Search

Emotional false memories are the erroneous recollection of events accompanied by an emotional experience. In high-risk domains like psychotherapy and the legal system, emotional false memories are of particular importance. Despite the systematic research conducted on emotional false memories in recent years, findings remain contradictory. Some studies have suggested that negative emotion reduces false memories, while others have suggested that negative emotion increases false memories. Research has mainly employed words and pictures as experimental stimuli, and studies using both types of memory stimuli are reviewed here. From this examination, it emerged that the main reasons for contradictory findings are as follows: (1) different materials have varying effects on inducing false memories, with pictures demonstrating a memory advantage compared to words; (2) recall and recognition tests have been used interchangeably, leading to different false-memory effects depending on the memory test employed; and (3) different studies have adopted different levels of control over valence and arousal when manipulating emotional variables. Future studies should distinguish between the use of different memory materials, examine specific differences in recall and recognition tests, and measure the impact of specific emotions on false memory beyond the dimensions of valence and arousal. [ABSTRACT FROM AUTHOR]

Background: Arg-gingipain A (RgpA) is the primary virulence factor of Porphyromonas gingivalis and contains hemagglutinin adhesin (HA), which helps bacteria adhere to cells and proteins. Hemagglutinin's functional domains include cleaved adhesin (CA), which acts as a hemagglutination and hemoglobin-binding actor. Here, we confirmed that the HA and CA genes are immunogenic, and using adjuvant chemokine to target dendritic cells (DCs) enhanced protective autoimmunity against P. gingivalis-induced periodontal disease., Methods: C57 mice were immunized prophylactically with pVAX1-CA, pVAX1-HA, pVAX1, and phosphate-buffered saline (PBS) through intramuscular injection every 2 weeks for a total of three administrations before P. gingivalis-induced periodontitis. The DCs were analyzed using flow cytometry and ribonucleic acid sequencing (RNA-seq) transcriptomic assays following transfection with CA lentivirus. The efficacy of the co-delivered molecular adjuvant CA DNA vaccine was evaluated in vivo using flow cytometry, immunofluorescence techniques, and micro-computed tomography., Results: After the immunization, both the pVAX1-CA and pVAX1-HA groups exhibited significantly elevated P. gingivalis-specific IgG and IgG1, as well as a reduction in bone loss around periodontitis-affected teeth, compared to the pVAX1 and PBS groups (p < 0.05). The expression of CA promoted the secretion of HLA, CD86, CD83, and DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) in DCs. Furthermore, the RNA-seq analysis revealed a significant increase in the chemokine (C-C motif) ligand 19 (p < 0.05). A notable elevation in the quantities of DCs co-labeled with CD11c and major histocompatibility complex class II, along with an increase in interferon-gamma (IFN-γ) cells, was observed in the inguinal lymph nodes of mice subjected to CCL19-CA immunization. This outcome effectively illustrated the preservation of peri-implant bone mass in rats afflicted with P. gingivalis-induced peri-implantitis (p < 0.05)., Conclusions: The co-administration of a CCL19-conjugated CA DNA vaccine holds promise as an innovative and targeted immunization strategy against P. gingivalis-induced periodontitis and peri-implantitis., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Aquaporin-0 (AQP0) is the main water channel in the mammalian lens and is involved in accommodation and maintaining lens transparency. AQP0 binds the Ca2+-sensing protein calmodulin (CaM) and this interaction is believed to gate its water permeability by closing the water-conducting pore. Here, we express recombinant and functional human AQP0 in Pichia pastoris and investigate how phosphorylation affects the interaction with CaM in vitro as well as the CaM-dependent water permeability of AQP0 in proteoliposomes. Using microscale thermophoresis and surface plasmon resonance technology we show that the introduction of the single phospho-mimicking mutations S229D and S235D in AQP0 reduces CaM binding. In contrast, CaM interacts with S231D with similar affinity as wild type, but in a different manner. Permeability studies of wild-type AQP0 showed that the water conductance was significantly reduced by CaM in a Ca2+-dependent manner, whereas AQP0 S229D, S231D and S235D were all locked in an open state, insensitive to CaM. We propose a model in which phosphorylation of AQP0 control CaMmediated gating in two different ways (1) phosphorylation of S229 or S235 abolishes binding (the pore remains open) and (2) phosphorylation of S231 results in CaM binding without causing pore closure, the functional role of which remains to be elucidated. Our results suggest that site-dependent phosphorylation of AQP0 dynamically controls its CaM-mediated gating. Since the level of phosphorylation increases towards the lens inner cortex, AQP0 may become insensitive to CaM-dependent gating along this axis. [ABSTRACT FROM AUTHOR]

Oxidation-reduction (redox) reactions are central to the existence of life. Reactive species of oxygen, nitrogen and sulfur mediate redox control of a wide range of essential cellular processes. Yet, excessive levels of oxidants are associated with ageing and many diseases, including cardiological and neurodegenerative diseases, and cancer. Hence, maintaining the fine-tuned steady-state balance of reactive species production and removal is essential. Here, we discuss new insights into the dynamic maintenance of redox homeostasis (that is, redox homeodynamics) and the principles underlying biological redox organization, termed the 'redox code'. We survey how redox changes result in stress responses by hormesis mechanisms, and how the lifelong cumulative exposure to environmental agents, termed the 'exposome', is communicated to cells through redox signals. Better understanding of the molecular and cellular basis of redox biology will guide novel redox medicine approaches aimed at preventing and treating diseases associated with disturbed redox regulation., (© 2024. Springer Nature Limited.)

Background: Porphyromonas gingivalis (P. gingivalis), a major pathogen of periodontitis, can evade host immune defenses. Previously, we found that P. gingivalis W83 sialidase gene mutant strain (ΔPG0352) was more easily cleared by macrophages. The aims of this study were to investigate the effects of sialidase in P. gingivalis on the polarization, antigen presentation, and phagocytosis of infected macrophages and to clarify the mechanism of P. gingivalis immune evasion. Methods: Human monocytes U937 were differentiated to macrophages and infected with P. gingivalis W83, ΔPG0352, com ΔPG0352, and Escherichia coli (E. coli). The phagocytosis of macrophages was observed by transmission electron microscopy and flow cytometry. ELISA or Griess reaction were used to examine the levels of interleukin-12 (IL-12), inducible nitric oxide synthase (iNOS) and interleukin-10 (IL-10), and the expressions of CD68, CD80 and CD206 were determined by flow cytometry. The expression of major histocompatibility complex-II (MHC-II) was detected by immunofluorescence. A rat periodontitis model was established to determine the M1 and M2 polarization of macrophages. Results: Compare with P. gingivalis W83, ΔPG0352 increased the levels of IL-12, iNOS, CD80, and MHC-II and inhibited the levels of IL-10 and CD206. Macrophages phagocytosed 75.4% of ΔPG0352 and 59.5% of P. gingivalis W83. In the rat periodontitis model, the levels of M1 and M2 macrophages in P. gingivalis W83 group were both higher than those in ΔPG0352 group, while the ratio of M1/M2 was higher in the ΔPG0352 group. Alveolar bone absorption was lower in ΔPG0352 group. Conclusion: Sialidase facilitates P. gingivalis immune evasion by reducing M1 polarization, antigen presentation, and phagocytosis of infected macrophages. [ABSTRACT FROM AUTHOR]

Objectives: Intrinsic apoptosis, which is regulated by Bcl‐2 family proteins, has an important role in chronic inflammatory diseases. The aim of the study was to identify the tissue levels and ratios of anti‐ and pro‐apoptotic Bcl‐2 family proteins in peri‐implant diseases. Materials and Methods: Twenty‐three individuals with peri‐implant mucositis, 25 individuals with peri‐implantitis, and 24 controls were included. The following clinical parameters were recorded: keratinized mucosa width, modified bleeding index, probing depth, modified plaque index, modified gingival index, and keratinized tissue thickness. Marginal alveolar bone assessments were performed by a software program. Granulation tissues were collected during treatments of peri‐implant diseases. The control tissue samples were collected during the second stage of implant surgery. The tissue levels of Bcl‐2 family pro‐apoptotic (Bak, Bax, active caspase‐3) and anti‐apoptotic (Bcl‐2, Bcl‐xL, Mcl‐1) proteins were determined by multiplex immunoassay method. Results: The pro‐apoptotic proteins; Bak, Bax and anti‐apoptotic proteins Bcl‐2, Bcl‐xL, Mcl‐1 were detected significantly higher in controls compared with patients with peri‐implant mucositis and peri‐implantitis (p <.001), respectively. The higher active caspase‐3 levels were also detected in controls in comparison with peri‐implant mucositis (p =.018) and peri‐implantitis (p =.005). Anti‐apoptotic: pro‐apoptotic protein ratios (Bcl‐2:Bax, p <.001; Bcl‐2:Bak, p =.01; Bcl‐xL: Bax, p =.006, Bcl‐xL:Bak, p =.011; Mcl‐1:Bak, p <.001) were significantly increased in diseased groups. A positive correlation was demonstrated between clinical variables and anti‐apoptotic: pro‐apoptotic ratios. Conclusion: Our findings indicate dysregulation of the Bcl‐2 family proteins in peri‐implant diseases. This unregulated response may disturb the homeostasis of peri‐implant tissue. [ABSTRACT FROM AUTHOR]

The primary aim of this research was to study the developmental trajectory of oscillatory synchronization in neural networks of normal healthy rats during adolescence, corresponding to the vulnerable age of schizophrenia prodrome in human. To monitor the development of oscillatory networks through adolescence we used a "pseudo-longitudinal" design. Recordings were performed in terminal experiments under urethane anesthesia, every day from PN32 to PN52 using rats-siblings from the same mother, to reduce individual innate differences between subjects. We found that hippocampal theta power decreased and delta power in prefrontal cortex increased through adolescence, indicating that the oscillations in the two different frequency bands follow distinct developmental trajectories to reach the characteristic oscillatory activity found in adults. Perhaps even more importantly, theta rhythm showed age-dependent stabilization toward late adolescence. Furthermore, sex differences was found in both networks, more prominent in the prefrontal cortex compared with hippocampus. Delta increase was stronger in females and theta stabilization was completed earlier in females, in postnatal days PN41-47, while in males it was only completed in late adolescence. Our finding of a protracted maturation of thetagenerating networks in late adolescence is overall consistent with the findings of longitudinal studies in human adolescents, in which oscillatory networks demonstrated a similar pattern of maturation. [ABSTRACT FROM AUTHOR]

Oral hygiene maintenance is important to maintain optimal oral health. Oral health is affected by dysbiotic oral microflora in the dental plaque. Virulent factors of pathogenic organisms, such as gingipain, are responsible for tissue degradation and host tissue invasion in periodontal disease. We sought to investigate the distribution of gingipain genotypes (rgpA and kgp) of P. gingivalis in patients with chronic periodontitis and healthy individuals. The study included individuals positive for P. gingivalis, with 95 samples in the chronic periodontitis (CP) group and 35 samples in the healthy (H) group. We found that kgp-I and kgp-II types were prevalent in 67.36% and 32.64% of the samples in the CP group, respectively. In the H group, kgp-II was highly prevalent (97.14%). The rgpA genotype, type A was found in 78.95% and 82.85% of the samples in the CP and H group, respectively. The mean level of PD and CAL were increased in the presence of kgp-I and decreased in the presence of kgp-II. The mean level of P. gingivalis was increased in the presence of kgp-I and rgpA, type A. Our results show that kgp-I and kgp-II are strongly associated with disease and health condition, respectively. [ABSTRACT FROM AUTHOR]

Methylmercury (MeHg) persists today as a priority public health concern. Mechanisms influencing MeHg metabolism, kinetics, and toxicity outcomes are therefore essential knowledge for informing exposure risks. Evidence points to different toxic potencies of MeHg and inorganic mercury (Hg2+), highlighting the role for biotransformation (demethylation) in regulating MeHg toxicokinetics/dynamics. Whereas microbial MeHg demethylation in the gut is seen to influence elimination kinetics, the potential for systemic demethylation in tissues and target organs to influence MeHg toxicity remains uncertain. To investigate the consequences of systemic MeHg demethylation across development, we engineered transgenic Drosophila to express the bacterial organomercurial lyase enzyme (merB) in a targeted and tissue-specific manner. With all combinations of merB-induced demethylation, ubiquitously (via an actin promoter) or in a tissue-specific manner (ie, gut, muscle, neurons), we observe a rescue of MeHg-induced eclosion failure at the pupal to adult transition. In MeHg-fed larvae with ubiquitous or targeted (gut and muscle) merB expression, we see a significant decrease in MeHg body burden at the pupal stage relative to control flies. We also observe a significant increase in the MeHg elimination rate with merB demethylation induced in adults (control, t 1/2 = 7.2 days; merB flies, t 1/2 = 3.1 days). With neuronal-specific merB expression, we observe a rescue of MeHg-induced eclosion failure without a decrease in Hg body burden, but a redistribution of Hg away from the brain. These results demonstrate the previously unidentified potential for intracellular MeHg demethylation to promote transport and elimination of Hg, and reduce developmental MeHg toxicity. Impact Statement : These findings demonstrate the potential for MeHg demethylation in situ to contribute significantly to the MeHg elimination and distribution kinetics of whole animals and thereby affords a means of protection against the toxic insult of MeHg. Therefore, this study reveals important insight into processes that can determine an individual's resistance or susceptibility to MeHg and provides rationale for therapies targeting a novel metabolism-based pathways to alleviate toxicity risk stemming from MeHg exposure. [ABSTRACT FROM AUTHOR]

Memory updating is an adaptive function that requires people's registry of changes of episodes. However, the research on the role of prior knowledge on memory updating among older adults is scant. We instructed young and older adults to learn two sets of pairs with overlapping scene (A) on Day 1 (A-B) and Day 2 (A-C) and tested the competing memories on Day 3. We further manipulated the schema-congruency between item (B/C) and scene (A). Young adults performed comparatively well in the A-B and A-C memory tests, and showed no difference under different congruency conditions. However, memory updating among older adults was moderated by prior knowledge, with better memory performance in A-C test relative to A-B test when the to-be-updated item C was schema-congruent, however, with poorer memory performance in the A-C test when the to-be-updated item is schema-incongruent. This study advances the understanding that prior knowledge significantly contributes to memory updating among older adults. They would experience retroactive interference when the to-be-updated memories were consistent with their prior knowledge, yet proactive interference when the to-be-updated memories were inconsistent with their prior knowledge. Meanwhile, prior knowledge among young adults does not affect memory updating, given that their memory patterns are consistent across congruency conditions. [ABSTRACT FROM AUTHOR]

The physiological variations during the crustacean molting cycle have intrigued researchers for many years. Maintaining osmotic homeostasis in the face of hemolymph dilution and dealing with dynamic intracellular and extracellular calcium fluctuations are challenges these animals continuously confront. It has recently been shown that water channels present in the cell membrane (aquaporins) are essential for water uptake during premolt and postmolt. This study aims to investigate whether hypoosmotic shock and intracellular and extracellular calcium variations can lead to translocation of Aquaporin 1 (AQP‐1) from the intracellular region to the plasma membrane during premolt and postmolt, thus allowing increased water flow in these stages. For this, we investigate in vitro the rapid change of AQP‐1 positions in the abdominal muscle cells in the freshwater shrimp, Palaemon argentinus. Using cell volume analysis and immunohistochemistry, we show that hypoosmotic conditions and an elevation of the intracellular and extracellular calcium concentrations are concurrent with the translocation of AQP‐1 to the plasma membrane. These results indicate that calcium flux and hypoosmotic shock may be regulators of AQP 1 in the translocation process. [ABSTRACT FROM AUTHOR]

Aquaporin (AQP) water channels are pivotal to renal water handling and therefore in the regulation of body water homeostasis. However, beyond the kidney, AQPs facilitate water reabsorption and secretion in other cells and tissues, including sweat and salivary glands and the gastrointestinal tract. A growing body of evidence has also revealed that AQPs not only facilitate the transport of water but also the transport of several small molecules and gases such as glycerol, H 2 O 2 , ions and CO 2 . Moreover, AQPs are increasingly understood to contribute to various cellular processes, including cellular migration, adhesion and polarity, and to act upstream of several intracellular and intercellular signalling pathways to regulate processes such as cell proliferation, apoptosis and cell invasiveness. Of note, several AQPs are highly expressed in multiple cancers, where their expression can correlate with the spread of cancerous cells to lymph nodes and alter the response of cancers to conventional chemotherapeutics. These data suggest that AQPs have diverse roles in various homeostatic and physiological systems and may be exploited for prognostics and therapeutic interventions., (© 2023. Springer Nature Limited.)

The article presents a study which investigate Aquaporins (AQPs) modulation at heart level of senescence-accelerated prone mice (SAMP8) respect relative controls, senescence accelerated resistant mice (SAMR1). It mentions that AQPs may have significant roles for the development of age-related hypertension and the tendency of cardiac ischemia, underlining their potential therapeutic implication at cardiovascular level.