Differential Changes Research Articles

Light-Emitting Diode Array with Optical Linear Detector Enables High-Throughput Differential Single-Cell Dielectrophoretic Analysis

This paper presents a lens-free imaging approach utilizing an array of light sources, capable of measuring the dielectric properties of many particles simultaneously. This method employs coplanar electrodes to induce velocity changes in flowing particles through dielectrophoretic forces, allowing the inference of individual particle properties from differential velocity changes. Both positive and negative forces are detectable. The light source utilized in this system is composed of LEDs with a wavelength of 470 nm, while detection is performed using a 256-element optical array detector. Measurements with 10 μm polystyrene beads demonstrate this method can resolve changes equivalent to a Clausius–Mossotti factor of 0.18. Simulations in this work, using values from the literature, predict that Clausius–Mossotti factor differences of 0.18 are sufficient to differentiate viable from nonviable cells and cancerous from multidrug-resistant cancerous cells. We demonstrate that for Chinese hamster ovary (CHO) cells, the method can collect a dielectric response spectrum for a large number of cells in several minutes. We demonstrate that for CHO cells, Clausius–Mossotti factor differences of 0.18 can be discriminated. Due to its simple detection apparatus and the utilization of high-throughput, wide, clog-resistant channels, this method holds promise for a wide range of applications.

Implementing the Multi-Disciplinary Expertise Team method to reduce involuntary care in intellectual disability care: multi-methods study evaluating adaptation and effectiveness.

Involuntary care in intellectual disability care may be reduced by deployment of multidisciplinary consultation. The Multi-Disciplinary Expertise Team (MDET) method proved effective in a previous trial on increasing involuntary care reduction. The current study aimed to examine how four organizations adapted MDET during implementation, and tested whether these versions were also effective. Semi-structured interviews with MDET-coordinators were analyzed using the Framework Reporting Adaptions and Modifications-Expanded. A quasi-experimental interrupted time-series design tested change in weekly counts of involuntary care recordings from before to during MDET implementation, in care homes that implemented MDET (n = 24) compared to care homes providing care-as-usual (CAU). Adaptations to MDET varied. These included implementing MDET without an independent MDET-team and loosening recordings of involuntary care. No differential changes in recordings were found between the implementation- and CAU-groups. Scaling-out MDET to other organizations led to adaptations that may have undermined its effects on reducing involuntary care.

Application of the Rasch Model to the Evaluation of Biological Problems

Evaluation of student abilities in Biology subjects often faces challenges in ensuring that the instruments used actually measure what they are supposed to measure. The data analysis used is the Rasch model, which is part of item response theory, offering a more accurate approach in analyzing evaluation data. This model allows the identification of items that are inappropriate or too difficult, as well as providing more in-depth information about individual student abilities. Through analysis of instruments and question items from 30 multiple choice questions that emphasize critical thinking skills, the aim of this research is to assess the quality of Biology questions for class X SMA. Testing was carried out using WinStep software and Rasch modeling analysis on 166 students from five high schools/vocational schools. The research method used is quantitative. The results of the instrument investigation show that the issue has very good dependability and the unidimensionality of the instrument is indicated by unexplained changes in the first differentiation. These results show that the Rasch test can help educators in selecting questions that meet the evaluation criteria and contribute to improving the quality of national education. The implications of this research are By applying the Rasch Model, educators can develop more accurate and fair evaluation tools, which are able to identify individual student difficulties and strengths.

MADRS single items differential changes among patients with melancholic and unspecified depression treated with ECT: an exploratory study.

Major depressive disorder (MDD) exhibits heterogeneity in treatment response. This exploratory analysis aims to evaluate the differential changes in individual items of the MADRS between melancholic MDD (M-MDD) and unspecified MDD (U-MDD) following electroconvulsive therapy (ECT). The study included 23 patients with unipolar MDD who received ECT. Patients were classified as M-MDD or U-MDD according to DSM-5 criteria. MADRS scores were assessed at baseline and one-month post-ECT. Differences between subtypes were analyzed using the Wilcoxon test and multiple linear regression. Among 23 participants receiving ECT for MDD, 10 had M-MDD and 13 had U-MDD. Baseline MADRS items showed significantly higher scores in the M-MDD group, except for reported sadness, suicidal ideation, and concentration difficulties. Total MADRS score reduction was significantly greater in the M-MDD group. This decline was especially pronounced in M-MDD patients for specific items, including apparent sadness, inability to feel, pessimistic thoughts, sleep disturbances, reduced appetite, and concentration difficulties, after adjusting for age and sex. MADRS score reductions were more substantial for M-MDD than U-MDD in both total and specific items following one month of ECT. Further research with larger samples is needed to clarify MADRS response differences after ECT between melancholic and unspecified depressive subtypes.

Electroacupuncture alleviates cerebral ischemia injury by regulating PI3K/AKT/NF-κB signaling in microglia of ischemic stroke rats.

This study aimed to investigate the potential of electroacupuncture as an intervention for inducing 'Awakening and Opening of the Brain' in rats with stroke models induced by middle cerebral artery occlusion/reperfusion (MCAO/R). The efficacy of electroacupuncture in alleviating cerebral ischemic injury was evaluated using Longa scores, triphenyl tetrazolium chloride staining, and hematoxylin and eosin staining. Non-targeted metabolomics analysis was conducted to identify differential metabolite changes before and after electroacupuncture treatment in MCAO/R rats. Network pharmacology analysis was then performed to correlate these differential metabolites with ischemic stroke. The PI3K/AKT/NF-κB signaling pathway was identified as a key target. In vivo experiments further validated the mechanism by which electroacupuncture promotes M2 microglial polarization through inhibition of the PI3K/AKT/NF-κB signaling in MCAO/R rats. This study demonstrated that electroacupuncture reduces brain damage and inhibits inflammation in MCAO/R rats by modulating the PI3K/AKT/NF-κB signaling pathway and promoting the polarization of microglia from M1 to M2.

Cable fault diagnosis with generalization capability using incremental learning and deep convolutional neural network

Power cable faults may exhibit dynamic and differential changes attributable to variations in operating times and environmental conditions. However, the existing artificial intelligence (AI)-based fault diagnosis methods are lack of capability to handle this complexity of fault development. They can only diagnose given faulty types and will malfunction when dealing with newly-emerged faults, which accounts for the lack of generalization capability for AI-based methods. Given that, this paper proposes a cable fault diagnosis method with generalization capability utilizing incremental learning and deep convolutional neural network (DCNN). The idea of knowledge distillation is introduced to reserve the diagnosis information of the DCNN for original faults, and meanwhile, the DCNN is also modified by the classification loss of newly-emerged faulty samples, which equips the DCNN with generalization capability. The category features are obtained utilizing the refined DCNN, and sent to the constructed classifier for accurate incremental fault diagnosis. Experiments are conducted with field and simulated data. The obtained results validate the feasibility and effectiveness of the proposed method.

Acid-sensing ion channel-1 contributes to the failure of myelin sheath regeneration following spinal cord injury by transcellular delivery of PGE2

BackgroundTraumatic injuries to spinal cord lead to severe motor, sensory, and autonomic dysfunction. The accumulation of inhibitory compounds plays a pivotal role in the secondary damage to sparing neural tissue and the failure of axonal regeneration and remyelination. Acid-sensing ion channel-1(ASIC1A) is widely activated following neurotrauma, including spinal cord injury (SCI). However, its role in SCI remains elusive.MethodsThe effects of acidic environment on the differentiation and genes changes of neural stem cells (NSCs) were assessed by immunofluorescence staining and RNA-sequencing analysis, respectively. The expression of ASIC1A and prostaglandin endoperoxide synthase 2 (PTGS2) were detected by western blot and immunofluorescence staining. The concentration of prostaglandin E2 (PGE2) within NSC-derived extracellular vesicles were evaluated by ELISA. Small-interfering RNAs (siRNAs) were used to knock down Asic1a and Ptgs2 expression in NSCs. The myelin sheath regeneration and axonal remyelination in rats and Asic1a-KO mice were assessed by immunofluorescence staining.ResultsFollowing injury to the spinal cord, ASIC1A was found to be colocalized and upregulated in NSCs. ASIC1A activation prevents the differentiation of NSCs into oligodendrocytes by upregulating PTGS2, which leads to increased production and release of PGE2 within extracellular vesicles (EVs). ASIC1A or PTGS2 deficiency in NSCs counters the ASIC1A-related effects on mediating NSC differentiation by reducing PGE2 expression within NSC-derived EVs. Furthermore, intervention in ASIC1A signaling by administration of ASIC1A inhibitors or genetic deletion of ASIC1A demonstrated a pronounced advantage in enhancing myelin sheath regeneration and axonal remyelination.ConclusionsThe activation of ASIC1A prevents NSC differentiation into oligodendrocytes via the transcellular NSC-to-NSC delivery of PGE2, resulting in the failure of myelin sheath regeneration and axonal remyelination following SCI. The inhibition of ASIC1A presents a promising therapeutic strategy for the treatment of SCI.Graphical

Highland barley ELNs and physiological responses to different concentrations of Cr (VI) stress.

This study is the first to use highland barley (HB) to study the toxic effects of Cr (VI) on seedlings and the response mechanism of HELNs to Cr (VI) stress. The outcomes indicated that the germination rate of HB seeds, plant height, root length, water content, and levels of proline (PRO) and soluble sugar in both leaves and roots were all impacted by varying concentrations of Cr (VI) treatments. Differential changes in the activities of antioxidant enzymes (SOD, POD, CAT) were observed in leaves and roots of HB. We also extracted HB-derived ELNs (HELNs) and characterized and sequenced HELNs. The average particle size of CK-HELNs was 79.0 nm, and the concentration of HELNs was 4.56 E+10 (particles/mL). As the concentration of Cr (VI) increased, the particle size of HELNs in HB seedlings also increased, while the concentration decreased. A total of 29 miRNA species were identified in CK-HELNs, Cr10-HELNs, and Cr40-HELNs. Out of these, 25 were newly predicted miRNAs, and the remaining four were known miRNAs. A total of 2 known miRNAs and 11 novel miRNAs were upregulated under different concentrations of Cr (VI) stress. 1 known and 5 novel miRNAs were downregulated under different concentrations of Cr (VI) stress. Enrichment of the GO and KEGG pathways revealed that the differential gene functions were mainly focused on binding and catalytic activities. This study reveals for the first time the changes of HELNs under different concentrations of Cr (VI) stress and the toxic effects of Cr (VI) on HB seedlings. This study provides a new perspective to explore the function and utilisation of ELNs.

Signaling pathways and bone marrow microenvironment in myelodysplastic neoplasms

Key signaling pathways within the bone marrow microenvironment (BMM), such as Notch, Phosphoinositide-Specific Phospholipase C (PI-PLCs), Transforming Growth Factor β (TGF-β), and Nuclear Factor Kappa B (NF-κB), play a vital role in the progression of myelodysplastic neoplasms (MDS). Among the various BMM cell types, mesenchymal stromal cells (MSCs) are particularly central to these pathways. While these signaling routes can independently affect both MSCs and hematopoietic stem cells (HSCs), they most importantly alter the dynamics of their interactions, leading to abnormal changes in survival, differentiation, and quiescence. Notch and PI-PLC signaling facilitate intercellular communication, TGF-β promotes quiescence and suppresses hematopoiesis, and NF-κB-driven inflammatory responses foster an environment detrimental to normal hematopoiesis. This review highlights the role of these pathways within the MDS microenvironment, driving the development and progression of the disease and paving the way for new possible therapeutic strategies.

BRD4 sustains p63 transcriptional program in keratinocytes

Here, we investigated the potential interaction between bromodomain-containing protein 4 (BRD4), an established epigenetic modulator and transcriptional coactivator, and p63, a member of the p53 transcription factor family, essential for epithelial development and skin homeostasis. Our protein–protein interaction assays demonstrated a strong and conserved physical interaction between BRD4 and the p53 family members—p63, p73, and p53—suggesting a shared binding region among these proteins. While the role of BRD4 in cancer development through its interaction with p53 has been explored, the effects of BRD4 and Bromodomain and Extra Terminal (BET) inhibitors in non-transformed cells, such as keratinocytes, remain largely unknown. Our functional analyses revealed changes in cellular proliferation and differentiation in keratinocytes depleted of either p63 or BRD4, which were further supported by using the BRD4 inhibitor JQ1. Transcriptomic analyses, chromatin immunoprecipitation, and RT-qPCR indicated a synergistic mechanism between p63 and BRD4 in regulating the transcription of keratinocyte-specific p63 target genes, including HK2, FOXM1, and EVPL. This study not only highlights the complex relationship between BRD4 and p53 family members but also suggests a role for BRD4 in maintaining keratinocyte functions. Our findings pave the way for further exploration of potential therapeutic applications of BRD4 inhibitors in treating skin disorders.

Effect of glucocerebrosidase on human bone marrow multipotent mesenchymal stromal

Introduction. During enzyme replacement therapy in patients with Gaucher disease (GD) with recombinant glucocerebrosidase (GCase), regression of bone manifestations is possible, but with prolonged therapy osteonecrosis may occur. These changes may be due to impaired differentiation of multipotent mesenchymal stromal cells (MSCs).Aim: to study changes in the MSCs of healthy donors and a patient with GD when cultured in the presence of GCase.Material and methods. MSCs were isolated from the bone marrow of 17 healthy donors and a female patient with GD by a standard method and cultured in the presence of various concentrations of GCase after the second passage from 2 to 7 weeks. Cell proliferation and the ability to differentiate were analyzed, including after induction. The assessment was carried out by differential staining, elution, and expression of differentiation marker genes by real-time PCR.Results. Low concentrations of recombinant GCase (0.25–1.5 U/ml) did not affect the proliferative activity of MSCs. Prolonged cultivation of MSCs in the presence of low doses of GCase led to a change in the differentiation potential of these cells in the direction of adipogenesis. Concentrations of GCase of 3–5 U/ml inhibited the proliferation of MSCs and caused significant changes in cell differentiation. High doses of the enzyme (7–10 U/ml) had a cytotoxic effect and led to cell death within one passage. The proliferative and differentiation potential of the MSCs of a patient with GD differed significantly from the cells of healthy donors in all the parameters studied.Conclusion. The cultivation of donor MSCs in the presence of recombinant GCase alters the proliferation and differentiation potential of these cells. These changes depend on the dose of the enzyme in the medium and the duration of cultivation.

Transient receptor potential a1b regulates primordial germ cell numbers and sex differentiation in developing zebrafish.

Temperature is a leading environmental factor determining the sex ratio of some animal populations, such as fish, amphibians, and reptiles. However, the underlying mechanism by which temperature affects gender is still poorly understood. Transient receptor potential a1b (Trpa1b) belongs to the ion channel family of transient receptor potentials and exhibits dual thermosensitivity to heat and cold. In this study, we have unveiled a novel function of the trpa1b gene. Zebrafish generated through clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 with Trpa1b-null manifest a male-biased sex ratio. The quantity of primordial germ cells (PGCs) in zebrafish is closely linked to gender determination and gonadal development. Yet the role of the trpa1b gene in zebrafish reproductive development remains unexplored in the literature. Our investigation revealed a significant reduction in PGCs in Trpa1b mutant zebrafish compared to their wild-type counterparts 24-h postfertilization (hpf). Transcriptome sequencing of tissues near the reproductive crest of embryos at 1.25 days postfertilization (dpf) revealed differential changes in PGC-related marker genes and genes related to sperm cell development and differentiation. The relative expression of ddx4 and sycp3 genes was significantly downregulated, whereas amh was significantly upregulated at 20 dpf in trpa1b-/- zebrafish. The results of this study provide valuable insights and references for studying the molecular mechanism of sex determination in zebrafish. Undoubtedly, these results will further enhance our understanding of gender differentiation and gonadal development in fish and other vertebrates.

Lead exposure at the feto-maternal interface: A cause for concern for fetal membrane trophoblasts.

The integrity of fetal membranes enables biological functions that protect the fetus and maintain the pregnancy. Any compromise in fetal membrane function can predispose a pregnant woman to prelabor rupture of the membranes (pPROM) and subsequently to preterm birth (PTB). Epidemiologic data suggest that lead exposure during pregnancy is one of several risk factors associated with PTB and pPROM. This heavy metal can cross placental and fetal membrane barriers, disrupting homeostasis in these tissues. Autophagy contributes to the maintenance of fetal membrane homeostasis during gestation, and dysfunctional autophagy is associated with pPROM. In this study, we determined the mechanistic impact of lead-induced cellular changes, autophagy, senescence, and inflammation in chorion trophoblast cells (CTCs) and amnion epithelial cells (AECs) of the fetal membranes. Lead exposure in CTCs induced autophagy disfunction (increase in LC3B-II), augmented senescence (increased SA-β-galactosidase activity) and increased the release of inflammation. In AECs, lead exposure did effect autophagy, senescence, nor inflammation. The differential changes observed in CTCs and AECs after exposure to high lead concentrations may promote the weakening of fetal membranes and contribute to preterm rupture.

Outcome of SARS-CoV-2 reinfection depends on genetic background in female mice

Antigenically distinct SARS-CoV-2 variants increase the reinfection risk for vaccinated and previously exposed population due to antibody neutralization escape. COVID-19 severity depends on many variables, including host immune responses, which differ depending on genetic predisposition. To address this, we perform immune profiling of female mice with different genetic backgrounds –transgenic K18-hACE2 and wild-type 129S1– infected with the severe B.1.351, 30 days after exposure to the milder BA.1 or severe H1N1. Prior BA.1 infection protects against B.1.351-induced morbidity in K18-hACE2 but aggravates disease in 129S1. H1N1 protects against B.1.351-induced morbidity only in 129S1. Enhanced severity in B.1.351 re-infected 129S1 is characterized by an increase of IL-10, IL-1β, IL-18 and IFN-γ, while in K18-hACE2 the cytokine profile resembles naïve mice undergoing their first viral infection. Enhanced pathology during 129S1 reinfection cannot be attributed to weaker adaptive immune responses to BA.1. Infection with BA.1 causes long-term differential remodeling and transcriptional changes in the bronchioalveolar CD11c+ compartment. K18-hACE2 CD11c+ cells show a strong antiviral defense expression profile whereas 129S1 CD11c+ cells present a more pro-inflammatory response upon restimulation. In conclusion, BA.1 induces cross-reactive adaptive immune responses in K18-hACE2 and 129S1, but reinfection outcome correlates with differential CD11c+ cells responses in the alveolar space.

HSP60 inhibits DF-1 apoptosis through its mitochondrial signal peptide

HSP60 is implicated in many biological functions and plays a key role in maintaining oxidative stress and preserving mitochondrial integrity. Our previous study showed that HSP60 inhibits apoptosis. In this study, we further investigated the mechanism of apoptosis inhibition by HSP60. First, the CRISPR-Cas9 system was employed to establish the HSP60 knockout DF-1 cell line (DF-1-HSP60-KO), and the apoptosis level of DF-1-HSP60-KO cell line was assessed by flow cytometry and ELISA apoptosis kit. Then, the effect of knockdout of HSP60 on relevant apoptotic factors was assessed by Western blotting and RT-PCR analysis. The results showed that compared with the control DF-1 cells, HSP60 knockdout cells indicated significantly increased apoptosis rates, decreased Bax expression, and enhanced Caspase 3 expression. This suggests that the HSP60 knockout induces apoptosis by up-regulating Caspase 3 and down-regulating Bax expression. The structure of the HSP60 mitochondrial signal peptide (MIT) protein was predicted using Pymol software, which revealed that His amino acid at the 21st position affects its spatial structure. In addition, the transfection of HSP60 mutant protein (TB) into DF-1-HSP60-KO cells and induction with Bardoxolone MethyI significantly increased the apoptosis rates and reduced cell viability compared to the wild-type HSP60 group, inducing differential changes in genes such as Bax, Bak, and Bcl-2. Together, these findings suggest that the HSP60 MIT's His amino acid at site 21 modulates the levels of genes associated with the apoptosis signaling pathway, thereby inhibiting apoptosis. This study reveals the regulatory role of HSP60 in apoptosis through its mitochondrial signal peptide, which will have potential medical value.

Identification of the NAC Family and a Functional Analysis of NoNAC36a Under Flooding Stress in Watercress (Nasturtium officinale R.Br.)

Watercress (Nasturtium officinale R.Br.) is a cruciferous aquatic vegetable that possesses significant nutritional value. The NAC family is a transcription factor family specific to plants that play an important role in regulating plant responses to abiotic stress. In order to investigate the response of NAC genes to flooding stress in watercress, we conducted a study on the NoNAC family. In this study, a total of 119 NoNAC genes were obtained through genome-wide identification. Phylogenetic analysis indicated that the NoNAC family members can be categorized into ten subgroups. The results of gene structure analysis revealed that each branch within the subgroups exhibited similar motif composition and gene structure. The heatmap analysis showed that several NoNAC genes demonstrated tissue-specific expression patterns, suggesting their potential as regulators of associated tissue development. As an aquatic plant, watercress serves as a valuable material for investigating plant resistance to flooding stress. This study found that flooding can significantly increase the watercress plant height, which is a typical escape strategy under flooding. The analysis of the expression of NoNAC genes in the stem transcriptome after flooding indicated that only NoNAC36a consistently exhibited significant differential changes and down-regulated expression at the three time points of flooding treatment. This suggests that NoNAC36a may be involved in regulating watercress plant height increases under flooding stress. The utilization of a virus-induced gene silencing assay to investigate the biological function of NoNAC36a revealed that NoNAC36a silencing caused cell elongation and expansion, thus increasing watercress plant height. The yeast one-hybrid and dual luciferase assays demonstrated that NoNAC36a binds the promoter of NoXTH33 and inhibits its expression. Subsequently, the results of yeast two-hybrid, luciferase complementary, and pull-down assays revealed the interaction between NoMOB1A and NoNAC36a in vivo and in vitro. Sequence alignment indicated that NoMOB1A and AtMOB1A share an identical amino acid sequence. RT-qPCR analysis indicated that flooding prompted the expression of NoMOB1A in stems. Thus, it is speculated that NoMOB1A may exhibit functions similar to AtMOB1A and that the up-regulation of NoMOB1A expression in stems may facilitate an increase in plant height under flooding. In summary, the NoNAC family was analyzed, and revealed a regulatory network centered on NoNAC36a that facilitates watercress resistance to flooding stress. This study enhanced the understanding of the NoNAC genes and established a theoretical foundation for investigating plant flooding tolerance.

Abstract 4138426: Geographic Disparities in Cardiometabolic Health Widened Across US States Between 2011 and 2021

Background: Geographic inequities in cardiovascular mortality are pervasive in the US. Pandemic-related delays in screening and treatment, economic loss, and worsening social determinants may have widened geographic disparities in cardiometabolic health, particularly in states that were hardest hit by these spillover effects. Understanding changes in state-based inequities could inform targeted public health efforts to advance cardiovascular health. Questions: Did the prevalence of cardiometabolic risk factors (diabetes, hypertension, hyperlipidemia, obesity) and lifestyle factors (alcohol consumption, physical inactivity, tobacco use) change between 2011 and 2021? How did between-state differences change over this period? Methods: We included adults from the CDC’s Behavioral Risk Factor Surveillance System. Survey-weighted logistic regressions models were used to calculate age and sex-adjusted risk difference between states with the highest and lowest adjusted prevalence rates of each risk factor in 2011 and 2011, respectively. An interaction term for state and year was included to assess for differential changes in between-state disparities. Results: From 2011 to 2021, there were increases in the age- and sex-adjusted prevalence of diabetes (10.9% [95% CI, 10.7,11.0] to 12.4% [12.2,12.6]), hypertension (32.4% [32.1,32.7] to 33.7% [33.4,34.0]), and obesity (27.5% [27.2,27.7] to 33.1% [32.8,33.5]). Geographic inequities widened, with increases in the difference between states with the highest vs lowest prevalence of diabetes (5.7% [5.3,6.1] to 7.8% [7.3,8.3]), hypertension (14.2% [13.6,14.8] to 17.2% [16.4,17.9]) and obesity (14.3% [13.6,15.0] to (15.7% [14.7,16.7]) (Table). The prevalence of alcohol consumption (18.0% [17.7,18.2] to 15.6% [15.3,15.8]), physical inactivity (25.7% [25.4,27.4] to 24.0% [23.6,23.7]), and tobacco use (44.9% [44.5,45.3] to 36.3% [35.8,36.8]) decreased, and between-state differences did not widen. Conclusion: In this national study, the prevalence of hypertension, obesity, and diabetes increased from 2011 to 2021, and state-based inequities widened. Our findings highlight the urgent need for public health interventions to address widening state-based disparities in cardiometabolic health.

Online driver license renewal and road user injury and fatality in Washington State

Objectives Washington State implemented a new policy in 2004 that allowed drivers younger than 70 years old to renew their driver license by mail or online at every other renewal. Drivers aged 70 years and older were still required to renew in-person every 6 years. The purpose of this study was to evaluate whether this policy change was associated with motor vehicle crash (MVC) injury and fatality among drivers, non-drivers, and all road users aged 45–69 years. Methods Controlled interrupted time series analysis models were fit to compare injury and fatality rates for these road users affected by the requirement to older road users not affected by the requirement (70 years and older). Differential level and slope changes in injury and fatality rates were used to estimate associations with the change in the license renewal requirement. Results We did not find evidence that implementation of online driver license renewal in Washington was associated with increased injury or fatality rates among drivers, non-drivers, or all road users aged 45–69 years relative to those aged 70 years and older. Conclusions Allowing driver license renewal online or by mail at every other renewal appears to be a safe strategy for less restrictive driver licensing for drivers aged 45–69 years. Future research should continue to evaluate the potential impacts of in-person and online renewal policies.

Structural and Functional Properties of Lower Extremity Tendons in Men.

Comstock, BA, Flanagan, SD, Denegar, CR, Newton, RU, Häkkinen, K, Volek, JS, Maresh, CM, Kraemer, WJ. Structural and functional properties of lower extremity tendons in men. J Strength Cond Res XX(X): 000-000, 2024-The purpose of this study was to understand further patellar and Achilles tendon structure and function, body composition, and serum collagen turnover biomarkers in young men who performed heavy resistance training (RT, n = 13, age: 22.2 ± 1.4 years) compared with recreationally active men who were not resistance-trained (NR, n = 13, age: 22.8 ± 2.2 years). Tendon properties were measured at rest and during maximal voluntary isometric efforts using ultrasonography and dynamometry. Lean body mass (LBM) and bone mineral density (BMD) were assessed with dual X-ray absorptiometry. Serum collagen turnover markers were analyzed and related to tendon measures. Resistance-trained men had significantly (p ≤ 0.05) greater LBM and BMD compared with recreationally active men. Resistance-trained men also showed significantly greater patellar tendon (PT) stiffness (45%) and Young's modulus (36%), though the PT cross-sectional area (CSA) did not differ significantly between groups. Achilles tendon CSA was significantly larger in resistance-trained men. Still, other properties such as stiffness and modulus did not differ significantly between the groups. Serum collagen turnover markers showed no significant differences between groups and were not correlated to any tendon or bone biomarkers. The findings support that resistance-trained men have greater LBM and BMD. However now, it reveals that tendon adaptations differ, as not all measures were similarly affected in both tendons. The blood biomarkers did not show any obvious roles in explaining the differential changes in tendons. Heavy RT induces differential tendon changes potentially due to complex interactions of training variables.

Race/Ethnic Differences in In-Hospital Mortality after Acute Ischemic Stroke.

Stroke mortality has declined, with differential changes by race; stroke is now the 5th leading cause of death overall, but 2nd leading cause of death in Black individuals. Little is known about recent race/ethnic and sex trends in in-hospital mortality after acute ischemic stroke (AIS) and whether system-level factors contribute to possible differences. Using the National Inpatient Sample, adults (≥18 years) with a primary diagnosis of AIS from 2006 to 2017 (n=643,912) were identified. We assessed in-hospital mortality by race/ethnicity (White, Black, Hispanic, Asian/Pacific Islander [API], other), sex, and age. Hospitals were categorized by proportion of White patients served: "75% White hospitals", "50-75% White hospitals", and "<50% White hospitals". Using survey adjusted logistic regression, the association between race/ethnicity and odds of mortality was assessed, adjusting for key sociodemographic, clinical, and hospital characteristics (e.g., age, comorbidities, stroke severity, do not resuscitate orders, and palliative care). Overall, mortality decreased from 5.0% in 2006 to 2.9% in 2017 (p<0.001). Comparing 2012-2017 to 2006-2011, there was a 68% reduction in mortality odds overall after adjusting for covariates, most prominent in White individuals (69%) and smallest in Black individuals (57%). Compared to White patients, Black and Hispanic patients had lower odds of mortality (adjusted odds ratio (aOR) 0.82, 95% CI 0.78-0.87 and aOR 0.93, 95% CI 0.87-1.00), primarily driven by those >65 years (age x ethnicity interaction p < 0.0001). Compared to White men, Black, Hispanic, and API men, and Black women had lower aOR of mortality. The differences in mortality between White and all the other race/ethnic groups combined were most pronounced in 75% White hospitals (aOR 0.80, 0.74-0.87) compared to 50-75% White hospitals (aOR 0.85, 0.79-0.91) and <50% White hospitals (aOR 0.88, 0.81-0.95; interaction effect: p=0.005). AIS mortality decreased dramatically in recent years in all race/ethnic subgroups. Overall, while individuals of other race/ethnic subgroups had lower mortality odds compared to White individuals, this effect was significantly lower in hospitals serving predominantly White patients compared to those serving minority populations. White patients had higher , mortality than the other race/ethnic groups, a difference that was most striking in hospitals predominantly serving White patients. Further study is needed to understand these differences and to what extent sociocultural, biological, and system-level factors play a role.