Effect of Immunosuppressive Regimens on Metabolic Dysfunction-associated Fatty Liver Disease Following Liver Transplantation.

Background: Metabolic dysfunction-associated fatty liver disease has been linked to negative outcomes in patients with end-stage liver disease following liver transplantation. However, the influence of immunosuppressive regimens on it has not been explored. Methods: A retrospective analysis was conducted using the preoperative and postoperative data from patients with end-stage liver disease. The study compared three different groups: tacrolimus-based group, sirolimus-based group, and combined tacrolimus- and sirolimus-based regimens. Binary logistic regression analysis was employed to identify risk factors for metabolic dysfunction-associated fatty liver disease. Results: A total of 171 patients participated in the study, consisting of 127 males and 44 females, with a mean age of 49.6 years. The prevalence of posttransplant metabolic dysfunction-associated fatty liver disease was 29.23%. Among the three groups, there were 111 liver transplant recipients in the tacrolimus-based group, 28 in the sirolimus-based group, and 32 in the combination group. A statistically significant difference was observed in the incidence of metabolic dysfunction-associated fatty liver disease (P < 0.05), whereas the other preoperative and postoperative parameters showed no significant differences. Multivariate analysis revealed that a low-calorie diet (95% confidence intervals: 0.15-0.90, P = 0.021) and a combination of tacrolimus- and sirolimus-based immunosuppressive regimen (95% confidence intervals: 1.01-2.77, P = 0.046) were associated with lower risk of posttransplant metabolic dysfunction-associated fatty liver disease. Conclusions: Our study indicates that implementing a low-calorie diet and utilizing a combination of tacrolimus- and sirolimus-based immunosuppressive regimen can effectively lower the risk of posttransplant metabolic dysfunction-associated fatty liver disease following liver transplantation.

SLC6A1 patient & organization perspective: founding of SLC6A1 connect, research, and ongoing efforts.

This paper describes the founding of the SLC6A1 Connect organization, which offers resources to patients and families with SLC6A1 diagnoses while keeping current with a scientific overview of the disorder. Following the birth of her two lovely twins, Amber Freed noticed how her son, Maxwell, missed motor development milestones and would often stare. Eventually, these signs led to a diagnosis of an SLC6A1 variant. The SLC6A1 gene is located on the short arm of chromosome 3 and the gene encodes for the gamma-aminobutyric acid (GABA) transporter 1 (GAT-1) protein. This transporter is responsible for the reuptake of the inhibitory neurotransmitter, GABA. The transporter usually removes GABA from the synapse space between two neurons, limiting over-excitability in the brain, which can lead to seizures and motor deficits as Amber noticed in her son, Maxwell. Amber realized that there were nearly no treatment options for her son's condition so she began forming connections with scientists and doctors. Initially, she flew to see Dr. Steven Gray, with whom she developed a research plan for a gene replacement therapy to treat the variant along with a design for a clinical trial. Not only this but they needed to raise four million dollars to fund these endeavors. Freed founded the SLC6A1 Connect organization to raise money and awareness and put together a network of dedicated researchers and families. Since then, the organization has raised over two million dollars and grown to offer families a base of support. The organization even hosts a yearly symposium with families, scientists, and biotech or pharmaceutical companies worldwide. In addition, we detail how the organization now offers informational resources to families to help them understand the science behind the variant and ways to help their children such as registry links and genetic testing options. These endeavors have led the organization to collaborate with scientists based on institutions such as Vanderbilt University Medical Center, UT Southwestern Medical Center, the Cleveland Clinic, and many industrial pharmaceutical partners.

Efforts of SLC6A1 Connect in providing educational, scientific, and support focused resources for those in the community SLC6A1 Connect offers many resources that patients and families afflicted by the SLC6A1 mutation benefit from. This mutation prevents a transporter from being encoded which typically allows for the proper levels of GABA in the brain to be maintained. Without this protein, there is a lack of GABA regulation and the brain is too excitable leading to seizures and motor delays. On our website, families are able to access scientific summaries of relevant publications in the field and can find plain-language summaries of the science behind the mutation. Additionally, symposiums are held once a year to allow families to hear from experts in the field and directly engage with them by asking questions. We aim to make scientific findings more understandable and accessible. The organization also allows them to become directly involved in the research, development, and medical treatment processes. Parents are able to help raise money through fundraising initiatives and receive regular information about genetic testing & registry programs. Overall, these organizational offerings have greatly benefited pediatric SLC6A1 patients, as seen through the patient family testimonies of Ms. Freed and the Fry family. Overall, throughout this paper we detail the resources made available to researchers, physicians, and families in the SLC6A1 Community.

ame-miR-5119-Eth axis modulates larval-pupal transition of western honeybee worker.

The miRNA plays a key role in the regulation of hormone signaling in insects. The pathways by which miRNAs affect hormone levels are unclear in the honeybee (Apis mellifera), an indispensable pollinator in nature. In this study, ame-miR-5119 was overexpressed and knocked down in larvae by feeding mimics and inhibitors, respectively, and we determined that ame-miR-5119 regulates hormone signaling through the target gene ecdysis triggering hormone (Eth), which affects the larval-pupal transition of workers. The results showed that ame-miR-5119 with a length of 19 nt targets six genes related to the hormone pathway. We focused on Eth and found that ame-miR-5119 and Eth exhibited reverse expression patterns during the transition from larval to pupal stages in workers. Dual luciferase assay confirmed the negative regulatory between ame-miR-5119 and Eth. Overexpression of ame-miR-5119 decreased the mRNA level of Eth, and the Eth receptor (Ethr) expression was not significantly affected, but the expression levels of juvenile hormone (JH) pathway related genes juvenile hormone acid methyltransferase (Jhamt) and Krüppel homolog 1 (Kr-h1) were significantly reduced. In contrast, knockdown of ame-miR-5119 increased the mRNA level of Eth, and the expression of Ethr, Jhamt and Kr-h1 was significantly upregulated. ame-miR-5119 did not affect larval body weight. The number of larvae overexpressing ame-miR-5119 survived in the prepupal stage was lower than that in the control group, and the number of pupations reduced at 11-day-old. The number of larvae that knocked down ame-miR-5119 survived in the prepupal stage was significantly higher than that in the control group, and the number of pupations increased at 11-day-old. These results indicated that ame-miR-5119 negatively regulates the expression of Eth, indirectly inhibits the expression of Ethr, Jhamt, and Kr-h1, and affects the JH biosynthesis, thereby preventing the metamorphic transition from larva to pupa in worker bees. These findings provide evidence that the miRNA regulation of hormone levels in honey bees.

Global prevalence of fatigue in patients with multiple sclerosis: a systematic review and meta-analysis.

Background: Fatigue is one of the most common and burdensome symptoms for patients with multiple sclerosis (PwMS), considerably impacting their quality of life and employment. Numerous reports have described the prevalence of MS-related fatigue, but there is no global consensus on this matter. Objective: To examine the global prevalence of MS-related fatigue and identify sources of heterogeneity in the published literature. Methods: A systematic review and meta-analysis were conducted. A comprehensive search of the PubMed, EMBASE, Cochrane Library, Web of Science, PsycINFO, CINAHL, China National Knowledge Infrastructure (CNKI), and Wanfang database for potential literature from 2000 to January 31, 2024. A random effects model was used to calculate the prevalence of MS-related fatigue. Subgroup analyses and a meta-regression were used to explore the sources of heterogeneity. Results: Sixty-nine studies from 27 countries were included. The global prevalence of MS-related fatigue was 59.1%, and it has decreased every decade since 2000. Fatigue was prevalent among females, those with lower education levels, those who were older, those with greater disability, and those with longer MS durations. The meta-regression revealed that fatigue measurement instruments were the largest source of heterogeneity. Conclusion: The prevalence of MS-related fatigue is quite high. Healthcare professionals should screen for and manage fatigue for PwMS as early as possible and pay attention to populations with a high prevalence of fatigue. The high heterogeneity among the prevalence rates due to differences in the fatigue scales suggests the importance of reaching a consensus on the best screening tools for MS-related fatigue.

A controlled study: Evaluating the clinical impact of a nurse-centred multidisciplinary hospice care model on anxiety, depression, and quality of life in patients with advanced malignant tumours.

OBJECTIVE: To explore the clinical effect of a nurse-centred multidisciplinary collaborative hospice care model in patients with advanced malignant tumours. METHODS: A total of 30 patients with advanced malignant tumours were hospitalised and randomly divided into a study group and a control group, each consisting of 15 cases. The study group received nurse-led multidisciplinary collaborative hospice care, whereas the control group underwent high-quality nursing intervention. Variables such as the self-rating anxiety scale (SAS) score, self-rating depression scale (SDS) score, quality of life scale (EORTC QLQ-C30) score, patient happiness, and nursing satisfaction were compared between the two groups. RESULTS: Post-intervention, the SAS and SDS scores in the study group were lower than those in the control group (p < 0.01). The overall quality of life score of the study group was higher than that of the control group (p < 0.01). The Memorial University of Newfoundland Scale of Happiness scores in the study group also surpassed those of the control group (p < 0.01). Additionally, nursing satisfaction in the study group exceeded that of the control group (p = 0.027). CONCLUSION: The nurse-led multidisciplinary collaborative hospice care model substantially alleviated negative emotions among patients, effectively improved their quality of life and happiness, and garnered positive evaluations of nursing satisfaction.

Up-regulation of myelin-associated glycoprotein is associated with the ameliorating effect of omega-3 polyunsaturated fatty acids on Alzheimer's disease progression in APP-PS1 transgenic mice.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive behavioral and cognitive impairments. Despite growing evidence of the neuroprotective action of omega-3 polyunsaturated fatty acids (PUFAs), the effects and mechanism of omega-3 PUFAs on AD control are yet to be clarified. By crossing male heterozygous fat-1 mice with female APP/PS1 mice, we assessed whether elevated tissue omega-3 PUFA levels could alleviate AD progression and their underlying mechanism among the offspring WT, APP/PS1 and APP/PS1 × fat-1 groups at various stages. We found that the fat-1 transgene significantly increased brain omega-3 PUFA and docosahexaenoic acid (DHA) levels, and cognitive deficits together with brain Aß-40 and Aß-42 levels in 6-month-old APP/PS1 × fat-1 mice were significantly lower than those in APP/PS1 mice. Subsequently, the tandem mass tag (TMT) method revealed the elevated expression of cortex and hippocampus myelin-associated glycoprotein (MAG) in APP/PS1 × fat-1 mice at 2-6 months. Furthermore, GO and KEGG pathway enrichment analysis suggested that the MAG-related myelin sheath pathway and its interaction with AD were regulated by omega-3 PUFAs. Moreover, subsequent western blot assays showed that both increased endogenous omega-3 levels and in vitro supplemented DHA up-regulated MAG expression, and the AD-protective effects of DHA on LPS-induced BV2 cells were significantly weakened when MAG was inhibited by si-RNA transfection. In summary, our study suggested that omega-3 PUFAs might protect against AD by up-regulating MAG expression.

A clinical study on the relationship between chronic rhinosinusitis and bronchial asthma.

Objective: To investigate the correlation between chronic rhinosinusitis (CRS) and bronchial asthma, focusing on the CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP), as well as their impact on lung function. Methods: A total of 141 patients diagnosed with chronic nasal-sinus inflammation were included in this study. Clinical data, including medical histories, nasal endoscopy scores, CT scores, symptom scores, and quality of life assessments, were collected. Results: Among the patients with CRSsNP, 23.8% had concomitant bronchial asthma. The incidence of asthma was significantly associated with the severity of sinus involvement in CRSsNP patients (p = 0.049). Pulmonary function impairment was correlated with the severity of sinus inflammation in CRSsNP patients (p = 0.019). Quality of life was significantly affected in patients with concomitant asthma and CRSsNP or CRSwNP. Conclusion: Chronic rhinosinusitis, both with and without nasal polyps, is closely correlated with bronchial asthma. Pulmonary function impairment is associated with the extent of inflammatory lesions in CRSsNP. Although CRSwNP does not significantly affect pulmonary function, the treatment of sinus diseases can contribute to the control of asthma.

Effects of Omega-3 Polyunsaturated Fatty Acids on the Formation of Adipokines, Cytokines, and Oxylipins in Retroperitoneal Adi-Pose Tissue of Mice.

Oxylipins and specialized pro-resolving lipid mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) are mediators that coordinate an active process of inflammation resolution. While these mediators have potential as circulating biomarkers for several disease states with inflammatory components, the source of plasma oxylipins/SPMs remains a matter of debate but may involve white adipose tissue (WAT). Here, we aimed to investigate to what extent high or low omega (n)-3 PUFA enrichment affects the production of cytokines and adipokines (RT-PCR), as well as oxylipins/SPMs (liquid chromatography-tandem mass spectrometry) in the WAT of mice during lipopolysaccharide (LPS)-induced systemic inflammation (intraperitoneal injection, 2.5 mg/kg, 24 h). For this purpose, n-3 PUFA genetically enriched mice (FAT-1), which endogenously synthesize n-3 PUFAs, were compared to wild-type mice (WT) and combined with n-3 PUFA-sufficient or deficient diets. LPS-induced systemic inflammation resulted in the decreased expression of most adipokines and interleukin-6 in WAT, whereas the n-3-sufficient diet increased them compared to the deficient diet. The n-6 PUFA arachidonic acid was decreased in WAT of FAT-1 mice, while n-3 derived PUFAs (eicosapentaenoic acid, docosahexaenoic acid) and their metabolites (oxylipins/SPMs) were increased in WAT by genetic and nutritional n-3 enrichment. Several oxylipins/SPMs were increased by LPS treatment in WAT compared to PBS-treated controls in genetically n-3 enriched FAT-1 mice. Overall, we show that WAT may significantly contribute to circulating oxylipin production. Moreover, n-3-sufficient or n-3-deficient diets alter adipokine production. The precise interplay between cytokines, adipokines, and oxylipins remains to be further investigated.

Glutathione-Conjugated Fluorometric Ratiometric NIR-Silicon Nanoparticles and Its Applications for In Vitro and In Vivo Imaging.

Glutathione (GSH), a tripeptide molecule, is the most abundant nonprotein biothiol in living cells, playing a crucial role in preventing oxidative damage to cellular components and maintaining intracellular redox homeostasis. As a thiol molecule, GSH contains a sulfhydryl (-SH) group that is vital for the body's response to reactive oxygen species (ROS). To confirm whether GSH can be used as a bioindicator or in the early diagnosis of cancers at the cellular level, it is essential to achieve highly selective detection and conjugation of GSH to silicon nanoparticles (SiNPs) under pathological conditions. We are herein excited to report a type of fluorescent ratiometric near-infrared silicon nanoparticle (NIR-SiNP) probe, that is, glutathione peptide conjugated (NIR-SiNPs-GSH), which simultaneously possess small pore sizes at an average of 6.7 nm, an emission of 670 nm, a bioimaging functionality of living cancer cells and animals, and favorable biocompatibility. Taking advantage of these virtues, we further manifest that such resulting NIR-SiNPs, NIR-SiNPs-GSH bioprobes are marvelously worthy for immunofluorescence imaging of cancer cells and living mice. Furthermore, it was shown that DAPI and probes could selectively stain malignant tumor cell nuclei, indicating the possibility for bioimaging and identification of cancer cells and animals. In summary, the suggested NIR-SiNPs-GSH probe has the potential to be a very effective chemical tool for early tumor detection in the future.

A gold nanoparticle-based photothermal hydrogel assisted by an N-halamine polymer for bacteria-infected skin wound healing.

Bacteria-infected wounds and antibiotic misuse have become a challenge in the treatment of clinical infections. Therefore, there is an urgent need to design non-antibiotic-dependent multifunctional wound dressings for the treatment of bacterially infected wounds. In this study, an injectable antibacterial hydrogel (pAMPS-Cl/AuNR@HA-DA) based on gold nanorods (AuNR) and N-halamine (pAMPS-Cl) with significant photothermal antibacterial properties was developed. The obtained pAMPS-Cl/AuNR@HA-DA hydrogel showed a sponge-like structure with excellent injectability, self-healing, tissue adhesion, and good hemocompatibility. In addition, the hydrogel exhibited excellent in vitro antibacterial capacity under near-infrared (NIR) laser irradiation through the synergistic action of photothermal therapy (PTT) and chemical release therapy. It also showed an excellent ability to eliminate bacterial infection and promote wound healing, indicating that the pAMPS-Cl/AuNR@HA-DA composite hydrogel could be a promising dressing for the treatment of skin wounds.

Genome-wide association studies on periodontitis: A systematic review.

OBJECTIVES: This study aims to systematically review the existing literature and critically appraise the evidence of genome-wide association studies (GWAS) on periodontitis. This study also aims to synthesise the findings of genetic risk variants of periodontitis from included GWAS. METHODS: A systematic search was conducted on PubMed, GWAS Catalog, MEDLINE, GLOBAL HEALTH and EMBASE via Ovid for GWAS on periodontitis. Only studies exploring single-nucleotide polymorphisms(SNPs) associated with periodontitis were eligible for inclusion. The quality of the GWAS was assessed using the Q-genie tool. Information such as study population, ethnicity, genomic data source, phenotypic characteristics(definition of periodontitis), and GWAS methods(quality control, analysis stages) were extracted. SNPs that reached conventional or suggestive GWAS significance level(5e-8 or 5e-06) were extracted and synthesized. RESULTS: A total of 15 good-quality GWAS on periodontitis were included (Q-genie scores ranged from 38-50). There were huge heterogeneities among studies. There were 11 identified risk SNPs (rs242016, rs242014, rs10491972, rs242002, rs2978951, rs2738058, rs4284742, rs729876, rs149133391, rs1537415, rs12461706) at conventional GWAS significant level (p<5x10-8), and 41 at suggestive level (p<5x10-6), but no common SNPs were found between studies. Three SNPs (rs4284742 [G], rs11084095 [A], rs12461706 [T]) from three large studies were from the same gene region-SIGLEC5. CONCLUSION: GWAS of periodontitis showed high heterogeneity of methodology used and provided limited SNPs statistics, making identifying reliable risk SNPs challenging. A clear guidance in dental research with requirement of expectation to make GWAS statistics available to other investigators are needed.

Acoustic, aerodynamic, and vibrational effects of ventricular folds adduction in an ex vivo experiment.

Objectives: The excessive adduction of ventricular folds has been observed in patients with dysphonia and professional singers. Whether these changes in the ventricular folds are the cause or just a result of disease progression remains unclear, and their potential pathological and physiological implications are yet to be determined. This study aimed to examine the impact of different degrees of ventricular adduction on acoustics, aerodynamics, and vocal fold vibration. Methods: The excised models of mild and severe ventricular adduction were established. We recorded the vibration pattern of vocal folds and ventricular folds and measured acoustic metrics, including fundamental frequency (F0), Jitter, Shimmer, harmonic-to-noise ratio (HNR), and sound pressure level (SPL). Furthermore, we evaluated the aerodynamics index through phonation threshold pressure (PTP), phonation instability pressure (PIP), mean flow rate (MFR), phonation threshold flow (PTF), and phonation instability flow (PIF). Results: Irregular vibrations of the ventricular fold were observed during ventricular adduction. Notably, mild and severe ventricular adduction conditions showed a significant increase in PTP, Shimmer, and Jitter, whereas MFR, PIF, and HNR decreased compared with the control condition. Conclusions: Ventricular adduction leads to the deterioration of acoustic and aerodynamic parameters. The aperiodic and irregular vibration of the ventricular folds may be responsible for this phenomenon, although further experiments are warranted. Understanding the functioning of ventricular folds can be beneficial in directing the treatment of muscle tension dysphonia and improving voice training techniques.Level of evidence: level 4.

Permeable Self-Association of Metal-Organic Framework 808/Ag-Based Fiber Membrane for Broad-Spectrum and Highly Efficient Degradation of Biological and Chemical War Agents.

The threat posed by biological and chemical warfare agents (BCWA) to national security, the environment, and personal health underscores the need for innovative chemical protective clothing. To address the limitations of conventional activated carbon materials, which are prone to falling off and adsorption saturation, an efficient self-association approach was introduced. In this study, we proposed the immobilization of metal-organic framework (MOF) 808 and Ag nanoparticles onto a polypropylene (PP) fiber membrane using a rapid self-association method facilitated by chitosan (CS). The MOF 808/Ag-based (PP-CS/808-Ag) fiber membrane demonstrated exceptional degradation efficiency, achieving a remarkable rate of t1/2 within 2 h for the mustard simulant 2-chloroethyl ethyl sulfide (2-CEES) and a rate of t1/2 = 4.12 min for the G-series simulant dimethyl 4-nitrophenylphosphate (DMNP). A theoretical computational model was developed to determine the overall reaction mechanism, and it was verified that MOF 808 and Ag nanoparticles were mainly involved in the hydrolysis process against 2-CEES and DMNP. The PP-CS/808-Ag composite fiber film was prepared as the core layer, and the fracture strength, bending resistance, and moisture permeability were better than those specified by many countries for biochemical protective clothing, showing that it has a broad application prospect in developing a generation of broad-spectrum bioprotective clothing.

Npc1 deficiency impairs microglia function via TREM2-mTOR signaling in Niemann-Pick disease type C.

Niemann-Pick disease Type C (NPC) is a neurodegenerative disease mainly caused by the mutation in NPC1 gene, leading to massive accumulation of unesterified cholesterol in the late endosome/lysosome of cells. Impaired phenotype of microglia is a hallmark in Npc1 mutant mice (Npc1-/- mice). However, the mechanism of Npc1 in regulating microglial function is still unclear. Here, we showed that the reactive microglia in the neonatal Npc1-/- mice indicated by the increased lysosome protein CD68 and phagocytic activity were associated with disrupted TREM2-mTOR signaling in microglia. Furthermore, in Npc1-deficient BV2 cells, genetic deletion of Trem2 partially restored microglial function, probably via restored mTOR signaling. Taken together, our findings indicated that loss of Npc1 in microglia caused changes of their morphologies and the impairment of lysosomal function, which were linked to the TREM2-mTOR signaling pathway.

Promotion of seedling germination in Arabidopsis by B-box zinc-finger protein BBX32.

Seed germination represents a determinant for plants to enter ecosystems and is thus regarded as a key ecological and agronomic trait. It is tightly regulated by a variety of environmental cues to ensure that seeds germinate under favorable conditions. Here, we characterize BBX32, a B-box zinc-finger protein, as an imbibition-stimulated positive regulator of seed germination. Belonging to subgroup V of the BBX family, BBX32 exhibits distinct characteristics compared with its close counterparts within the same subgroup. BBX32 is transiently induced at both the transcriptional and post-transcriptional levels in the embryo upon water absorption. Genetic evidence indicates that BBX32 acts upstream of the master transcription factor PHYTOCHROME-INTERACTING FACTOR 1 (PIF1) to facilitate light-induced seed germination. BBX32 directly interacts with PIF1, suppressing its protein-interacting and DNA-binding capabilities, thereby relieving PIF1's repression on seed germination. Furthermore, the imbibition-stimulated BBX32 functions in parallel with the light-induced transcription regulator HFR1 to collectively attenuate the transcriptional activities of PIF1. The BBX32-PIF1 de-repression module serves as a molecular connection that enables plants to integrate signals of water availability and light exposure, effectively coordinating the initiation of seed germination.

Technical note: A GPU-based shared Monte Carlo method for fast photon transport in multi-energy x-ray exposures.

BACKGROUND: The Monte Carlo (MC) method is an accurate technique for particle transport calculation due to the precise modeling of physical interactions. Nevertheless, the MC method still suffers from the problem of expensive computational cost, even with graphics processing unit (GPU) acceleration. Our previous works have investigated the acceleration strategies of photon transport simulation for single-energy CT. But for multi-energy CT, conventional individual simulation leads to unnecessary redundant calculation, consuming more time. PURPOSE: This work proposes a novel GPU-based shared MC scheme (gSMC) to reduce unnecessary repeated simulations of similar photons between different spectra, thereby enhancing the efficiency of scatter estimation in multi-energy x-ray exposures. METHODS: The shared MC method selects shared photons between different spectra using two strategies. Specifically, we introduce spectral region classification strategy to select photons with the same initial energy from different spectra, thus generating energy-shared photon groups. Subsequently, the multi-directional sampling strategy is utilized to select energy-and-direction-shared photons, which have the same initial direction, from energy-shared photon groups. Energy-and-direction-shared photons perform shared simulations, while others are simulated individually. Finally, all results are integrated to obtain scatter distribution estimations for different spectral cases. RESULTS: The efficiency and accuracy of the proposed gSMC are evaluated on the digital phantom and clinical case. The experimental results demonstrate that gSMC can speed up the simulation in the digital case by ∼37.8% and the one in the clinical case by ∼20.6%, while keeping the differences in total scatter results within 0.09%, compared to the conventional MC package, which performs an individual simulation. CONCLUSIONS: The proposed GPU-based shared MC simulation method can achieve fast photon transport calculation for multi-energy x-ray exposures.

n-3 PUFA ameliorate functional outcomes following repetitive mTBI in the fat-1 mouse model.

Purpose: Repeated mild traumatic brain injuries (mTBI) are a continuing healthcare concern worldwide, given its potential for enduring adverse neurodegenerative conditions. Past research suggests a potential protective effect of n-3 polyunsaturated fatty acids (PUFA) in experimental models of mTBI. The aim of this study was to investigate whether the neuroprotective benefits of n-3 PUFA persist following repetitive weight drop injury (WDI). Methods: Male fat-1 mice (n = 12), able to endogenously convert n-6 PUFA to n-3 PUFA, and their wild type (WT) counterparts (n = 12) were maintained on a 10% w/w safflower diet. At 9-10 weeks of age, both groups received one mild low-impact WDI on the closed cranium daily, for three consecutive days. Following each WDI, time to righting reflex and seeking behaviour were measured. Neurological recovery, cognitive, motor, and neurobehavioural outcomes were assessed using the Neurological Severity Score (NSS) over 7 days (168 h) post-last WDI. Brains were assessed for cerebral microhemorrhages by Prussian blue and cellular damage by glial fibrillary acidic protein (GFAP) staining. Results: Fat-1 mice exhibited significantly faster righting reflex and seeking behaviour time, and lower mean NSS scores and at all post-WDI time points (p ≤ 0.05) compared to WT mice. Immunohistochemistry showed no significant difference in presence of cerebral microhemorrhage however, fat-1 mice had significantly lower GFAP staining in comparison to WT mice (p ≤ 0.05). Conclusion: n-3 PUFA is effective in restoring cognitive, motor, and behavioural function after repetitive WDI, which may be mediated through reduced cellular damage of the brain.

Investigating the Relationship between Oral Health and Severe Mental Illness: Analysis of NHANES 1999-2016.

OBJECTIVES: To explore whether: (i) people with severe mental illness (SMI) experience worse oral health than the general population, and (ii) the risk factors for poor oral health in people with SMI. METHODS: Cross-sectional data were extracted from the National Health and Nutrition Examination Survey (1999-2016), including on self-rated oral health, oral pain, tooth loss, periodontitis stage, and number of decayed, missing, and filled teeth. Candidate risk factors for poor oral health included demographic characteristics, lifestyle factors, physical health comorbidities, and dental hygiene behaviours. Ordinal logistic regression and zero-inflated negative binomial models were used to explore predictors of oral health outcomes. RESULTS: There were 53,348 cases included in the analysis, including 718 people with SMI. In the fully adjusted model, people with SMI were more likely to suffer from tooth loss (OR 1.60, 95% CI: 1.34-1.92). In people with SMI, risk factors identified for poor oral health outcomes were older age, white ethnicity, lower income, smoking history, and diabetes. Engaging in physical activity and daily use of dental floss were associated with better oral health outcomes. CONCLUSIONS: People with SMI experience higher rates of tooth loss than the general population, and certain subgroups are particularly at risk. Performing regular physical exercise and flossing may lower the risk of poor oral health, while smoking and diabetes may increase the risk. These findings suggest opportunities for targeted prevention and early intervention strategies to mitigate adverse oral health outcomes in people with SMI.