalidade foram observadas ao longo de 72 horas para determinar a eficácia dos tratamentos. O componente citronelal (86,64) predominou em E. citriodora, limoneno em E. staigeriana (41,68), eugenol em E. caryophyllus (87,76) e mentol em M. arvensis (50,73%). Os OEs exibiram atividade larvicida a partir de 10 ppm, com grande eficácia a 85 ppm, onde os de E. staigeriana e M. arvensis causaram mortalidade máxima de larvas de Ae. aegypti. Os resultados revelaram padrões de eficácia distintos entre os OEs, com E. staigeriana exibindo maior toxicidade dentro de 24 horas, alcançando valores de CL50 e CL95 de 47,04 ppm e 97,35 ppm, respectivamente. Efeitos larvicidas dentro de 1 hora foram observados para E. citriodora e E. caryophyllus. Este estudo destaca a eficácia larvicida contra Ae. aegypti, especialmente E. staigeriana, que teve o menor valor de CL50. Concluímos que esses OEs são potencialmente larvicidas para o controle eficaz de Ae. aegypti.

Protective adaptive immunity to Zika virus (ZIKV) has been mainly attributed to cytotoxic CD8 + T cells and neutralizing antibodies, while the participation of CD4 + T cells in resistance has remained largely uncharacterized. Here, we show a neutralizing antibody response, dependent on CD4 + T cells and IFNγ signaling, which we detected during the first week of infection and is associated with reduced viral load in the brain, prevention of rapid disease onset and survival. We demonstrate participation of these components in the resistance to ZIKV during primary infection and in murine adoptive transfer models of heterologous ZIKV infection in a background of IFNR deficiency. The protective effect of adoptively transferred CD4 + T cells requires IFNγ signaling, CD8 + T cells and B lymphocytes in recipient mice. Together, this indicates the importance of CD4 + T cell responses in future vaccine design for ZIKV. Characterization of protective immunity to Zika virus has largely focussed on CD8 + T cells and antibody-mediated protection. Here the authors show roles for CD4 + T cells and the associated IFNγ signaling in antibody-mediated resistance to Zika virus infection.