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In this qualitative study, we analyzed the processes of a collaborative online international learning (COIL) collaboration between two higher education institutions in Japan and the United States from the perspective of the technological, pedagogical, and content knowledge (TPACK) framework. The research question this study aimed to address was: What is the utility of the TPACK framework, as a lens of analysis, for this online cultural exchange? To address this question, we conducted semi-structured interviews with student participants and examined their written works. From the student participants' learning experiences, we identified evidence of cultural exchange as well as evidence of missed opportunities for cultural exchange arising from the limited knowledge of technology, pedagogy, content, and culture. COIL and TPACK both share a common goal of increasing students' access to multiple knowledge systems using educational technology. As a result, COIL conceptually aligns well with the TPACK framework. This collaboration showed an ongoing need for the centering of cultural knowledge and cultural exchange in both COIL and TPACK. We, accordingly, outline potential for a TPACCK, a modified TPACK framework to center cultural knowledge in both with the hope of taking steps towards a more culturally sustaining framework of international collaboration.

As a field established on improving the lives of individuals, families, and communities, Family and Consumer Sciences (FCS) is well-positioned to address the challenges and opportunities faced by justice-involved families (Nickols et al., 2009). From reentry and rehabilitation to parenting and family relationships, the support of justice-involved families is intrinsically linked to individual well-being, family strengths, and community vitality. Embedded within the FCS Body of Knowledge (BOK), the integrative element of human ecosystems provides practitioners with a lens for viewing the justice system's impact on families. The foundation of FCS emphasizes the importance of strong family relationships. For justice-involved families, these relationships may be strained due to the effects of incarceration. Multiple barriers, within and outside of the justice system, can impact a family's ability to interact and communicate with their justice-involved loved ones. Using the BOK as a model for practice, this paper details five ways in which the FCS profession can utilize the foundations of the field to support justice-involved families.

ObjectiveMitophagy removes damaged mitochondria to maintain cellular homeostasis. Aryl hydrocarbon receptor (AhR) expression in the liver plays a crucial role in supporting normal liver functions, but its impact on mitochondrial function is unclear. Here, we identified a new role of AhR in the regulation of mitophagy to control hepatic energy homeostasis.MethodsIn this study, we utilized primary hepatocytes from AhR knockout (KO) mice and AhR knockdown AML12 hepatocytes. An endogenous AhR ligand, kynurenine (Kyn), was used to activate AhR in AML12 hepatocytes. Mitochondrial function and mitophagy process were comprehensively assessed by MitoSOX and mt-Keima fluorescence imaging, Seahorse XF-based oxygen consumption rate measurement, and Mitoplate S-1 mitochondrial substrate utilization analysis.ResultsTranscriptomic analysis indicated that mitochondria-related gene sets were dysregulated in AhR KO liver. In both primary mouse hepatocytes and AML12 hepatocyte cell lines, AhR inhibition strongly suppressed mitochondrial respiration rate and substrate utilization. AhR inhibition also blunted the fasting response of several essential autophagy genes and the mitophagy process. We further identified BCL2 interacting protein 3 (BNIP3), a mitophagy receptor that senses nutrient stress, as an AhR target gene. AhR is directly recruited to the Bnip3 genomic locus, and Bnip3 transcription was enhanced by AhR endogenous ligand treatment in wild-type liver and abolished entirely in AhR KO liver. Mechanistically, overexpression of Bnip3 in AhR knockdown cells mitigated the production of mitochondrial reactive oxygen species (ROS) and restored functional mitophagy.ConclusionsAhR regulation of the mitophagy receptor BNIP3 coordinates hepatic mitochondrial function. Loss of AhR induces mitochondrial ROS production and impairs mitochondrial respiration. These findings provide new insight into how endogenous AhR governs hepatic mitochondrial homeostasis.

Protein- and peptide-based proton-conducting biomaterials have been touted as particularly promising for bioelectronics applications because of their advantageous chemical and physical characteristics, typically excellent biocompatibilities, and readily understood electrical properties. Within this context, our laboratory has previously discovered and systematically investigated bulk proton conduction for a unique family of cephalopod structural proteins called reflectins. Herein, we leverage a combination of experimental and computational methodologies to investigate the bulk electrical properties of hierarchically nanostructured films self-assembled from a previously reported truncated reflectin variant. Our findings indicate that the truncated reflectin variant exhibits protonic conductivities and associated figures of merit on par with those reported for both full-length reflectins and other proteinaceous proton-conducting materials. The combined studies enhance current understanding of reflectins’ functional properties within the framework of bioengineering and bioelectronics applications and may ultimately facilitate the development of other protein- and peptide-based conductive biomaterials.

Knowledge of drug concentrations in the brains of behaving subjects remains constrained on a number of dimensions, including poor temporal resolution and lack of real-time data. Here, however, we demonstrate the ability of electrochemical aptamer-based sensors to support seconds-resolved, real-time measurements of drug concentrations in the brains of freely moving rats. Specifically, using such sensors, we achieve 1.5 hours. These results demonstrate the utility of such sensors in (i) the determination of the site-specific, seconds-resolved neuropharmacokinetics, (ii) enabling the study of individual subject neuropharmacokinetics and concentration-response relations, and (iii) performing high-precision control over intracranial drug levels.

The microenvironment that surrounds pancreatic ductal adenocarcinoma (PDAC) is profoundly desmoplastic and immunosuppressive. Understanding triggers of immunosuppression during the process of pancreatic tumorigenesis would aid in establishing targets for effective prevention and therapy. Here, we interrogated differential molecular mechanisms dependent on cell of origin and subtype that promote immunosuppression during PDAC initiation and in established tumors. Transcriptomic analysis of cell-of-origin-dependent epithelial gene signatures revealed that Nt5e/CD73, a cell-surface enzyme required for extracellular adenosine generation, is one of the top 10% of genes overexpressed in murine tumors arising from the ductal pancreatic epithelium as opposed to those rising from acinar cells. These findings were confirmed by IHC and high-performance liquid chromatography. Analysis in human PDAC subtypes indicated that high Nt5e in murine ductal PDAC models overlaps with high NT5E in human PDAC squamous and basal subtypes, considered to have the highest immunosuppression and worst prognosis. Multiplex immunofluorescent analysis showed that activated CD8+ T cells in the PDAC tumor microenvironment express high levels of CD73, indicating an opportunity for immunotherapeutic targeting. Delivery of CD73 small-molecule inhibitors through various delivery routes reduced tumor development and growth in genetically engineered and syngeneic mouse models. In addition, the adenosine receptor Adora2b was a determinant of adenosine-mediated immunosuppression in PDAC. These findings highlight a molecular trigger of the immunosuppressive PDAC microenvironment elevated in the ductal cell of origin, linking biology with subtype classification, critical components for PDAC immunoprevention and personalized approaches for immunotherapeutic intervention.SignificanceDuctal-derived pancreatic tumors have elevated epithelial and CD8+GZM+ T-cell CD73 expression that confers sensitivity to small-molecule inhibition of CD73 or Adora2b to promote CD8+ T-cell-mediated tumor regression. See related commentary by DelGiorno, p. 977.

Abstract While Prospect Theory helps to explain decision-making under risk, studies often base frames on hypothetical events and fail to acknowledge that many individuals lack the ability and motivation to engage in complex thinking. We use an original survey of US adults (N = 2813) to test Prospect Theory in the context of the May 2023 debt ceiling negotiations in the US Congress and assess whether objective numeracy moderates framing effects. We hypothesize and find evidence to suggest that most respondents are risk-averse to potential gains and risk-accepting to potential losses; however, high numerates are more risk-averse and risk-accepting to gains and losses, respectively, than low numerates. We also find that need for cognition interacts with numeracy to moderate framing effects for prospective losses, such that higher need for cognition attenuates risk-acceptance among low numerates and exacerbates risk-acceptance among high numerates. Our results are robust to a range of other covariates and in models accounting for the interaction between political knowledge and need for cognition, indicating joint moderating effects from two knowledge domains similarly conditioned by the desire to engage in effortful thinking. Our findings demonstrate that those who can understand and use objective information may remain subjectively persuaded by certain policy frames.

Abstract Background B-type lamins are critical nuclear envelope proteins that interact with the three-dimensional genomic architecture. However, identifying the direct roles of B-lamins on dynamic genome organization has been challenging as their joint depletion severely impacts cell viability. To overcome this, we engineered mammalian cells to rapidly and completely degrade endogenous B-type lamins using Auxin-inducible degron technology. Results Using live-cell Dual Partial Wave Spectroscopic (Dual-PWS) microscopy, Stochastic Optical Reconstruction Microscopy (STORM), in situ Hi-C, CRISPR-Sirius, and fluorescence in situ hybridization (FISH), we demonstrate that lamin B1 and lamin B2 are critical structural components of the nuclear periphery that create a repressive compartment for peripheral-associated genes. Lamin B1 and lamin B2 depletion minimally alters higher-order chromatin folding but disrupts cell morphology, significantly increases chromatin mobility, redistributes both constitutive and facultative heterochromatin, and induces differential gene expression both within and near lamin-associated domain (LAD) boundaries. Critically, we demonstrate that chromatin territories expand as upregulated genes within LADs radially shift inwards. Our results indicate that the mechanism of action of B-type lamins comes from their role in constraining chromatin motion and spatial positioning of gene-specific loci, heterochromatin, and chromatin domains. Conclusions Our findings suggest that, while B-type lamin degradation does not significantly change genome topology, it has major implications for three-dimensional chromatin conformation at the single-cell level both at the lamina-associated periphery and the non-LAD-associated nuclear interior with concomitant genome-wide transcriptional changes. This raises intriguing questions about the individual and overlapping roles of lamin B1 and lamin B2 in cellular function and disease.

Wetting functionalities of rough surfaces are largely determined by the Laplace pressure generated across liquid–gas interfaces formed within surface structures. Typically, rough wetting surfaces create negative Laplace pressures, enabling capillary wicking, while rough non-wetting surfaces create positive Laplace pressures, exhibiting fluid repellency. Here, with microfabricated reentrant structures, it is shown that the same surface can exhibit either a negative or positive Laplace pressure, regardless of its intrinsic wettability. This material-independent Laplace pressure duality enables or enhances a range of wetting functionalities including wicking, switchability, and selectivity. On the same surface, capillary rise, capillary dip, and the combination of the two which leads to further enhancement of the total sustainable capillary height and Laplace pressure, the driving force for wicking is demonstrated. Further, active switching of wetting states between the hemiwicking and the repellent Cassie state on reentrant structures is shown. Moreover, with a water-hexane mixture system, selective wetting of reentrant structures are demonstrated, that is, water can be selectively wicked or repelled in the presence of hexane, and vice versa. These functionalities are achieved, which would typically require complex chemical coatings, solely using surface structures, thus largely expanding the design space for a wide range of thermofluidic applications.

Taï Forest virus (TAFV) is a negative-sense RNA virus in the Filoviridae family. TAFV has caused only a single human infection, but several disease outbreaks in chimpanzees have been linked to this virus. Limited research has been done on this human-pathogenic virus. We sought to establish an animal model to assess TAFV disease progression and pathogenicity at our facility. We had access to two different viral stock preparations from different institutions, both originating from the single human case. Type I interferon receptor knockout mice were inoculated with TAFV stock 1 or stock 2 by the intraperitoneal route. Inoculation resulted in 100% survival with no disease regardless of viral stock preparation or infectious dose. Next, cynomolgus macaques were inoculated with TAFV stock 1 or stock 2. Inoculation with TAFV stock 1 resulted in 100% survival and robust TAFV glycoprotein-specific IgG responses including neutralizing antibodies. In contrast, macaques infected with TAFV stock 2 developed disease and were euthanized 8-11 days after infection exhibiting viremia, thrombocytopenia, and increased inflammatory mediators identified by transcriptional analysis. Histopathologic analysis of tissue samples collected at necropsy confirmed classic filovirus disease in numerous organs. Genomic differences in both stock preparations were mapped to several viral genes which may have contributed to disease severity. Taken together, we demonstrate that infection with the two TAFV stocks resulted in no disease in mice and opposing disease phenotypes in cynomolgus macaques, highlighting the impact of viral stock propagation on pathogenicity in animal models.

It is increasingly recognized that interspecies interactions may modulate the pathogenicity of Pseudomonas aeruginosa during chronic lung infections. Nevertheless, while the interaction between P. aeruginosa and pathogenic microorganisms co-infecting the lungs has been widely investigated, little is known about the influence of other members of the lung microbiota on the infection process. In this study, we focused on investigating the impact of Prevotella species isolated from the sputum of people with cystic fibrosis (pwCF) on biofilm formation and virulence factor production by P. aeruginosa. Screening of a representative collection of Prevotella species recovered from clinical samples showed that several members of this genus (8 out 10 isolates) were able to significantly reduce biofilm formation of P. aeruginosa PAO1, without impact on growth. Among the tested isolates, the strongest biofilm-inhibitory activity was observed for Prevotella intermedia and Prevotella nigrescens, which caused a reduction of up to 90% in the total biofilm biomass of several P. aeruginosa isolates from pwCF. In addition, a strain-specific effect of P. nigrescens on the ability of P. aeruginosa to produce proteases and pyocyanin was observed, with significant alterations in the levels of these virulence factors detected in LasR mutant strains. Overall, these results suggest that non-pathogenic bacteria from the lung microbiota may regulate pathogenicity traits of P. aeruginosa, and possibly affect the outcome of chronic lung infections.

Objective: To determine whether chronic pain persists after complete spinal cord injury (SCI). Design: Prospective observational study regarding the outcome of pre-existent chronic pain of inpatients admitted with new clinically diagnosed complete cervical SCI. For patients who acknowledged chronic pain of ≥3 years duration before the SCI, further questions explored whether they still experienced that pain, whether they were experiencing current posttraumatic pain, and whether they had any past exposure to opioids. The included patients were identified during the initial consultation in the trauma center for treatment of the SCI. Setting: Level I trauma center. Participants: From a total of 49 participants with acute cervical SCI with clinically diagnosed complete motor and sensory tetraplegia admitted between 2018 and 2020, 7 were selected on the basis of a history of chronic pain. Intervention: Collected complete history and performed physical examination with serial follow-ups during the acute hospital stay until death or discharge. Main Outcome Measures: The primary outcome was a finding of chronic pain experienced before new clinical diagnosis of complete SCI, compared with whether or not that pain continued after the SCI injury. The secondary outcome was the relation of persistent pain with opioid use; it was formulated after data collection. Results: Among 49 patients with clinically diagnosed complete cervical SCIs, 7 had experienced prior chronic pain. Four participants experienced a continuation of the prior pain after their complete tetraplegia (4/7), whereas 3 participants did not (3/7). All the participants with continued pain had been previously treated with opioids, whereas those whose pain ceased had not received chronic opioid therapy. Conclusions: There may be a unique form of chronic pain that is based in the brain, irrespective of peripheral pain or spinal mechanisms. Otherwise healthy people with longstanding antecedent chronic pain whose pain persists after acute clinically complete SCI with tetraplegia may provide a new model for evaluation of brain-based pain. Opioids may be requisite for this type of pain.

There is growing interest in the kinematic analysis of human functional upper extremity movement (FUEM) for applications such as health monitoring and rehabilitation. Deconstructing functional movements into activities, actions, and primitives is a necessary procedure for many of these kinematic analyses. Advances in machine learning have led to progress in human activity and action recognition. However, their utility for analyzing the FUEM primitives of reaching and targeting during reach-to-grasp and reach-to-point tasks remains limited. Domain experts use a variety of methods for segmenting the reaching and targeting motion primitives, such as kinematic thresholds, with no consensus on what methods are best to use. Additionally, current studies are small enough that segmentation results can be manually inspected for correctness. As interest in FUEM kinematic analysis expands, such as in the clinic, the amount of data needing segmentation will likely exceed the capacity of existing segmentation workflows used in research laboratories, requiring new methods and workflows for making segmentation less cumbersome. This paper investigates five reaching and targeting motion primitive segmentation methods in two different domains (haptics simulation and real world) and how to evaluate these methods. This work finds that most of the segmentation methods evaluated perform reasonably well given current limitations in our ability to evaluate segmentation results. Furthermore, we propose a method to automatically identify potentially incorrect segmentation results for further review by the human evaluator. Clinical impact: This work supports efforts to automate aspects of processing upper extremity kinematic data used to evaluate reaching and grasping, which will be necessary for more widespread usage in clinical settings.

Abstract Background The relationship between obesity and non-Hodgkin’s lymphoma (NHL) was controversial, which may be due to the crudeness definition of obesity based on body mass index (BMI). As obesity and metabolic abnormalities often coexist, we aimed to explore whether the classification of obesity based on metabolic status can help to evaluate the real impact of obesity on the readmission of NHL. Methods In this retrospective cohort study, utilizing the 2018 Nationwide Readmissions Database, we identified NHL-related index hospitalizations and followed them for non-elective readmission. The patients with NHL were classified as metabolically healthy non-obese (MHNO) and obese (MHO) and metabolically unhealthy non-obese (MUNO) and obese (MUO). Readmission rates for each phenotype were calculated at 30-day intervals. Multiple COX regression was used to analyze the association of metabolic-defined obesity with 30-day, 90-day, and 180-day readmission rates in patients with NHL. Results There were 22,086 index hospitalizations with NHL included. In the multivariate COX regression, MUNO was associated with increased 30-day (HR = 1.113, 95% CI 1.036–1.195), 90-day (HR = 1.148, 95% CI 1.087–1.213), and 180-day readmission rates (HR = 1.132, 95% CI 1.077–1.189), and MUO was associated with increased 30-day (HR=1.219, 95% CI: 1.081-1.374), 90-day (HR = 1.228, 95% CI 1.118–1.348), and 180-day readmission rates (HR = 1.223, 95% CI 1.124–1.33), while MHO had no associations with readmission rates. Conclusions The presence of metabolic abnormalities with or without obesity increased the risk of non-selective readmission in patients with NHL. However, obesity alone had no associations with the risk of non-selective readmission, suggesting that interventions for metabolic abnormalities may be more important in reducing readmissions of NHL patients.

In this conceptual essay, we weave concepts of critical race theory, joy, [anti-]disciplinarity, and humanization toward a critique of the disciplinary organization of teacher preparation program curricula through what we term a pedagogy of humanizing co-creatorship. In this essay, we seek to position disciplinarity as needed, but find that antiracist practices, such as the centering of joy and humanization, are even more ethically fundamental to creating culturally sustaining early-career teachers.

This article presents a study that explored the implementation of a "Say Yes to FCS" Teaching Camp, a local community initiative in Texas, to address the critical shortage of family and consumer sciences (FCS) teachers in secondary schools. Aimed at incoming 9th- and 10th-grade students, the 4-day camp offered hands-on learning experiences across various FCS-related secondary courses, mentorship from local FCS educators, and insights into the diverse career paths within the field. Despite not significantly increasing the participants' interest in pursuing the FCS teaching profession, the camp was positively received, prompting interest in FCS-related high-school courses. In addition, this study emphasizes the necessity of evaluating the camp's success and adjusting strategies to ensure this initiative increases participants' interest in pursuing an FCS teaching profession in the future.

In this paper, the author uses an AsianCrit analysis of US Department of War Educational Manual No. 42, Our Chinese Ally (EM42), a document of military curriculum from WWII. Their argues that EM42 demonstrates both a state-sanctioned [re]racialization of Chinese and Chinese Americans through simultaneous technologies of Sinophobia and Sinocentrism. Their analysis of EM42 has implications for the construction of Asian Americans as a "model minority" in the United States, and highlights EM42's contemporary reverberations on the construction of Asian American identity, as well as how nation-states challenged stereotypes of Chinese people without decentring whiteness.

The purpose of this paper is to introduce the Five-Level Qualitative Data Analysis (5LQDA) method for ATLAS.ti as a way to intentionally design methodological approaches applicable to the field of evaluation. To demonstrate my analytical process using ATLAS.ti, I use examples from an existing evaluation of a STEM Peer Learning Assistant program. Aligned with the 5LQDA method for ATLAS.ti, I first contextualize the strategies used to develop the analytical framework (Levels 1 & 2) and then deconstruct the translation process (Level 3) of pairing conceptual strategies with software tools. I then demonstrate the potential of the software in terms of selected and constructed tools (Levels 4 & 5) and discuss the importance of choosing tools aligned with the project's conceptual strategies. This paper acts as a resource to convey the value of integrating 5LQDA for ATLAS.ti throughout qualitative evaluation by engaging in an iterative process that creates opportunity for engagement.