The most common complication of active brucellosis in humans is osteoarticular injury. In the bone marrow microenvironment, mesenchymal stem cells (MSCs) can differentiate into either adipocytes or osteoblasts, and this balance is tightly regulated because an increase in adipogenesis may negatively affect bone formation and favor bone loss. The differentiation of MSCs into adipocytes or osteoblasts is tightly regulated by mechanisms that promote cell fate toward one lineage while repressing the other. Our study demonstrated that Brucella abortus infects MSCs but does not affect the deposition of organic and mineral matrix during osteoblast differentiation. However, the infection upregulates Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL) expression in osteoblasts, which may contribute to osteoclast activation and bone resorption. Conversely, B. abortus infection significantly influences adipocyte differentiation by modulating lipolysis, lipogenesis, and interactions between lipid droplets and mitochondria. This leads to increased cellular cholesterol levels and reduced intracellular triglycerides, accompanied by glycerol release. These changes result in more differentiated adipocytes and larger lipid droplets. Consequently, we observed increased IL-6 secretion and a higher leptin/adiponectin ratio. Importantly, these effects were independent of a functional type IV secretion system (T4SS), as purified Brucella DNA fully reproduced the adipogenic phenotype. Moreover, inhibition of TLR9-the primary sensor of bacterial DNA-significantly reduced the DNA-induced adipogenic response, demonstrating that adipocyte modulation is at least in part mediated through TLR9 signaling. In summary, B. abortus promotes MSC differentiation toward an inflammatory adipocyte phenotype. It involves a TLR-9-mediated DNA detection. It may contribute to osteoarticular injury and infection-associated bone resorption.
Canine overweight and obesity mirrors human trends, emphasizing a One Health perspective. This prospective study evaluated haematological, biochemical and urinary parameters, alongside systolic blood pressure (SBP), in client-owned dogs: normal-weight (NW, n = 10), overweight (OW, n = 10) and obese (OB, n = 10). Overweight and obese dogs followed a 150-day caloric restriction programme (high-protein, high-fibre, low-energy) with biweekly veterinary follow-up. At baseline, triglycerides were significantly higher in OB (126.6 mg/dL) compared to controls (57.6 mg/dL; p < 0.05). While serum total protein, globulin, C-reactive protein and calcium were significantly higher in OB (p < 0.05), mean values remained within clinical reference intervals. Baseline SBP in OB (191.3 mmHg) was significantly higher (p < 0.05) than in NW. Post-intervention, mean weight loss reached 9.43% (OW) and 9.83% (OB). Success in achieving ideal body condition was higher in OW (87.5%) than OB (30%) (p < 0.05). In obese group, hypertriglyceridaemia normalised (126.6 to 78.4 mg/dl; p < 0.01) and SBP significantly decreased (191.3 to 174 mmHg; p < 0.05). Programme success strongly correlated with improved physical activity (p < 0.05) and quality of life (p < 0.01). These findings confirm that canine obesity induces metabolic and inflammatory dysregulation, even in apparently healthy dogs. Results demonstrate that structured nutritional programmes can significantly mitigate these alterations, although certain inflammatory markers, like C-reactive protein, may not fully reach control levels within the study timeframe. Notably, clinically relevant improvements occurred before achieving ideal body condition, highlighting the efficacy of early intervention and sustained veterinary-owner engagement in weight management strategies.
The interaction of large, membrane-bound vesicles leads to the development of extended diaphragms that act as intermediates in the fusion process. Such hemifusion diaphragms confined inside a stiffer container may disassemble through energetically distinct rim-pore expansion modes (radial or lateral), and the preferred mode depends on diaphragm size and lipid reabsorption costs. We propose a theoretical model based on constrained-wetting physics to explain why large hemifusion diaphragms favor lateral rim-pore propagation while small hemifusion diaphragms prefer radial growth. We combine coarse-grained unbiased molecular dynamics of confined vesicle-in-vesicle systems in the μs-scale, with an analytical geometrical model derived from interface wetting. Energies include line tensions for membrane building blocks (edges, arcs and Y-junctions), diaphragm lateral tension, and a lipid reabsorption term accounting for area transfer and flip-flop controlled stress-asymmetry. Simulation observables (rim-pore area, arc/edge/Y-junction lengths and contact angles) are directly compared to model predictions. The wetting-inspired energy model predicts two regimes. For large hemifusion diaphragms lateral propagation minimizes both edge length and reabsorption costs and therefore is energetically preferred, producing rapid lateral expansion and micelle formation via a final fission. For small hemifusion diaphragms radial propagation is favored, producing slow bleb reabsorption without fragment excision. Independent unbiased trajectory replicas (n=10 per regime) reproduce these predictions quantitatively (rim-pore area, contact angles, expansion timescales). Results unify geometric and wetting analogies with numerical simulation evidence, and reveal a mechanistic pathway for selective fast or slow hemifusion diaphragm disassembly with implications for controlled membrane self-reorganization under spatial confinement.
Congenital anomalies (CA) can be detected prenatally through imaging and specialized procedures. On December 30, 2020, Argentina passed the Termination of pregnancy (TOP) law. This study assesses the impact of this legislation on the epidemiological profile of CA, in relation to access to prenatal diagnosis and the practice of legal termination of pregnancy due to fetal anomalies. A before-and-after study design was used, comparing two three-year periods: 2015–2017 and 2021–2023, using data from the National Network of Congenital Anomalies of Argentina (RENAC). A survey was also conducted among obstetric and prenatal diagnosis professionals from 70 maternity hospitals. In the second period, a significant decrease was observed in the prevalence of anencephaly, hydrocephalus, Down syndrome, and disruptive anomalies. The percentage of hospitals performing prenatal procedures (nuchal translucency measurement, first trimester screening, detailed ultrasound, and karyotyping) increased. While 51% of the institutions reported performing legal terminations in the first trimester for fetal anomalies in the first period, this rose to 87.1% in the second. The decline in major nervous system anomalies is likely associated with greater access to prenatal screening and legal terminations. The decrease in Down syndrome prevalence, despite rising maternal age, may reflect improved prenatal detection and access to TOP. The reduction in disruptive anomalies may be related to a decrease in unsafe, clandestine abortions following the legalization of TOP.
Oropouche virus (OROV) is an arbovirus that has caused multiple epidemic outbreaks in several Latin American countries. In 2024, cases of possible vertical transmission with congenital microcephaly were reported, raising concerns about potential teratogenic effects. However, the causal relationship between OROV infection during pregnancy and congenital anomalies remains poorly defined. This study aimed to analyze the evidence on the potential teratogenic effect of OROV in humans through a systematic literature review, applying Shepard's criteria for causality. The available evidence supports a temporal relationship between exposure during critical periods of prenatal development and observed effects in offspring. Reported cases share certain common characteristics that could suggest a specific syndrome. Experimental studies in animal models demonstrate vertical transmission of OROV and harmful effects in offspring. Considering the documented vertical transmission, viral presence in the central nervous system, and known pathogenic mechanisms, biological plausibility exists for a teratogenic effect. However, no epidemiological study has yet evaluated the association between OROV infection and teratogenicity. Furthermore, given that infection occurs during epidemic outbreaks rather than through sporadic environmental exposure, the criterion of infrequent exposure associated with an infrequent defect is not met. Therefore, Shepard's teratogenicity criteria are not yet fully fulfilled. In conclusion, while suggestive evidence exists, definitive proof of OROV teratogenicity remains lacking. Health authorities should prioritize research initiatives, strengthen epidemiological surveillance groups, ensure availability of serological testing for OROV infection, and enhance congenital defect surveillance systems to better characterize this potential association.
The development of biomimetic scaffolds from decellularized porcine reproductive tissues represents a promising approach to addressing challenges in reproductive medicine, with high translational potential. However, most available protocols are based on tissues from prepubertal animals because they are more uniform and are not influenced by estrous-cycle fluctuations. These protocols may not be applicable to adult animals due to increased tissue thickness and higher extracellular matrix (ECM) density. Therefore, this study aimed to optimize a detergent-based decellularization protocol to generate decellularized scaffolds from oviducts and uteri of cyclic sows. To this end, oviductal and uterine tissues from adult females in the early follicular stage were subjected to two, three, or four cycles of detergent exposure. The resulting scaffolds were subsequently characterized by morphometric and histological analysis, DNA quantification, biomechanical testing, and biocompatibility analysis by co-incubation with porcine spermatozoa. Histological results showed acellular scaffolds from the second decellularization cycle. However, DNA quantification showed significantly lower levels after four decellularization cycles. The protocol well preserved ECM components, such as collagen and elastin, while a decrease in glycosaminoglycans was observed independent of the number of cycles. Biomechanical properties were preserved in the oviduct, with no changes observed, whereas uterine decellularization resulted in a decrease in deformation capacity. Biocompatibility assays demonstrated that the generated scaffolds were cytocompatible, largely preserving sperm viability and motility. In conclusion, reproductive tissues of adult animals benefit from increased exposure to detergents, as this ensures greater DNA removal without compromising the integrity of the ECM or the cytocompatibility of the scaffolds.
Secretory vesicles discharge their contents into the extracellular space through fusion pores; the behaviour of these structures regulates release kinetics. In sperm, acrosomal contents are released after the expansion of multiple pores formed when the plasma and acrosomal membranes fuse. Alpha-synuclein is required after pore opening during the human sperm acrosome reaction (AR). Here, we investigated its role in AR kinetics, specifically in pore expansion. We introduced cell-penetrating His6-TAT-alpha-synuclein into human sperm and monitored progesterone-induced AR by time-lapse fluorescence microscopy using an anti-CD46 antibody. Fluorescence traces from individual cells revealed that the AR follows a sigmoidal profile with a steeper slope in cells exposed to His6-TAT-alpha-synuclein plus progesterone than in progesterone-only controls. This acceleration was most pronounced in the later phase of the curves, which suggests that alpha-synuclein enhances pore dilation. It is generally assumed that pore expansion proceeds immediately after opening without modulation; our results challenge this view. Thus, the contribution of this study to the sperm biology field is that pore dilation is regulated. Its contribution to the cell biology field is to provide new insight into the physiological role of alpha-synuclein beyond the nervous system and to raise the possibility of its conserved function across different cell types.
The structural and electrophysiological stability of the adult heart depends on coordinated transcriptional repression governed by chromatin remodeling and nuclear architecture. The Chd4/NuRD complex is essential to maintain cardiomyocyte identity, and its deletion leads to arrhythmias, aberrant expression of skeletal muscle sarcomeric genes, and dysregulation of key components of the cardiac conduction system, including Hcn4, Cntn2, and Cx40. However, while the mechanisms by which Chd4 cooperates with additional transcriptional regulators to preserve adult cardiac homeostasis remain poorly understood, previous studies have identified ThPOK, a lamina-associated transcription factor, as a candidate Chd4 partner in cardiomyocytes. Using cardiomyocyte-specific conditional mouse models, we show that combined loss of Chd4 and ThPOK markedly exacerbates conduction defects, leading to more severe arrhythmias and accelerated sudden cardiac death compared with Chd4 loss alone. Transcriptomic profiling revealed a synergistic upregulation of Sprr1a, a protein normally expressed in the epidermis where it contributes to keratinocyte differentiation and cornification. Sprr1a induction correlated with downregulation of the cardioprotective microRNA miR-150-5p, a change driven by Chd4 deletion; however, miR-150-5p levels were not further reduced in double-knockout hearts, indicating that ThPOK contributes to Sprr1a de-repression through a distinct mechanism. Notably, Sprr1a upregulation was also observed in Lmna mutant hearts, suggesting a link between its de-repression and cardiac-specific nuclear lamina dysfunction. Together, these findings uncover a cooperative Chd4;ThPOK regulatory axis that preserves transcriptional integrity and safeguards structural and electrical homeostasis in the adult murine heart.
South American camelids are domestic species native to the Andean region and display distinctive reproductive features relevant to their productive management. Although embryo transfer has been adopted as a genetic improvement tool, important knowledge gaps persist regarding embryo quality assessment and early embryonic morphophysiology. This study aimed to describe morphometric characteristics, steroidogenic capacity, and the presence of primordial germ cells in preimplantation llama embryos. Sixteen adult females were superovulated with 650 IU equine chorionic gonadotropin (eCG) and used as embryo donors. Embryos were recovered non-surgically on days 7, 8, and 10 post-mating, yielding a total of 32 embryos. Sixteen embryos were processed for histological and immunohistochemical analyses. Embryos were photographed, analyzed using ImageJ-FIJI®, and classified according to shape and size as spherical, irregular, elongated, or filamentous. Histological sections were stained with haematoxylin-eosin and periodic acid-Schiff, and embryo dimensions and trophoblastic wall thickness were recorded. Immunohistochemical detection of P450 aromatase and DDX4 was performed. Day 7 embryos were spherical or irregular, day 8 embryos exhibited spherical, irregular, and elongated forms, and day 10 embryos were exclusively filamentous. All embryos were hatched blastocysts lacking the zona pellucida. Mean embryo diameter increased markedly with developmental stage. Aromatase immunoexpression intensified with development and was localized to trophoblastic cells, whereas DDX4-positive cells were detected within the inner cell mass. These findings provide novel insights into early llama blastocyst biology and support the development of objective embryo evaluation criteria in South American camelids.
Alzheimer's disease (AD) is a complex disorder involving multiple cellular and molecular mechanisms. Recent evidence suggests that metabolic alterations play a crucial role in AD progression. Likewise, diabetes and obesity-two major metabolic diseases-are well-established risk factors for AD. These conditions are associated with a significant expansion of white adipose tissue (WAT). Here, we hypothesize that visceral WAT may act as a key mediator between peripheral metabolic dysfunction and brain illnesses. Immunohistochemistry and biochemical approaches were used to evaluate the WAT from WT and db/db mice. Similar techniques were applied to examine the brain tissue of 3xTg-AD mice that received white epididymal fat pads from WT or db/db donors and determine the impact of adipose tissue transplantation on tau and Aβ pathology. Our study revealed that recipient 3xTg-AD mice that received db/db fat pads developed profound changes in tau pathology due to increased expression of the cyclin-dependent kinase 5 activator p25 compared with 3xTg-AD mice that received fad pads from WT or sham mice. This increment in p25/cdk5 was associated with a prominent inflammatory response induced by the WAT transplant. Moreover, the opposite effect on Aβ pathology was found. The reduction in Aβ levels was correlated with an increase in microglial phagocytic capacity. Overall, our study demonstrated a novel crosstalk between AD and metabolic disorders through white adipose signaling resulting in differential effects on tau and Aβ pathology mediated by an activated immune response.
Prenatal alcohol exposure (PAE) is a major early-life stressor associated with long-lasting neurodevelopmental and neurocognitive alterations. Increasing evidence from human studies indicates that PAE leaves persistent molecular signatures that can be detected in the placenta and in clinically accessible biological fluids. This Mini Review summarizes recent advances in the identification of epigenetic, immune, endocrine, and RNA-based biomarkers measured in placental tissue, umbilical cord blood, and peripheral fluids, and their associations with neurodevelopmental outcomes. We highlight convergent findings across heterogeneous study designs, discuss current methodological challenges and research gaps, and consider future directions toward integrative and longitudinal biomarker approaches. Together, the reviewed evidence supports the potential of placental and circulating biomarkers to improve early risk stratification and to advance understanding of neurodevelopmental alterations following PAE.
The renin-angiotensin system (RAS) contributes to inflammatory and neuropathic pain, but whether its primary receptors, AT1R and AT2R, regulate the K2P channel TWIK1 in sensory neurons remains unknown. We investigated whether Ang-II receptors modulate TWIK1 expression and whether this pathway influences neuropathic pain. Adult female rats underwent chronic constriction injury (CCI) of the sciatic nerve and received continuous subcutaneous administration of vehicle, telmisartan (AT1R antagonist), PD123319 (AT2R antagonist), or their combination for 14 days. TWIK1, AT1R, and AT2R expression were analyzed in dorsal root ganglia (DRG) by immunohistochemistry and RT-qPCR. Behavioral outcomes included spontaneous foot lifting, cold allodynia, and mechanical hypersensitivity. Plasma cytokines were quantified by ELISA. Satellite glial cell (SGC) activation was assessed via GFAP immunoreactivity. In vitro DRG cultures were exposed to inflammatory stimuli to evaluate TWIK1 transcriptional regulation. CCI reduced TWIK1 expression in DRG neurons, accompanied by dynamic regulation of AT1R and AT2R. Pharmacological blockade, particularly combined receptor inhibition, restored or increased TWIK1 expression, attenuated mechanical and cold hypersensitivity, reduced circulating pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and decreased SGC activation. Inflammatory stimulation in vitro reduced TWIK1 mRNA, supporting cytokine-mediated regulation. AT1R and AT2R regulate TWIK1 expression in sensory neurons through an integrated mechanism involving inflammatory signaling and glial activation. Dual receptor blockade produces the most consistent molecular and behavioral effects, supporting RAS modulation as a potential strategy for neuropathic pain management.
Feeding transcends mere nourishment by integrating social and cultural factors. The foods we consume hold significant economic and social relevance within territories and are rich in bioactive compounds that confer health benefits. In the context of an aging population and increased life expectancy, functional foods represent a healthy alternative for Chilean women. Evidence among Chilean women suggests that incorporating functional foods into the diet, alongside modifying behaviors and risk factors such as the desynchronization of biological rhythms, can aid in preventing non-communicable chronic diseases such as obesity, diabetes, and hypertension. This review examines the potential beneficial effects that locally sourced functional foods may have on the health of Chilean women during critical life stages, including pregnancy, the climacteric, and advanced adulthood. A healthy diet incorporating functional foods commonly consumed in Chile, particularly those endemic to the country, could contribute to improved women's health across key stages of the life course, reduce obesity rates, and exert both short- and long-term effects on the prevalence of diseases affecting older women, mothers, and their offspring.
Metabolic syndrome (MetS) and periodontal disease (PD) are prevalent inflammatory conditions with global health implications. Their bidirectional interaction amplifies systemic and metabolic inflammation, worsening periodontal destruction while PD exacerbates metabolic disturbances. This study evaluates the combined impact of MetS and PD on periodontal and hepatic health and examines melatonin (MEL) as a therapeutic agent. Male Wistar rats were assigned to Control, MetS, PD, MetS + PD, and MetS + PD + MEL groups. MetS was induced with 10% fructose intake for 35 days and PD by ligature placement for 4 days. MEL (10 mg/kg) was administered to assess its anti-inflammatory effects. Body weight, glycemia, lipid profile, and liver enzymes were measured. Radiographic and histomorphometric analyses were performed on the jaw, and NLRP3 and IL-10 expression assessed by immunohistochemistry in jaw and liver. MetS + PD animals showed aggravated hyperglycemia, dyslipidemia, hepatic injury, and severe periodontal destruction, with increased NLRP3 and reduced IL-10 levels. MEL attenuated these alterations, improving metabolic outcomes, preserving periodontal bone, restoring hepatic histology and enzyme levels, and modulating inflammation by decreasing NLRP3 and increasing IL-10. These findings indicate that MetS and PD synergistically intensify inflammatory and metabolic disturbances, and that MEL counteracts this exacerbated inflammatory burden, emerging as a promising adjunct therapeutic candidate for systemic-oral inflammatory conditions. KEY MESSAGES: Metabolic syndrome and periodontitis synergistically exacerbate liver and periodontal damage. Melatonin mitigates these combined metabolic and inflammatory alterations. Melatonin protective effect is associated with reduced NLRP3 activation and restored IL-10 expression.
Nerve growth factor (NGF) is a member of the neurotrophin family, essential for neuronal survival and phenotypic maintenance. However, in vitro, its function can be disrupted by oxidative posttranslational modifications such as tyrosine nitration. Nitrated NGF (NO2NGF) has been shown to have a gain-of-toxic, pro-apoptotic, activity in motoneuron cultures. Herein, we report the generation and characterization of monoclonal antibodies (mAbs) that specifically recognize NO2NGF to unravel its formation in vivo. Using hybridoma technology, we produced mAbs with high affinity and selectivity for NO2NGF, as demonstrated immunochemically and by surface plasmon resonance. The antibodies elicit neutralizing capacity to NO2NGF in neuronal cells. Nitrated Tyr52 within the NGF48-58 sequence was identified as the primary antigenic determinant by crystallographic analysis of antibody:peptide complexes at atomic resolution, peptide-based epitope mapping and molecular dynamics simulations, whereas local sequence NGF motifs around the nitrated tyrosine are important for protein specificity. The antibodies revealed NO2NGF accumulation in amyotrophic lateral sclerosis (ALS) rodent models and human subjects. Indeed, immunofluorescence showed selective accumulation of NO2NGF in spinal cord regions undergoing motor neuron degeneration, as well as in sciatic nerves and neuromuscular junctions. Our findings establish NGF nitration as an oxidative hallmark in ALS and demonstrate that monoclonal antibodies targeting this chemical modification are powerful tools for both mechanistic studies and biomarkers development. This work proposes a link between neurotrophin nitration and neurodegenerative disease progression and opens avenues for therapeutic exploration along the peroxynitrite-tyrosine nitration pathway.
We recently demonstrated that the human pathogen Acinetobacter baumannii exhibits light-regulated daily and circadian rhythms, suggesting that the physiological state of the bacterium varies along the day. Because this temporal dimension may influence host-pathogen interactions, we investigated here whether key bacterial processes relevant to pathogenesis fluctuate according to light-dark-induced rhythms and whether these fluctuations impact infection outcome. In particular, β-lactamase activity displayed significant daily variation in several multidrug-resistant strains, with higher activity at the end of the light phase compared to the dark phase, in light-dark entrained cultures. Consistent with these findings, macrocolony ring formation also followed a rhythmic pattern. In addition, we show that both prior bacterial entrainment and the time of infection critically determine disease progression in a murine skin-wound infection model. Specifically, higher bacterial titers were recovered when light-dark entrained bacteria infected mice at the end of the dark phase (morning) with respect to infections caused by arrhythmic bacteria, while the opposite occurred in the evening. Together, these results demonstrate that A. baumannii displays diurnal regulation of physiological and pathogenic traits that influence infection dynamics and antibiotic-inactivating activity, introducing a new temporal dimension to bacterial pathogenesis with important implications for understanding disease progression and treatment strategies.
The Neotropical Nannopterum brasilianus is a piscivorous bird feeding on aquatic organisms, can ingest various infectious forms of helminths, such as those from the phylum Acanthocephala. In their adult stage, these parasites attach to the intestinal mucosa of their definitive hosts, causing varying degrees of tissue damage. Between 2020 and 2023, 35 individuals of N. brasilianus were analyzed, and 20 of them (57.1%) presented acanthocephalan infection. Morphological and histopathological analyses identified the species as Southwellina hispida, we described the tissue alterations associated with its presence in detail. The results contribute to the taxonomic knowledge of the parasite and provide important information for diagnosing and monitoring of infections in birds housed at Wildlife Triage and Rehabilitation Centers (WTRC). Nannopterum brasilianus, uma ave piscívora neotropical que se alimenta de organismos aquáticos, pode ingerir diversas formas infecciosas de helmintos, como os do filo Acanthocephala. Em sua fase adulta, esses parasitas se fixam à mucosa intestinal de seus hospedeiros definitivos, causando diferentes graus de danos aos tecidos. A caracterização microscópica dessas lesões tem sido realizada por meio de análises histopatológicas. Entre os anos de 2020 e 2023, foram analisados 35 indivíduos de N. brasilianus, dos quais 20 (57.1%) apresentaram infecção por acantocéfalos. A partir de análises morfológicas e histopatológicas, foi possível identificar a espécie Southwellina hispida, além de descrever detalhadamente as alterações teciduais associadas à sua presença. Os resultados obtidos contribuem para o conhecimento da taxonomia do parasito e oferecem subsídios importantes para diagnóstico e o monitoramento de infecções em aves acolhidas por Centros de Triagem e Reabilitação de Animais Silvestres (CETRAS).
The molecular behavior of viruses within respiratory aerosols plays a critical role in airborne disease transmission yet remains largely inaccessible to experimental characterization. Here, we use a billion-atom all-atom molecular dynamics simulation of a virus-laden respiratory aerosol to uncover how respiratory proteins, lipids, ions, and water collectively assemble around SARS-CoV-2, giving rise to structured microenvironments that influence viral stability and spike dynamics. We find that respiratory components rapidly evolve into heterogeneous networks characterized by protein-rich aggregates, patchy lipid assemblies, and spatially structured ion and water dynamics. These features create distinct microenvironments that constrain molecular transport and stabilize regions surrounding the virion. Within this crowded aerosol context, we observe sustained and selective interactions between aerosol components and the viral spike protein, including preferential recruitment of surfactant lipids and persistent coordination by divalent cations. These interactions modulate spike conformational dynamics, enhancing domain breathing motions and flexibility at key hinge regions while preserving a stable membrane anchor. Together, these observations reveal a condensate-like physical regime in which multivalent aerosol components coalesce into a soft, heterogeneous matrix that selectively modulates viral protein dynamics under extreme crowding. By framing virus-laden respiratory aerosols within this physical context, this work establishes an in situ molecular framework for understanding how aerosols influence viral persistence and offers a platform for exploring mechanisms relevant to airborne disease transmission and mitigation strategies.
The bacterial-like identity of membranes in modern eukaryotes and the formation and disassembly of large hemifusion diaphragms during organelle fusion, remain unresolved problems in cell biology. In this forum, we comment on a noncanonical fusion pathway, supported by molecular simulations, which offers a unified physicochemical framework to rationalize these phenomena.
The calcaneonavicular ligament (spring ligament) plays a fundamental role in calcaneonavicular static stability and medial longitudinal arch, injury which is related to flatfoot. The primary objective was to compare the biomechanical behaviour of the spring ligament in a healthy foot and after section and repair with augmentation and transfer of the flexor digitorum longus (FDL). As secondary objectives we have the biomechanical comparison between isolated repair with augmentation associated or not with transfer. This experimental biomechanical cadaver study evaluates the medial complex in four phases: intact ankle (1); spring injury (2); repair and augmentation (3), and after FDL transfer (4). Talonavicular angular displacement was measured in the three planes of space using an arthrometer and manual spring ligament exploration manoeuvres. Significant differences were found after sectioning the ligament with the abduction and external rotation manoeuvre in the coronal (p=.050) and sagittal (p=.045) planes. Upon augmentation, there was significance in the horizontal plane (p=.047) and after FDL transfer in the horizontal plane (p=.002). However, no significant differences were identified between repair and augmentation and FDL transfer. Ligament section generated instability in the coronal and sagittal plane with abduction and external rotation movements. It should be noted that both surgical techniques were able to restore joint stability, even surpassing that achieved with the ligament intact.