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BACKGROUND: Synaptic dysfunction, characterized by synapse loss and structural alterations, emerges as a prominent correlate of cognitive decline in Alzheimer's disease (AD). Actin cytoskeleton, which serves as the structural backbone of synaptic architecture, is observed to be lost from synapses in AD. Actin cytoskeleton loss compromises synaptic integrity, affecting glutamatergic receptor levels, neurotransmission, and synaptic strength. Understanding these molecular changes is crucial for developing interventions targeting synaptic dysfunction, potentially mitigating cognitive decline in AD. METHODS: In this study, we investigated the synaptic actin interactome using mass spectrometry in a mouse model of AD, APP/PS1. Our objective was to explore how alterations in synaptic actin dynamics, particularly the interaction between PSD-95 and actin, contribute to synaptic and cognitive impairment in AD. To assess the impact of restoring F-actin levels on synaptic and cognitive functions in APP/PS1 mice, we administered F-actin stabilizing agent, jasplakinolide. Behavioral deficits in the mice were evaluated using the contextual fear conditioning paradigm. We utilized primary neuronal cultures to study the synaptic levels of AMPA and NMDA receptors and the dynamics of PSD-95 actin association. Furthermore, we analyzed postmortem brain tissue samples from subjects with no cognitive impairment (NCI), mild cognitive impairment (MCI), and Alzheimer's dementia (AD) to determine the association between PSD-95 and actin. RESULTS: We found a significant reduction in PSD-95-actin association in synaptosomes from middle-aged APP/PS1 mice compared to wild-type (WT) mice. Treatment with jasplakinolide, an actin stabilizer, reversed deficits in memory recall, restored PSD-95-actin association, and increased synaptic F-actin levels in APP/PS1 mice. Additionally, actin stabilization led to elevated synaptic levels of AMPA and NMDA receptors, enhanced dendritic spine density, suggesting improved neurotransmission and synaptic strength in primary cortical neurons from APP/PS1 mice. Furthermore, analysis of postmortem human tissue with NCI, MCI and AD subjects revealed disrupted PSD-95-actin interactions, underscoring the clinical relevance of our preclinical studies. CONCLUSION: Our study elucidates disrupted PSD-95 actin interactions across different models, highlighting potential therapeutic targets for AD. Stabilizing F-actin restores synaptic integrity and ameliorates cognitive deficits in APP/PS1 mice, suggesting that targeting synaptic actin regulation could be a promising therapeutic strategy to mitigate cognitive decline in AD.

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To ensure the reliability of machining quality, it is crucial to predict tool wear accurately. In this paper, a novel deep learning-based model is proposed, which synthesizes the advantages of power spectral density (PSD), convolutional neural networks (CNN), and vision transformer model (ViT), namely PSD-CVT. PSD maps can provide a comprehensive understanding of the spectral characteristics of the signals. It makes the spectral characteristics more obvious and makes it easy to analyze and compare different signals. CNN focuses on local feature extraction, which can capture local information such as the texture, edge, and shape of the image, while the attention mechanism in ViT can effectively capture the global structure and long-range dependencies present in the image. Two fully connected layers with a ReLU function are used to obtain the predicted tool wear values. The experimental results on the PHM 2010 dataset demonstrate that the proposed model has higher prediction accuracy than the CNN model or ViT model alone, as well as outperforms several existing methods in accurately predicting tool wear. The proposed prediction method can also be applied to predict tool wear in other machining fields.

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Chronic pain, as a social public health problem, has a serious impact on the quality of patients' life. Currently, the main drugs used to treat chronic pain are opioids, antipyretic, and nonsteroidal anti-inflammatory drugs (NSAIDs). But the obvious side effects limit their use, so it is urgent to find new therapeutic targets. Postsynaptic density (PSD)-95 protein plays an important role in the occurrence and development of chronic pain. The over-expression of the PSD-95 protein and its interaction with other proteins are closely related to the chronic pain. Besides, the PSD-95-related drugs that inhibit the expression of PSD-95 as well as the interaction with other protein have been proved to treat chronic pain significantly. In conclusion, although more deep studies are needed in the future, these studies indicate that PSD-95 and the related proteins, such as NMDA receptor (NMDAR) subunit 2B (GluN2B), AMPA receptor (AMPAR), calmodulin-dependent protein kinase II (CaMKII), 5-hydroxytryptamine 2A receptor (5-HT2AR), and neuronal nitric oxide synthase (nNOS), are the promising therapeutic targets for chronic pain.

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BACKGROUND: Limited observational research has explored the relationship between the non-high-density lipoprotein cholesterol (non-HDL-C) to high-density lipoprotein cholesterol (HDL-C) ratio (NHHR) and the risk of post-stroke depression (PSD). This study aims to investigate the potential associations between NHHR and PSD. METHODS: A cross-sectional study was conducted using data from stroke participants aged 20 and older, sourced from the National Health and Nutrition Examination Survey (NHANES) spanning 2005 to 2018. Depression was assessed using the PHQ-9 questionnaire. The association between NHHR and PSD risk was evaluated through weighted multivariate logistic regression and restricted cubic spline (RCS) models. Subgroup and sensitivity analyses were performed to validate the findings. RESULTS: In the continuous model, the NHHR value for the PSD group (3.23±1.84) was significantly higher than that of the non-PSD group (2.79±1.40, p=0.015). Logistic regression analysis in the fully adjusted model revealed a positive association between NHHR and PSD (OR 1.16, 95 % CI 1.03-1.30, p=0.016). Interaction tests showed no significant differences across strata (p > 0.05 for interaction). Restricted cubic spline results indicated a linear dose-response relationship between NHHR and PSD risk (P for non-linearity = 0.6). This association persisted in various subgroup analyses. CONCLUSION: NHHR was significantly correlated with an increased risk of PSD among U.S. adults. Further re-search on NHHR could contribute to the prevention and treatment of PSD.

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The functional activities of the brain during any task like imaginary, motor, or cognitive are different in pattern as well as their area of activation in the brain is also different. This variation in pattern is also found in the brain's electrical variations that can be measured from the scalp of the brain using an electroencephalogram (EEG). This work exclusively studied a group of subjects' EEG data (available at: https://archive.physionet.org/physiobank/database/eegmat/) to unravel the activation pattern of the human brain during a mental arithmetic task. Since any cognitive task creates variations in EEG signal pattern, the relative changes in the signal power also occur which is also known as event-related desynchronization/synchronization (ERD/ERS). In this work, ERD/ERS have calculated the band-wise power spectral density (PSD) using Welch's method from the EEG signals. Besides, the coherence analysis was also performed to verify the results of ERD/ERS analysis from several randomly chosen subjects' EEG data. Here, subjects performing mental arithmetic tasks were grouped based on their performances: good (subtraction solved > 10 on average) and bad (subtraction solved ≤ 10 on average) to conduct group-specific ERD/ERS analysis regarding their performance in cognitive tasks. It was found that when the brain is on count condition, the variations found in the band power of theta and beta. The amounts of ERS in the left hemisphere are increased. When the task complexity increases, it contributes to an increase in relative ERD/ERS amounts and durations. The left and right hemispheres were asymmetrically distributed by both the pre-stimulus stages of the corresponding band power and relative ERD/ERS.

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The melanocortin-4 receptor (MC4R) is a G protein-coupled receptor (GPCR) that is expressed in several brain locations encompassing the hypothalamus and the brainstem, where the receptor controls several body functions, including metabolism. In a well-defined pathway to decrease appetite, hypothalamic proopiomelanocortin (POMC) neurons localized in the arcuate nucleus (Arc) project to MC4R neurons in the paraventricular nuclei (PVN) to release the natural MC4R agonist α-melanocyte-stimulating hormone (α-MSH). Arc neurons also project excitatory glutamatergic fibers to the MC4R neurons in the PVN for a fast synaptic transmission to regulate a satiety pathway potentiated by α-MSH. By using super-resolution microscopy, we found that in hypothalamic neurons in a primary culture, postsynaptic density protein 95 (PSD95) colocalizes with GluN1, a subunit of the ionotropic N-methyl-D-aspartate receptor (NMDAR). Thus, hypothalamic neurons form excitatory postsynaptic specializations. To study the MC4R distribution at these sites, tagged HA-MC4R under the synapsin promoter was expressed in neurons by adeno-associated virus (AAV) gene transduction. HA-MC4R immunofluorescence peaked at the center and in proximity to the PSD95- and NMDAR-expressing sites. These data provide morphological evidence that MC4R localizes together with glutamate receptors at postsynaptic and peri-postsynaptic sites.

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Insufficient sleep is a global problem with serious consequences for cognition and mental health.1 Synapses play a central role in many aspects of cognition, including the crucial function of memory consolidation during sleep.2 Interference with the normal expression or function of synapse proteins is a cause of cognitive, mood, and other behavioral problems in over 130 brain disorders.3 Sleep deprivation (SD) has also been reported to alter synapse protein composition and synapse number, although with conflicting results.4,5,6,7 In our study, we conducted synaptome mapping of excitatory synapses in 125 regions of the mouse brain and found that sleep deprivation selectively reduces synapse diversity in the cortex and in the CA1 region of the hippocampus. Sleep deprivation targeted specific types and subtypes of excitatory synapses while maintaining total synapse density (synapse number/area). Synapse subtypes with longer protein lifetimes exhibited resilience to sleep deprivation, similar to observations in aging and genetic perturbations. Moreover, the altered synaptome architecture affected the responses to neural oscillations, suggesting that sleep plays a vital role in preserving cognitive function by maintaining the brain's synaptome architecture.

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Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by selective dopaminergic loss. Non dopaminergic neurotransmitters such as glutamate are also involved in PD progression. NMDA receptor/postsynaptic density protein 95 (PSD-95)/neuronal nitric oxide synthase (nNOS) activation is involved in neuronal excitability in PD. Here, we are focusing on the evaluating these post-synaptic protein levels in the 6-OHDA model of PD. Adult male C57BL/6 mice subjected to unilateral striatal injury with 6-OHDA were assessed at 1-, 2-, or 4-weeks post-lesion. Animals were subjected to an apomorphine-induced rotation test followed by the analysis of protein content, synaptic structure, and NOx production. All biochemical analysis was performed comparing the control versus lesioned sides of the same animal. 6-OHDA mice exhibited contralateral rotation activity, difficulties in coordinating movements, and changes in Iba-1 and glial fibrillary acidic protein (GFAP) expression during the whole period. At one week of survival, the mice showed a shift in NMDA composition, favoring the GluN2A subunit and increased PSD95 and nNOS expression and NOx formation. After two-weeks, a decrease in the total number of synapses was observed in the lesioned side. However, the number of excitatory synapses was increased with a higher content of GluN1 subunit and PSD95. After four weeks, NMDA receptor subunits restored to control levels. Interestingly, NOx formation in the serum increased. This study reveals, for the first time, the temporal course of behavioral deficits and glutamatergic synaptic plasticity through NMDAr subunit shift. Together, these data demonstrate that dopamine depletion leads to a fine adaptive response over time, which can be used for further studies of therapeutic management adjustments with the progression of PD.

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Depressive states in both healthy individuals and those with major depressive disorder exhibit differences primarily in symptom severity rather than symptom type, suggesting that there is a spectrum of depressive symptoms. The increasing prevalence of mild depression carries lifelong implications, emphasizing its clinical and social significance, which parallels that of moderate depression. Early intervention and psychotherapy have shown effective outcomes in subthreshold depression. Electroencephalography serves as a non-invasive, powerful tool in depression research, with many studies employing it to discover biomarkers and explore underlying mechanisms for the identification and diagnosis of depression. However, the efficacy of these biomarkers in distinguishing various depressive states in healthy individuals and in understanding the associated mechanisms remains uncertain. In our study, we examined the power spectrum density and the region-based phase-locking value in healthy individuals with various depressive states during their resting state. We found significant differences in neural activity, even among healthy individuals. Participants were categorized into high, middle, and low depressive state groups based on their response to a questionnaire, and eyes-open resting-state electroencephalography was conducted. We observed significant differences among the different depressive state groups in theta- and beta-band power, as well as correlations in the theta-beta ratio in the frontal lobe and phase-locking connections in the frontal, parietal, and temporal lobes. Standardized low-resolution electromagnetic tomography analysis for source localization comparing the differences in resting-state networks among the three depressive state groups showed significant differences in the frontal and temporal lobes. We anticipate that our study will contribute to the development of effective biomarkers for the early detection and prevention of depression.

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Introduction: Deletion or mutation of members of the spectrin gene family contributes to many neurologic and neuropsychiatric disorders. While each spectrinopathy may generate distinct neuropathology, the study of ßΙ spectrin's role (Sptb) in the brain has been hampered by the hematologic consequences of its loss. Methods: Jaundiced mice (ja/ja) that lack ßΙ spectrin suffer a rapidly fatal hemolytic anemia. We have used exchange transfusion of newborn ja/ja mice to blunt their hemolytic pathology, enabling an examination of ßΙ spectrin deficiency in the mature mouse brain by ultrastructural and biochemical analysis. Results: ßΙ spectrin is widely utilized throughout the brain as the ßΙΣ2 isoform; it appears by postnatal day 8, and concentrates in the CA1,3 region of the hippocampus, dentate gyrus, cerebellar granule layer, cortical layer 2, medial habenula, and ventral thalamus. It is present in a subset of dendrites and absent in white matter. Without ßΙ spectrin there is a 20% reduction in postsynaptic density size in the granule layer of the cerebellum, a selective loss of ankyrinR in cerebellar granule neurons, and a reduction in the level of the postsynaptic adhesion molecule NCAM. While we find no substitution of another spectrin for ßΙ at dendrites or synapses, there is curiously enhanced ßΙV spectrin expression in the ja/ja brain. Discussion: ßΙΣ2 spectrin appears to be essential for refining postsynaptic structures through interactions with ankyrinR and NCAM. We speculate that it may play additional roles yet to be discovered.

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Corrosion deterioration of materials is a major problem affecting economic, safety, and logistical issues, especially in the aeronautical sector. Detecting the correct corrosion type in metal alloys is very important to know how to mitigate the corrosion problem. Electrochemical noise (EN) is a corrosion technique used to characterize the behavior of different alloys and determine the type of corrosion in a system. The objective of this research is to characterize by EN technique different aeronautical alloys (Al, Ti, steels, and superalloys) using different analysis methods such as time domain (visual analysis, statistical), frequency domain (power spectral density (PSD)), and frequency-time domain (wavelet decomposition, Hilbert Huang analysis, and recurrence plots (RP)) related to the corrosion process. Optical microscopy (OM) is used to observe the surface of the tested samples. The alloys were exposed to 3.5 wt.% NaCl and H2SO4 solutions at room temperature. The results indicate that HHT and recurrence plots are the best options for determining the corrosion type compared with the other methods due to their ability to analyze dynamic and chaotic systems, such as corrosion. Corrosion processes such as passivation and localized corrosion can be differentiated when analyzed using HHT and RP methods when a passive system presents values of determinism between 0.5 and 0.8. Also, to differentiate the passive system from the localized system, it is necessary to see the recurrence plot due to the similarity of the determinism value. Noise impedance (Zn) is one of the best options for determining the corrosion kinetics of one system, showing that Ti CP2 and Ti-6Al-4V presented 742,824 and 939,575 Ω·cm2, while Rn presented 271,851 and 325,751 Ω·cm2, being the highest when exposed to H2SO4.

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BACKGROUND: The study of tactile perception during a childhood is extremely important for understanding the social and communicative aspects of the child's development. Tactile perception of stimuli with different valence can have different normative stages of development. METHODS: In the present study, we examined changes in linear and nonlinear electroencephalogram (EEG) parameters during the presentation of pleasant (C-tactile optimal stroking), unpleasant (ice stroking), and neutral tactile stimuli in three groups of healthy volunteers: preschoolers 4 and 5 years, school-age children from 8 to 10 years, and adults from 20 to 40 years. RESULTS: According to our findings, child maturation plays a significant role in the perception of pleasant and neutral tactile stimuli. Patterns of EEG dynamics related to tactile perception showed greater similarity between adult volunteers and school-aged children than preschoolers. CONCLUSIONS: Non-linear EEG parameters such as fractal dimension (FD), envelope mean frequency (EMF), and power spectral density (PSD) dynamics of the theta-rhythm were particularly sensitive to developmental changes in tactile perception. Hjorth complexity and peak alpha frequency (PAF) scores may serve as indicators of mature perception of С-tactile (CT)-stimuli.

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The potential role of adenosine, a natural neuroprotective agent, and its receptors in the pathogenesis of Alzheimer's disease has been proposed. The present study aims to examine the effect of administering both an A1 receptor agonist and an A2A adenosine receptor antagonist simultaneously on memory, inflammatory factors, and PSD-95 in an LPS-induced Alzheimer's disease model in rats. Fifty-six male Wistar rats were randomly divided into seven groups: Saline, LPS, Saline + Vehicle, LPS + Vehicle, LPS + SCH58261 (A2A receptor antagonist), LPS + CPA (A1 receptor agonist), LPS + SCH58261+CPA. LPS (3 mg/kg/ip) was used to cause memory impairment. Treatment was performed by intraventricular injection of CPA at a dose of 700 µg and SCH-58261 at 40 µg for ten days. Passive avoidance and Y-maze tests were performed to examine animals' memories. IL-10, TNF-α, and PSD-95 levels were measured in the brain using ELISA and western blot, respectively. Compared to the groups receiving each medication separately, the simultaneous administration of CPA and SCH58261 improved memory (P<0.05). Additionally, compared to the single medication groups, there was a significant increase in IL-10, PSD-95, and a significant decrease in TNF-α in the brain tissue (P<0.05). These findings suggest that the activation of A1 receptors along with A2A receptor inhibition could be a potential therapeutic strategy for Alzheimer's disease. These findings suggest that A1 receptor activation combined with A2A receptor inhibition may be a promising therapeutic approach for Alzheimer's disease.

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Botrytis cinerea is an important fungal pathogen that causes gray mold disease in plants. Previously, Bacillus velezensis TCS001 live culture presented broad-spectrum antifungal activity against various plant pathogenic fungi and oomycetes, particularly B. cinerea. Here, the bioactivity of lipopeptides produced by TCS001 against B. cinerea was investigated. The IC50 values of the crude lipopeptide extract (CLE) from TCS001 to suppress mycelial growth and conidial germination were 14.20 and 49.39 mg/L, respectively. SEM and TEM imaging revealed that CLE caused morphological deformities and ultrastructural changes in the mycelium. Transcriptomic analyses combined with ΔBcpsd mutant construction demonstrated that the CLE could confer antifungal activity via suppressing Bcpsd expression in the pathogen. In addition, the CLE activated the plant immune system by increasing the content of defense-related enzymes and the expression of marker genes in immunity signaling pathways in cucumber plants. Therefore, TCS001 CLE could be potentially developed into biopesticides for the biocontrol of gray mold disease.

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The panoramic stereo video has brought a new visual experience for the audience with its immersion and stereo effect. In panoramic stereo video, the face is an important element. However, the face image in panoramic stereo video has varying degrees of deformation. This brings new challenges to face recognition. Therefore, this paper proposes a face recognition model DCM2Net (Deformable Convolution MobileFaceNet) for panoramic stereo video. The model mainly integrates the feature information between channels during feature fusion, redistributes the information between channels in the deeper part of the network, and fully uses the information between different channels for feature extraction. This paper also built a panoramic stereo video live system, using the DCM2Net model to recognize the face in panoramic stereo video, and the recognition results are displayed in the video. After experiments on different datasets, the results show that our model has better results on popular datasets and panoramic datasets.

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The key DNA repair enzyme DNA-PKcs has several and important cellular functions. Loss of DNA-PKcs activity in mice has revealed essential roles in immune and nervous systems. In humans, DNA-PKcs is a critical factor for brain development and function since mutation of the prkdc gene causes severe neurological deficits such as microcephaly and seizures, predicting yet unknown roles of DNA-PKcs in neurons. Here we show that DNA-PKcs modulates synaptic plasticity. We demonstrate that DNA-PKcs localizes at synapses and phosphorylates PSD-95 at newly identified residues controlling PSD-95 protein stability. DNA-PKcs -/- mice are characterized by impaired Long-Term Potentiation (LTP), changes in neuronal morphology, and reduced levels of postsynaptic proteins. A PSD-95 mutant that is constitutively phosphorylated rescues LTP impairment when over-expressed in DNA-PKcs -/- mice. Our study identifies an emergent physiological function of DNA-PKcs in regulating neuronal plasticity, beyond genome stability.

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Historically, the analysis of stimulus-dependent time-frequency patterns has been the cornerstone of most electroencephalography (EEG) studies. The abnormal oscillations in high-frequency waves associated with psychotic disorders during sensory and cognitive tasks have been studied many times. However, any significant dissimilarity in the resting-state low-frequency bands is yet to be established. Spectral analysis of the alpha and delta band waves shows the effectiveness of stimulus-independent EEG in identifying the abnormal activity patterns of pathological brains. A generalized model incorporating multiple frequency bands should be more efficient in associating potential EEG biomarkers with first-episode psychosis (FEP), leading to an accurate diagnosis. We explore multiple machine-learning methods, including random-forest, support vector machine, and Gaussian process classifier (GPC), to demonstrate the practicality of resting-state power spectral density (PSD) to distinguish patients of FEP from healthy controls. A comprehensive discussion of our preprocessing methods for PSD analysis and a detailed comparison of different models are included in this paper. The GPC model outperforms the other models with a specificity of 95.78% to show that PSD can be used as an effective feature extraction technique for analyzing and classifying resting-state EEG signals of psychiatric disorders.

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During development, microglia prune excess synapses to refine neuronal circuits. In neurodegeneration, the role of microglia-mediated synaptic pruning in circuit remodeling and dysfunction is important for developing therapies aimed at modulating microglial function. Here we analyzed the role of microglia in the synapse disassembly of degenerating postsynaptic neurons in the inner retina. After inducing transient intraocular pressure elevation to injure retinal ganglion cells, microglia increase in number, shift to ameboid morphology, and exhibit greater process movement. Furthermore, due to the greater number of microglia, there is increased colocalization of microglia with synaptic components throughout the inner plexiform layer and with excitatory synaptic sites along individual ganglion cell dendrites. Microglia depletion partially restores ganglion cell function, suggesting that microglia activation may be neurotoxic in early neurodegeneration. Our results demonstrate the important role of microglia in synapse disassembly in degenerating circuits, highlighting their recruitment to synaptic sites early after neuronal injury.

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BACKGROUND: Post-stroke depression (PSD) is a significant impediment to successful rehabilitation and recovery after a stroke. Current therapeutic options are limited, leaving an unmet demand for specific and effective therapeutic options. Our objective was to investigate the safety of Maraviroc, a CCR5 antagonist, as a possible mechanism-based add-on therapeutic option for PSD in an open-label proof-of-concept clinical trial. METHODS: We conducted a 10-week clinical trial in which ten patients with subcortical and cortical stroke, suffering from PSD. were administered a daily oral dose of 300 mg Maraviroc. Participants were then monitored for an additional eight weeks. The primary outcome measure was serious treatment-emergent adverse events (TEAEs) and TEAEs leading to discontinuation. The secondary outcome measure was a change in the Montgomery-Asberg Depression Rating Scale (MADRS). RESULTS: Maraviroc was well tolerated, with no reports of serious adverse events or discontinuations due to intolerance. The MADRS scores substantially reduced from baseline to week 10 (mean change: -16.4 ± 9.3; p < 0.001). By the conclusion of the treatment phase, a favorable response was observed in five patients, with four achieving remission. The time to response was relatively short, approximately three weeks. After the cessation of treatment, MADRS scores increased at week 18 by 6.1 ± 9.6 points (p = 0.014). CONCLUSIONS: Our proof-of-concept study suggests that a daily dosage of 300 mg of Maraviroc may represent a well-tolerated and potentially effective pharmacological approach to treating PSD. Further comprehensive placebo-controlled studies are needed to assess the impact of Maraviroc augmentation on PSD. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT05932550, Retrospectively registered: 28/06/2023.

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This study aimed to retrospectively examine the computed tomography (CT) features of lung adenocarcinoma across different demographic groups. Preoperative chest CT findings from 1266 surgically resected lung adenocarcinoma cases were retrospectively analyzed. Lung adenocarcinomas were categorized based on CT characteristics into pure ground glass (pGGO), nodule-containing ground glass opacity (mGGO), and pure solid without containing ground glass opacity (pSD). These categories were correlated with sex, age, EGFR status, and five histopathological subtypes. The diameters of pGGO, mGGO, and pSD significantly increased across all patient groups (P < 0.05). Males exhibited a significantly higher proportion of pSD than females (P = 0.002). The mean diameters of pGGO and pSD were significantly larger in males than in females (P = 0.0017 and P = 0.043, respectively). The frequency of pGGO was higher in the younger age group (≤ 60 years) compared to the older group (> 60 years) for both males (P = 0.002) and females (P = 0.027). The frequency of pSD was higher in the older age group for both sexes. A linear correlation between age and diameter was observed in the entire cohort as well as in the male and female groups (P < 0.0001 for all groups). EGFR mutations were less frequent in pSD compared to pGGO (P = 0.0002) and mGGO (P < 0.0001). The frequency of lesions containing micropapillary components increased from pGGO to mGGO and pSD (P < 0.0001 for all). The frequency of lesions containing solid components also increased from pGGO to mGGO and pSD (P = 0.045, P < 0.0001, and P < 0.0001, respectively). The CT features of lung adenocarcinoma exhibit differences across genders and age groups. Male gender and older age are risk factors for lung adenocarcinoma growth.

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