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Research on graphene has been developing at a relentless pace as it holds the promise of delivering composites with exceptional properties. In particular, the excellent mechanical properties of graphene make it a potentially good reinforcement ingredient in ceramic composites while their impressive electrical conductivity has roused interest in the area of multifunctional applications. However, the potential of graphene can only be fully exploited if they are homogenously embedded into ceramic matrices. Thus, suitable processing route is critical in obtaining ceramic composites with desired properties. This paper reviews the current understanding of graphene ceramic matrix composites (GCMC) with three particular topics: (i) principles and techniques for graphene dispersion, (ii) processing of GCMC, and (iii) effects of graphene on properties of GCMC. Besides, toughening mechanisms and percolation phenomenon that may occur in these composites are elaborated with appropriate examples. Challenges and perspectives for future progress in applications are also highlighted.

Cases of foodborne disease caused by Salmonella are frequently associated with the consumption of minimally processed produce. Bacterial cell surface components are known to be important for the attachment of bacterial pathogens to fresh produce. The role of these extracellular structures in Salmonella attachment to plant cell walls has not been investigated in detail. We investigated the role of flagella, fimbriae and cellulose on the attachment of Salmonella Typhimurium ATCC 14028 and a range of isogenic deletion mutants (ΔfliC fljB, ΔbcsA, ΔcsgA, ΔcsgA bcsA and ΔcsgD) to bacterial cellulose (BC)-based plant cell wall models [BC-Pectin (BCP), BC-Xyloglucan (BCX) and BC-Pectin-Xyloglucan (BCPX)] after growth at different temperatures (28°C and 37°C). We found that all three cell surface components were produced at 28°C but only the flagella was produced at 37°C. Flagella appeared to be most important for attachment (reduction of up to 1.5 log CFU/cm2) although both cellulose and fimbriae also aided in attachment. The csgD deletion mutant, which lacks both cellulose and fimbriae, showed significantly higher attachment as compared to wild type cells at 37°C. This may be due to the increased expression of flagella-related genes which are also indirectly regulated by the csgD gene. Our study suggests that bacterial attachment to plant cell walls is a complex process involving many factors. Although flagella, cellulose and fimbriae all aid in attachment, these structures are not the only mechanism as no strain was completely defective in its attachment.

Robust data on trends in stroke hospitalisation rate and outcomes are needed to improve stroke care, yet are sparse and show conflicting results. We investigated the trends in hospitalisation rate, survival, and risk of stroke recurrence following an acute stroke using population-wide data from Australia and New Zealand over a 10-year period. We included adults aged ≥ 18 years hospitalised with an acute stroke from 2008 to 17. Age- and sex-standardized trends of stroke hospitalisation were calculated. Flexible parametric survival models were used to estimate and assess trends in survival and cumulative incidence of stroke recurrence at 30 days, 1 year and 5 years. 331,016 patients were included (mean age 73.2 ± 14.5 years, 48.0% female), with ischaemic stroke (185,800, 56.1%) being the most common type, followed by haemorrhagic stroke (81,877, 24.7%) and unspecified stroke (63,339, 19.1%). The overall age- and sex-standardised stroke hospitalisation rate decreased by 13.5% (179.3/100,000 person-years in 2008 to 155.1/100,000 person-years in 2017, P for trend < 0.01). However, the decline was limited to those ≥ 65 years, with the hospitalisation rate rising in those aged 55–64 years and stagnant in those aged 18–54 years. The adjusted survival probability at 30-day (83.4% in 2008/2009 to 85.9% in 2016/2017), 1-year (70.5% to 74.3%), and 5-year (51.4% to 53.0%) following a stroke has improved over time ( P for trend < 0.01). The adjusted risk of stroke recurrence at 30 days and 5 years was unchanged over time, whereas the 1-year risk increased from 9.8% in 2008–2009 to 10.8% in 2016 ( P for trend < 0.01). In patients hospitalised for acute stroke in Australia and New Zealand, the overall stroke hospitalisation rate and mortality declined over 10 years. However, this was accompanied by a static or rising stroke hospitalisation rate in younger patients and a concerning lack of improvement in the risk of stroke recurrence.

Graphene-based materials have gained remarkable attention in numerous disciplines owing to their unique electrochemical properties. Out of various hybridized nanocomposites, graphene-zirconia nanocomposite (GZ) was distinctive due to its biocompatibility. Zirconia nanoparticles serve as spacers that reduce the stacking of graphene and improve the electrochemical performance of the material. Considering that lungs and skin suffer the greatest exposure to nanoparticles, this study aimed to evaluate the cytotoxicity of the as-synthesized GZ nanocomposites on MRC5 (lung cells) and HaCaT (skin cells) via morphological observation and cell viability assay using 3-(4,5 dimethylthiazol-2-yl)-(2,5-diphenyltetrazolium bromide) tetrazolium (MTT). GZ-treated cells showed a comparable proliferation rate and morphology with untreated cells under microscopic evaluation. Based on MTT results, the IC 50 values of GZ were > 500 µg/ml for MRC5 and HaCaT cells. The excellent biocompatibility was the supremacy of GZ over other nanocomposites applied as electrode materials in biosensors. GZ was functionalized with biolinker for the detection of carcinoembryonic antigen (CEA). The proposed immunosensor exhibited good responses towards CEA detection, with a 4.25 pg/ml LOD and correlation coefficient of R 2  = 0.99 within a linear working range from 0.01 to 10 ng/ml. The performance of the immunosensor to detect CEA present in human serum was also evaluated. Good recovery of CEA was found, suggesting that the proposed immunosensor possess a high affinity to CEA even in a complex biological matrix, rendering it a promising sensing platform for real sample analysis and open a new way for the detection of cancer-associated proteins.

Although alterations in myeloid cells have been observed in COVID-19, the specific underlying mechanisms are not completely understood. Here, we examine the function of classical CD14 + monocytes in patients with mild and moderate COVID-19 during the acute phase of infection and in healthy individuals. Monocytes from COVID-19 patients display altered expression of cell surface receptors and a dysfunctional metabolic profile that distinguish them from healthy monocytes. Secondary pathogen sensing ex vivo leads to defects in pro-inflammatory cytokine and type-I IFN production in moderate COVID-19 cases, together with defects in glycolysis. COVID-19 monocytes switch their gene expression profile from canonical innate immune to pro-thrombotic signatures and are functionally pro-thrombotic, both at baseline and following ex vivo stimulation with SARS-CoV-2. Transcriptionally, COVID-19 monocytes are characterized by enrichment of pathways involved in hemostasis, immunothrombosis, platelet aggregation and other accessory pathways to platelet activation and clot formation. These results identify a potential mechanism by which monocyte dysfunction may contribute to COVID-19 pathology. Although myeloid cell dysfunction has been observed in COVID-19, the underlying mechanisms remain incompletely understood. Here, the authors demonstrate that monocytes from patients with mild to moderate COVID-19 show a blunted innate immune response and a pro-thrombotic signature following secondary SARS-CoV-2 challenge.

Cumulative data suggest the involvement of Fyn tyrosine kinase in Alzheimer's disease (AD). Previously, our group has shown increased immunoreactivities of the FynT isoform in AD neocortex (with no change in the alternatively spliced FynB isoform) which associated with neurofibrillary degeneration and reactive astrogliosis. Since both the aforementioned neuropathological features are also variably found in Lewy Body dementias (LBD), we investigated potential perturbations of Fyn expression in the post‐mortem neocortex of patients with AD, as well as those diagnosed as having one of the two main subgroups of LBD: Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB). We found selective upregulation of FynT expression in AD, PDD, and DLB which also correlated with cognitive impairment. Furthermore, increased FynT expression correlated with hallmark neuropathological lesions, soluble β‐amyloid, and phosphorylated tau, as well as markers of microglia and astrocyte activation. In line with the human post‐mortem studies, cortical FynT expression in aged mice transgenic for human P301S tau was upregulated and further correlated with accumulation of aggregated phosphorylated tau as well as with microglial and astrocytic markers. Our findings provide further evidence for the involvement of FynT in neurodegenerative dementias, likely via effects on tauopathy and neuroinflammation. Splice variant‐specific upregulation of FynT kinase correlated with clinical and neuropathological markers of Alzheimer's Disease (AD) and Lewy body Dementias (LBD). Our results suggest that FynT should be further evaluated as a novel therapeutic target in AD and LBD.

Migraine is a chronic neurological problem with a psychological comorbidity. However, anxiety and depression among patients with migraine have not been thoroughly investigated in Southeast Asia. Thus, we aimed to elucidate the prevalence of anxiety and depression in patients with migraine, as well as the associated factors. This cross-sectional study was conducted between March 2022 and March 2024 at the National University of Malaysia. The participants' data were collected prior to completing two questionnaires, including the Patient Health Questionnaire-9 (PHQ-9) and the Generalized Anxiety Disorder-7 (GAD-7), which were used to evaluate depression and anxiety, respectively. A total of 246 participants who were diagnosed with migraine were recruited for this study. The mean age of the participants was 46.19 years (SD: ± 14.75). Additionally, 77.6% of the participants were female. Moreover, 27.7% of the participants had anxiety alone, 15.9% had depression alone, and 11.8% had both anxiety and depression. A younger age (p = 0.03), earlier age of migraine onset (r(246) -0.178, p < 0.01), background history of asthma (r(246) 0.161, p < 0.05), lower household income range (r(246) -0.179, p < 0.01), increased pain severity (r(246) 0.211, p < 0.01), frequency of attack (r(246) 0.139, p < 0.05), use of NSAIDs (r(246) 0.134, p < 0.05), use of pizotifen (r(246) 0.169, p < 0.01), use of propranolol (r(246) 0.286, p < 0.01), use of sodium valproate (r(246) 0.146, p < 0.05), use of topiramate (r(246) 0.178, p < 0.01), use of more than one medication (r(246) 0.240, p < 0.01), use of cold therapy (r(246) 0.223, p < 0.01) and use of acupuncture (r(246) 0.260, p < 0.01) were associated with anxiety and depression in migraine patients. Anxiety and depression are commonly observed in patients with migraine in Asia. Routine assessments for anxiety and depression should be performed to ensure holistic management of migraine.

Background Unpaid carers of older people, and older unpaid carers, experience a range of adverse outcomes. Supporting carers should therefore be a public health priority. Our understanding of what works to support carers could be enhanced if future evaluations prioritise under-researched interventions and outcomes. To support this, we aimed to: map evidence about interventions to support carers, and the outcomes evaluated; and identify key gaps in current evidence. Methods Evidence gap map review methods were used. Searches were carried out in three bibliographic databases for quantitative evaluations of carer interventions published in OECD high-income countries between 2013 and 2023. Interventions were eligible if they supported older carers (50 + years) of any aged recipient, or any aged carers of older people (50 + years). Findings 205 studies reported across 208 publications were included in the evidence map. The majority evaluated the impact of therapeutic and educational interventions on carer burden and carers’ mental health. Some studies reported evidence about physical exercise interventions and befriending and peer support for carers, but these considered a limited range of outcomes. Few studies evaluated interventions that focused on delivering financial information and advice, pain management, and physical skills training for carers. Evaluations rarely considered the impact of interventions on carers’ physical health, quality of life, and social and financial wellbeing. Very few studies considered whether interventions delivered equitable outcomes. Conclusion Evidence on what works best to support carers is extensive but limited in scope. A disproportionate focus on mental health and burden outcomes neglects other important areas where carers may need support. Given the impact of caring on carers’ physical health, financial and social wellbeing, future research could evaluate interventions that aim to support these outcomes. Appraisal of whether interventions deliver equitable outcomes across diverse carer populations is critical.

Background We aimed to identify specific multimorbidity latent classes among multi-ethnic community-dwelling adults aged ≥ 18 years in Malaysia. We further explored the risk factors associated with these patterns and examined the relationships between the multimorbidity patterns and 11-year all-cause mortality risk, as well as health-related quality of life (HRQoL). Methods Using data from 18,101 individuals (aged 18–97 years) from the baseline Census 2012, Health Round 2013, and Verbal Autopsies 2012–2023 of the South East Asia Community Observatory (SEACO) health and demographic surveillance system, latent class analysis was performed on 13 chronic health conditions to identify statistically and clinically meaningful groups. Multinomial logistic regression and Cox proportional hazards regression models were conducted to investigate the adjusted association of multimorbidity patterns with the risk factors and mortality, respectively. HRQoL was analyzed by linear contrasts in conjunction with ANCOVA adjusted for baseline confounders. Results Four distinct multimorbidity latent classes were identified: (1) relatively healthy ( n  = 10,640); (2) cardiometabolic diseases ( n  = 2428); (3) musculoskeletal, mobility and sensory disorders ( n  = 2391); and (4) complex multimorbidity (a group with more severe multimorbidity with combined profiles of classes 2 and 3) ( n  = 699). Significant variations in associations between socio-demographic characteristics and multimorbidity patterns were discovered, including age, sex, ethnicity, education level, marital status, household monthly income and employment status. The complex multimorbidity group had the lowest HRQoL across all domains compared to other groups ( p  < 0.001), including physical health, psychological, social relationships and environment. This group also exhibited the highest mortality risk over 11 years even after adjustment of confounders (age, sex, ethnicity, education and employment status), with a hazard of death of 1.83 (95% CI 1.44–2.33), followed by the cardiometabolic group (HR 1.42, 95% CI 1.18–1.70) and the musculoskeletal, mobility and sensory disorders group (HR 1.29, 95% CI 1.04–1.59). Conclusions Our study advances the understanding of the complexity of multimorbidity and its implications for health outcomes and healthcare delivery. The findings suggest the need for integrated healthcare approaches that account for the clusters of multiple conditions and prioritize the complex multimorbidity cohort. Further longitudinal studies are warranted to explore the underlying mechanisms and evolution of multimorbidity patterns.

Alzheimer’s disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown. To identify and characterize selectively vulnerable neuronal populations, we used single-nucleus RNA sequencing to profile the caudal entorhinal cortex and the superior frontal gyrus—brain regions where neurofibrillary inclusions and neuronal loss occur early and late in AD, respectively—from postmortem brains spanning the progression of AD-type tau neurofibrillary pathology. We identified RORB as a marker of selectively vulnerable excitatory neurons in the entorhinal cortex and subsequently validated their depletion and selective susceptibility to neurofibrillary inclusions during disease progression using quantitative neuropathological methods. We also discovered an astrocyte subpopulation, likely representing reactive astrocytes, characterized by decreased expression of genes involved in homeostatic functions. Our characterization of selectively vulnerable neurons in AD paves the way for future mechanistic studies of selective vulnerability and potential therapeutic strategies for enhancing neuronal resilience. Leng et al. uncover the molecular signature of neuronal subpopulations that are selectively vulnerable to tau aggregation and death early in Alzheimer’s disease in the human entorhinal cortex and other brain regions, validating RORB as a marker.