Reliability and Validity Analyses of the Practical Assessment of Dysphagia Test in Stroke.

To investigate the validity and reliability of the Practical Assessment of Dysphagia (PAD) test as a quantitative and organ-specific test for stroke patients. In this study, PAD test data from 109 patients with stroke were used. The internal consistency of the PAD was analyzed using Cronbach's α value. Inter- and intra-rater reliabilities of the PAD were analyzed using Kappa coefficient. Concurrent validity was evaluated based on the correlation between PAD and the videofluoroscopic swallowing study (VFSS). The diagnostic accuracy of the PAD test in patients with stroke was measured using the area under the receiver operating characteristic (ROC) curve. Intra- and inter-rater reliabilities (Intra-class Correlation Coefficient (ICC) = 0.98 and 0.99, respectively) were significant (p < 0.001) for the total PAD score. The functional dysphagia scale (FDS) score and penetration-aspiration score (PAS) correlated significantly with PAD (p < 0.001). The results of the ROC curve analysis with various cut-off points showed that the PAD test had high sensitivity and specificity. The PAD has high reliability and validity. Therefore, it is a useful screening test for dysphagia in patients with stroke.

Autotaxin inhibition attenuates the aortic valve calcification by suppressing inflammation-driven fibro-calcific remodeling of valvular interstitial cells.

BACKGROUND: Patients with fibro-calcific aortic valve disease (FCAVD) have lipid depositions in their aortic valve that engender a proinflammatory impetus toward fibrosis and calcification and ultimately valve leaflet stenosis. Although the lipoprotein(a)-autotaxin (ATX)-lysophosphatidic acid axis has been suggested as a potential therapeutic target to prevent the development of FCAVD, supportive evidence using ATX inhibitors is lacking. We here evaluated the therapeutic potency of an ATX inhibitor to attenuate valvular calcification in the FCAVD animal models. METHODS: ATX level and activity in healthy participants and patients with FCAVD were analyzed using a bioinformatics approach using the Gene Expression Omnibus datasets, enzyme-linked immunosorbent assay (ELISA), immunohistochemistry, and western blotting. To evaluate the efficacy of ATX inhibitor, interleukin-1 receptor antagonist-deficient (Il1rn-/-) mice and cholesterol-enriched diet-induced rabbits were used as the FCAVD models, and primary human valvular interstitial cells (VICs) from patients with calcification were employed. RESULTS: The global gene expression profiles of the aortic valve tissue of patients with severe FCAVD demonstrated that ATX gene expression was significantly upregulated and correlated with lipid retention (r = 0.96) or fibro-calcific remodeling-related genes (r = 0.77) in comparison to age-matched non-FCAVD controls. Orally available ATX inhibitor, BBT-877, markedly ameliorated the osteogenic differentiation and further mineralization of primary human VICs in vitro. Additionally, ATX inhibition significantly attenuated fibrosis-related factors' production, with a detectable reduction of osteogenesis-related factors, in human VICs. Mechanistically, ATX inhibitor prohibited fibrotic changes in human VICs via both canonical and non-canonical TGF-ß signaling, and subsequent induction of CTGF, a key factor in tissue fibrosis. In the in vivo FCAVD model system, ATX inhibitor exposure markedly reduced calcific lesion formation in interleukin-1 receptor antagonist-deficient mice (Il1rn-/-, P = 0.0210). This inhibition ameliorated the rate of change in the aortic valve area (P = 0.0287) and mean pressure gradient (P = 0.0249) in the FCAVD rabbit model. Moreover, transaortic maximal velocity (Vmax) was diminished with ATX inhibitor administration (mean Vmax = 1.082) compared to vehicle control (mean Vmax = 1.508, P = 0.0221). Importantly, ATX inhibitor administration suppressed the effects of a high-cholesterol diet and vitamin D2-driven fibrosis, in association with a reduction in macrophage infiltration and calcific deposition, in the aortic valves of this rabbit model. CONCLUSIONS: ATX inhibition attenuates the development of FCAVD while protecting against fibrosis and calcification in VICs, suggesting the potential of using ATX inhibitors to treat FCAVD.

Decline in case rates of youth onset type 2 diabetes in year three of the COVID-19 pandemic.

OBJECTIVES: To determine changes in case rates of youth onset type 2 diabetes in the three years following the COVID-19 pandemic. METHODS: A single-center, retrospective medical record review was conducted for patients newly diagnosed with T2D between 3/1/18 and 2/28/23 at a pediatric tertiary care center. The number of patients referred to CHLA with a T2D diagnosis date between 3/1/2020 and 2/28/2023 was compared to historical rates between 3/1/2018 and 2/29/2020. χ2 or Fisher's exact test was used to compare categorical variables between each year and 2019. RESULTS: Compared to prepandemic baseline (3/1/19-2/29/20, 11.8±3.7 cases/month), there was a significant increase in new T2D monthly case rates in pandemic year 1 (3/1/20-2/28/21, 20.1±6.0 cases/month, 171 %, p=0.005) and pandemic year 2 (3/1/21-2/28/22, 25.9±8.9 cases/month, 221 %, p=0.002). Case rates declined in pandemic year 3 to 14.5±4.1 cases/month (3/1/22-2/28/23, p=0.43). Compared to prepandemic year 1, the frequency of DKA at diagnosis was higher in pandemic year 1 (13.3 vs. 5.0 %, p=0.009). The DKA rate in pandemic years 2 (6.8 %) and 3 (3.4 %) were comparable to prepandemic year 1 (p=0.53 and 0.58, respectively). CONCLUSIONS: Youth onset type 2 diabetes cases and DKA rates in year 3 of the pandemic have returned to prepandemic level.

Concomitant induction of SLIT3 and microRNA-218-2 in macrophages by toll-like receptor 4 activation limits osteoclast commitment.

BACKGROUND: Toll-like receptor 4 (TLR4) conducts a highly regulated inflammatory process by limiting the extent of inflammation to avoid toxicity and tissue damage, even in bone tissues. Thus, it is plausible that strategies for the maintenance of normal bone-immunity to prevent undesirable bone damage by TLR4 activation can exist, but direct evidence is still lacking. METHODS: Osteoclast precursors (OCPs) obtained from WT or Slit3-deficient mice were differentiated into osteoclast (OC) with macrophage colony-stimulating factor (M-CSF), RANK ligand (RANKL) and lipopolysaccharide (LPS) by determining the number of TRAP-positive multinuclear cells (TRAP+ MNCs). To determine the alteration of OCPs population, fluorescence-activated cell sorting (FACS) was conducted in bone marrow cells in mice after LPS injection. The severity of bone loss in LPS injected WT or Slit3-deficient mice was evaluated by micro-CT analysis. RESULT: We demonstrate that TLR4 activation by LPS inhibits OC commitment by inducing the concomitant expression of miR-218-2-3p and its host gene, Slit3, in mouse OCPs. TLR4 activation by LPS induced SLIT3 and its receptor ROBO1 in BMMs, and this SLIT3-ROBO1 axis hinders RANKL-induced OC differentiation by switching the protein levels of C/EBP-ß isoforms. A deficiency of SLIT3 resulted in increased RANKL-induced OC differentiation, and the elevated expression of OC marker genes including Pu.1, Nfatc1, and Ctsk. Notably, Slit3-deficient mice showed expanded OCP populations in the bone marrow. We also found that miR-218-2 was concomitantly induced with SLIT3 expression after LPS treatment, and that this miRNA directly suppressed Tnfrsf11a (RANK) expression at both gene and protein levels, linking it to a decrease in OC differentiation. An endogenous miR-218-2 block rescued the expression of RANK and subsequent OC formation in LPS-stimulated OCPs. Aligned with these results, SLIT3-deficient mice displayed increased OC formation and reduced bone density after LPS challenge. CONCLUSION: Our findings suggest that the TLR4-dependent concomitant induction of Slit3 and miR-218-2 targets RANK in OCPs to restrain OC commitment, thereby avoiding an uncoordinated loss of bone through inflammatory processes. These observations provide a mechanistic explanation for the role of TLR4 in controlling the commitment phase of OC differentiation. Video Abstract.

Institutional role conflict in the digital age: The case of diabetes management at school.

As the prevalence of pediatric diabetes grows and new technologies to manage diabetes emerge, there is increasing concern about consistency in health management across institutional settings, particularly in schools. While much is known about barriers at school, there are still gaps in understanding the institutional dynamics that shape health management in this setting. Using focus groups with 19 youth with type 1 diabetes (T1D) and applying institutional role theory, we find healthcare providers' recommendations conflict with school rules and norms, making it difficult to enact both the "sick role" and the "student role." These conflicts elicit negative responses from teachers and peers and stigmatize youth with T1D in school. Caregiver involvement often heightens rather than ameliorates conflict and teachers do not intervene in effective ways. Ultimately, youth must manage conflicts and stigma. By reframing challenges in health management as institutional role conflict, this paper contributes to sociological research by highlighting the importance of institutional roles, especially beyond healthcare. More broadly, the study suggests health research and policy should investigate how to better align institutional roles-rather than relying on youth and their families-to support health management of chronic illnesses across institutional settings.

Near-peer mentoring and virtual reality for adult basic life support education in high school students.

Bystander cardiopulmonary resuscitation (CPR) can improve cardiac arrest survival; however, lack of willingness or community training lead to low bystander CPR rates. Virtual Reality (VR) Cardiopulmonary Resuscitation (CPR) training among high-school students is an innovative method to train bystander CPR skills. VR is well received by "technology natives" inherent among high school students and induces a greater sense of presence and agency compared to office-based CPR training. We describe a pilot trial with high school students using a near-peer mentoring framework using a single- player VR CPR training software (CBS, TetraSignum, Seoul, KR) in which both students collaboratively coach each other while performing in-VR CPR. Our pilot program recruited 3 pairs (n = 6) high school students during a local summer camp. During each 1.5-hour session, each pair learned about CPR and basic life support through a VR avatar either in-VR or displayed on a TV screen. The in-VR student practiced on the manikin while the other student could take notes on paper. Then each student was assessed on their CPR skills in-VR on a cardiac arrest avatar superimposed onto a real QCPR manikin, coached by the other student who could visualize CPR quality projected on the TV screen. The students then switched roles and debriefed about their experience. Overall, the students universally performed well and appreciated the collaborative nature of the learning experience. Further study is needed to explore barriers and enablers to implementation of VR CPR training at the high school level.

Sphingosine-1-phosphate hinders the osteogenic differentiation of dental pulp stem cells in association with AKT signaling pathways.

Sphingosine-1-phosphate (S1P) is an important lipid mediator that regulates a diverse range of intracellular cell signaling pathways that are relevant to tissue engineering and regenerative medicine. However, the precise function of S1P in dental pulp stem cells (DPSCs) and its osteogenic differentiation remains unclear. We here investigated the function of S1P/S1P receptor (S1PR)-mediated cellular signaling in the osteogenic differentiation of DPSCs and clarified the fundamental signaling pathway. Our results showed that S1P-treated DPSCs exhibited a low rate of differentiation toward the osteogenic phenotype in association with a marked reduction in osteogenesis-related gene expression and AKT activation. Of note, both S1PR1/S1PR3 and S1PR2 agonists significantly downregulated the expression of osteogenic genes and suppressed AKT activation, resulting in an attenuated osteogenic capacity of DPSCs. Most importantly, an AKT activator completely abrogated the S1P-mediated downregulation of osteoblastic markers and partially prevented S1P-mediated attenuation effects during osteogenesis. Intriguingly, the pro-inflammatory TNF-α cytokine promoted the infiltration of macrophages toward DPSCs and induced S1P production in both DPSCs and macrophages. Our findings indicate that the elevation of S1P under inflammatory conditions suppresses the osteogenic capacity of the DPSCs responsible for regenerative endodontics.

Predictive hyperglycemia and hypoglycemia minimization: In-home double-blind randomized controlled evaluation in children and young adolescents.

OBJECTIVE: The primary objective of this trial was to evaluate the feasibility, safety, and efficacy of a predictive hyperglycemia and hypoglycemia minimization (PHHM) system vs predictive low glucose suspension (PLGS) alone in optimizing overnight glucose control in children 6 to 14 years old. RESEARCH DESIGN AND METHODS: Twenty-eight participants 6 to 14 years old with T1D duration ≥1 year with daily insulin therapy ≥12 months and on insulin pump therapy for ≥6 months were randomized per night into PHHM mode or PLGS-only mode for 42 nights. The primary outcome was percentage of time in sensor-measured range 70 to 180 mg/dL in the overnight period. RESULTS: The addition of automated insulin delivery with PHHM increased time in target range (70-180 mg/dL) from 66 ± 11% during PLGS nights to 76 ± 9% during PHHM nights (P<.001), without increasing hypoglycemia as measured by time below various thresholds. Average morning blood glucose improved from 176 ± 28 mg/dL following PLGS nights to 154 ± 19 mg/dL following PHHM nights (P<.001). CONCLUSIONS: The PHHM system was effective in optimizing overnight glycemic control, significantly increasing time in range, lowering mean glucose, and decreasing glycemic variability compared to PLGS alone in children 6 to 14 years old.

Mobile-Based Video Learning Outcomes in Clinical Nursing Skill Education: A Randomized Controlled Trial.

Mobile devices are a regular part of daily life among the younger generations. Thus, now is the time to apply mobile device use to nursing education. The purpose of this study was to identify the effects of a mobile-based video clip on learning motivation, competence, and class satisfaction in nursing students using a randomized controlled trial with a pretest and posttest design. A total of 71 nursing students participated in this study: 36 in the intervention group and 35 in the control group. A video clip of how to perform a urinary catheterization was developed, and the intervention group was able to download it to their own mobile devices for unlimited viewing throughout 1 week. All of the students participated in a practice laboratory to learn urinary catheterization and were blindly tested for their performance skills after participation in the laboratory. The intervention group showed significantly higher levels of learning motivation and class satisfaction than did the control. Of the fundamental nursing competencies, the intervention group was more confident in practicing catheterization than their counterparts. Our findings suggest that video clips using mobile devices are useful tools that educate student nurses on relevant clinical skills and improve learning outcomes.