Background: This cross-sectional study aimed to identify the prevalence of Candida albicans and Malassezia globosa in children with severe early childhood caries and caries-free children in Hong Kong. Methods: This study first recruited a total of 80 children aged between 48 and 72 months old, 40 children with severe early childhood caries, and 40 caries-free children. The children were then further divided into four groups, with 20 children in each group: Group 1: Severe early childhood caries-C. albicans, Group 2: Severe early childhood caries-M. globosa, Group 3: Caries-free-C. albicans and Group 4: Caries-free-M. globosa. Saliva, plaque, and caries lesion samples were collected from participants with severe early childhood caries, while only saliva and plaque samples were collected from caries-free participants. Caries status of the primary molars was assessed using WHO\'s decayed, missing, and filled tooth index, and the severity of cavitated lesions was determined based on International Caries Diagnosis and Assessment System criteria as caries code 5 or 6. The samples were analyzed using an Internal Transcribed Space and Quantitative Real-Time Polymerase Chain Reaction. Results:C. albicans was more prevalent in saliva and plaque samples of severe early childhood caries than in the caries-free group. Proportion of C. albicans in both saliva and plaque samples differed significantly between severe early childhood caries and caries-free groups (p < 0.05). Within the severe early childhood caries group, the proportion of children with C. albicans varied between 6 and 46%. No significant difference in M. globosa load was found between plaque samples of the severe early childhood caries and caries-free groups (p = 0.159). Conversely, no significant difference in M. globosa load was observed between saliva samples of severe early childhood caries and caries-free groups (p = 0.051). Conclusions: This study demonstrated a strong association between C. albicans and severe early childhood caries. M. globosa was detected in both the caries-free and severe early childhood caries groups, albeit at low levels.

UNASSIGNED: We investigated the relationship between remnant cholesterol and carotid intraplaque neovascularization (IPN) assessed by contrast-enhanced ultrasonography (CEUS) in patients with ischemic stroke.
UNASSIGNED: This was a single-center study. Remnant cholesterol is calculated as total cholesterol minus low-density lipoprotein cholesterol (LDL-C) minus high-density lipoprotein cholesterol (HDL-C). All patients underwent CEUS. IPN is graded according to the presence and location of microbubbles within each plaque.
UNASSIGNED: The cohort included 110 patients with ischemic stroke. Patients with an IPN grading of 2 had higher triglyceride (TG), non-HDL-C, and remnant cholesterol concentrations than those with an IPN grading of < 2 (TG: 1.45 ± 0.69 vs. 0.96 ± 0.24 mmol/L, P < 0.001; non-HDL-C: 2.63 ± 0.85 vs. 2.31 ± 0.64 mmol/L, P = 0.037; remnant cholesterol: 0.57 ± 0.23 vs. 0.44 ± 0.07 mmol/L, P < 0.001). The multivariate-adjusted odds ratio (95% confidence interval) for remnant cholesterol was 27.728 (2.714 - 283.253) for an IPN grading of 2 in the subset of patients with an optimal LDL-C concentration.
UNASSIGNED: The remnant cholesterol concentration is significantly associated with carotid IPN on CEUS in patients with ischemic stroke with an optimal LDL-C concentration. Remnant cholesterol may be an important indicator of risk stratification in patients with ischemic stroke.

Accurate evaluation of the nature and composition of coronary plaque involves clinical follow-up and prognosis. Coronary CT angiography is the most commonly non-invasive method for plaque evaluation, however, the qualitative and quantitative evaluation of plaque based on CT value is inaccurate, due to the influence of luminal attenuation, tube voltage, parameter setting and the subjectivity.

Background Periodontal disease poses a significant oral health challenge, involving inflammatory conditions impacting tooth-supporting structures. Treponema denticola, a \"red complex\" organism, plays a crucial role in periodontal pathogenesis, forming biofilms in subgingival environments and contributing to dysbiosis. Antimicrobial therapy is pivotal in managing periodontal disease, requiring a nuanced understanding of susceptibility patterns exhibited by key pathogens like T. denticola. Aims and objectives This study aims to investigate the antimicrobial susceptibility and resistance profiles of Treponema denticola, a prominent bacterium in periodontal disease, by examining its responses to various antimicrobial agents commonly used in periodontal therapy. Methodology Plaque samples were meticulously collected from individuals diagnosed with periodontal disease to ensure a diverse representation of the oral microbiome. All the samples were cultured, and red complex bacteria were isolated under anaerobic culture. Treponema denticola isolates were cultured from these samples under anaerobic conditions, and molecular techniques were employed for species identification. A comprehensive panel of antimicrobial agents was selected to assess the response of Treponema denticola. In vitro antimicrobial susceptibility testing (AST) was conducted using the antimicrobial gradient method, employing a hybrid approach combining elements of disk-diffusion and dilution methods. Results Treponema denticola had exhibited resistance to metronidazole, a commonly used antibiotic effective against anaerobic bacteria, emphasizing limitations in its applicability. However, the bacterium displayed sensitivity to tetracycline, imipenem, cefoperazone, chloramphenicol, clindamycin, and moxifloxacin, offering diverse therapeutic options. The antimicrobial gradient strip test provided detailed minimum inhibitory concentration (MIC) values, contributing to a nuanced understanding of susceptibility and resistance patterns. Conclusion This study significantly advances our understanding of Treponema denticola\'s antimicrobial susceptibility and resistance profiles in the context of periodontal disease. The findings underscore the importance of tailored treatment strategies and contribute to broader efforts in antimicrobial stewardship, aligning with global initiatives to combat antibiotic resistance. This research lays the foundation for more effective and personalized approaches to periodontal care, emphasizing the intricate microbial dynamics associated with periodontal health and disease.

OBJECTIVE: To compare the efficacy of test (ultrasonic cleaner combined with immersion in denture cleanser solution) and control (immersion in denture cleanser solution followed by conventional brushing) denture cleaning interventions in enhancing denture cleanliness, reducing denture stomatitis, and improving patient satisfaction.
METHODS: A prospective, single-blind, block-randomised, two-period crossover, superiority-controlled clinical trial was conducted of a 3-month intervention. The study design included a pre-intervention period (2 weeks), intervention period one (3 months), washout period (2 weeks), and intervention period two (3 months). A total of 56 community-dwelling elders were block-randomized into either sequence Test/Control or sequence Control/Test. The intervention, period, and carryover effects for the changes in the cleanliness of extensive partial and complete acrylic dentures, denture stomatitis, and changes in patient satisfaction were estimated using Generalized Estimating Equations models.
RESULTS: Percentage plaque area coverage, patient satisfaction, and denture stomatitis were significantly improved for both intervention and control arms after 3 months (P < 0.05). The intervention arm was found to significantly improve denture cleanliness (P < 0.001) and patient satisfaction (P = 0.002) more than the control arm. Denture-wearing habits and denture age were also significantly associated with the changes in denture plaque coverage (P < 0.05). However, the effect of the test intervention on denture stomatitis was not significantly different compared to the control arm (P = 0.284).
CONCLUSIONS: This study revealed that the test intervention group was significantly more effective than the control group in improving denture cleanliness and patient satisfaction among community-dwelling elders. This test intervention is recommended for maintaining optimum denture hygiene among older adults.
CONCLUSIONS: Removable dentures can harbor opportunistic pathogens, emphasizing the need for effective denture hygiene intervention using ultrasonic cleaner combined with immersion in denture cleanser solution to eliminate denture biofilm in community-dwelling elders.

This review paper examines the evolution of photodynamic therapy (PDT) as a novel, minimally invasive strategy for treating atherosclerosis, a leading global health concern. Atherosclerosis is characterized by the accumulation of lipids and inflammation within arterial walls, leading to significant morbidity and mortality through cardiovascular diseases such as myocardial infarction and stroke. Traditional therapeutic approaches have primarily focused on modulating risk factors such as hypertension and hyperlipidemia, with emerging evidence highlighting the pivotal role of inflammation. PDT, leveraging a photosensitizer, specific-wavelength light, and oxygen, offers targeted treatment by inducing cell death in diseased tissues while sparing healthy ones. This specificity, combined with advancements in nanoparticle technology for improved delivery, positions PDT as a promising alternative to traditional interventions. The review explores the mechanistic basis of PDT, its efficacy in preclinical studies, and the potential for enhancing plaque stability and reducing macrophage density within plaques. It also addresses the need for further research to optimize treatment parameters, mitigate adverse effects, and validate long-term outcomes. By detailing past developments, current progress, and future directions, this paper aims to highlight PDT\'s potential in revolutionizing atherosclerosis treatment, bridging the gap from experimental research to clinical application.

UNASSIGNED: The inflammatory response is a pivotal factor in accelerating the progression of atherosclerosis. The high-sensitivity C-reactive protein-to-albumin ratio (CAR) has emerged as a novel marker of systemic inflammation. However, few studies have shown the CAR to be a promising prognostic marker for carotid atherosclerotic disease. This study aimed to analyse the predictive role of the CAR in carotid atherosclerotic disease.
UNASSIGNED: This community-based cohort study recruited 2003 participants from the Rose asymptomatic IntraCranial Artery Stenosis (RICAS) study who were free of stroke or transient ischemic attack. Carotid atherosclerotic plaques and their stability were identified via carotid ultrasound. Logistic regression models were utilized to investigate the association between CAR and the presence of carotid atherosclerotic plaques.
UNASSIGNED: The prevalence of carotid atherosclerotic plaques was 38.79% in this study. After adjusting for clinical risk factors, including sex, age, dyslipidemia, hypertension, diabetes mellitus (DM), and smoking and drinking habits, a high CAR-level was independently associated with carotid plaque (odds ratio [OR] of upper: 1.46, 95% confidence interval [CI]: 1.13-1.90, P = 0.004; P for trend = 0.011). The highest CAR tertile was still significantly associated with carotid plaques among middle-aged (40-64 years) or female participants. Notably, an elevated CAR may be an independent risk factor for vulnerable carotid plaques (OR of upper: 2.06, 95% CI: 1.42-2.98, P < 0.001; P for trend <0.001).
UNASSIGNED: A high CAR may be correlated with a high risk of carotid plaques, particularly among mildly aged adults (40-64 years) or females. Importantly, the CAR may be associated with vulnerable carotid plaques, suggesting that the CAR may be a new indicator for stroke prevention.

UNASSIGNED: Despite intense investigations, no effective treatment is yet available to reduce plaques and protect memory and learning in patients with Alzheimer\'s disease (AD), the most common neurodegenerative disorder. Therefore, it is important to identify a non-toxic, but effective, treatment option for AD.
UNASSIGNED: Cinnamein, a nontoxic compound, is naturally available in Balsam of Peru and Tolu Balsam. We examined whether cinnamein treatment could decrease plaques and improve cognitive functions in 5XFAD mouse model of AD.
UNASSIGNED: We employed in silico analysis, time-resolved fluorescence energy transfer assay, thermal shift assay, primary neuron isolation, western blot, immunostaining, immunohistochemistry, Barnes maze, T maze, and open field behavior.
UNASSIGNED: Oral administration of cinnamein led to significant reduction in amyloid-β plaque deposits in the brain and protection of spatial learning and memory in 5XFAD mice. Peroxisome proliferator-activated receptor alpha (PPARα), a nuclear hormone receptor, is involved in plaque lowering and increase in hippocampal plasticity. While investigating underlying mechanisms, we found that cinnamein served as a ligand of PPARα. Accordingly, oral cinnamein upregulated the level of PPARα, but not PPARβ, in the hippocampus, and remained unable to decrease plaques from the hippocampus and improve memory and learning in 5XFAD mice lacking PPARα. While A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) is one of the drivers of nonamyloidogenic pathway, transcription factor EB (TFEB) is considered as the master regulator of autophagy. Cinnamein treatment was found to upregulate both ADAM10 and TFEB in the brain of 5XFAD mice via PPARα.
UNASSIGNED: Our results suggest that this balsam component may have therapeutic importance in AD.

We review the technique for carotid endarterectomy (CEA) and direct carotid access for distal thrombectomy after attempted proximal thrombectomy in the setting of tandem occlusions. A patient in their 70s presented with right facial droop and drooling and was found to have critical left carotid stenosis with filling defect in the cavernous segment of the left internal carotid artery consistent with vessel occlusion, Thrombolysis in Cerebral Infarction (TICI) 0, and left M2 middle cerebral artery (MCA) occlusion. After multiple attempts with different wire shapes guided by microcatheter injections within the carotid bulb, we were unable to cross the occlusion. Conversion to open CEA with distal thrombectomy was elected. Following closure of the arteriotomy, direct carotid access using a 5Fr radial artery sheath was achieved within the open surgical field for distal thrombectomy. A 5Fr aspiration catheter was navigated to the left M2 MCA where a stent retriever was then recaptured and TICI 2B reperfusion was achieved.

Amyloid beta (Aβ) peptides, which aggregate to form neocortical plaques in Alzheimer\'s disease, exist in states that range from soluble monomers and oligomers/protofibrils to insoluble fibrillar amyloid. The present study evaluated the effects of mAb158, a mouse monoclonal antibody version of lecanemab that preferentially binds to soluble Aβ protofibrils, in aged transgenic mice (Tg2576) with Aβ pathology. Female Tg2576 mice (12 months old) received weekly intraperitoneal mAb158 (35 mg/kg) or vehicle for 4 weeks or for 18 weeks, with or without a subsequent 12-week off-treatment period. Aβ protofibril levels were significantly lower in mAb158-treated animals at both 4 and 18 weeks, while longer treatment duration (18 weeks) was required to observe significantly lower Aβ42 levels in insoluble brain fractions and lower Aβ plaque load. Following the off-treatment period, comparison of the vehicle- and mAb158-treated mice demonstrated that the Aβ protofibril levels, insoluble Aβ42 levels and Aβ plaque load remained significantly lower in mAb158-treated animals, as compared with age-matched controls. However, there was a significant increase of brain accumulation of both the Aβ protofibril levels, insoluble Aβ42 levels and Aβ plaque load after treatment cessation. Thus, repeated mAb158 treatment of aged Tg2576 mice first reduced Aβ protofibril levels within 4 weeks of treatment, which then was followed by a reduction of amyloid plaque pathology within 18 weeks of treatment. These effects were maintained 12 weeks after the final dose, indicating that mAb158 had a disease-modifying effect on the Aβ pathology in this mouse model. In addition, brain accumulation of both Aβ protofibril levels and amyloid pathology progressed after discontinuation of the treatment which supports the importance of continued treatment with mAb158 to maintain the effects on Aβ pathology.