Educational needs of community visiting nurses for infection prevention and control: Application of the Borich needs assessment and the Locus for Focus models.

OBJECTIVES: This study aimed to assess the educational needs and analyze the priorities of infection prevention and control (IPC) for community-visiting nurses. DESIGN: This is a cross-sectional descriptive study. SAMPLE: This study was conducted with 144 visiting nurses working in public health centers and long-term care facilities in South Korea. METHOD: A total of 23 questions in five subcategories were used to measure the current knowledge and perceived importance of IPC in community-visiting nursing. Data were collected from June 23 to October 30, 2021, during the COVID-19 pandemic. Data were analyzed paired t-test, the Borich needs assessment, and the Locus for Focus models. RESULTS: Top-priority content was defined as content belonging to two models, the first 10 contents of Borich needs assessment and the contents located in the Quadrant I of the Locus for Focus models. "Reporting in case of infection-related accidents," "Mandatory vaccination for visiting nurses," "Standard precaution," "Airborne precaution," "Contact precautions," "Respiratory infection control," and "Post-visit management." CONCLUSIONS: This study suggests that it is necessary to provide visiting nurses with more opportunities for IPC education and to develop standardized IPC programs that consider educational priorities.

Piezo1 regulates meningeal lymphatic vessel drainage and alleviates excessive CSF accumulation.

Piezo1 regulates multiple aspects of the vascular system by converting mechanical signals generated by fluid flow into biological processes. Here, we find that Piezo1 is necessary for the proper development and function of meningeal lymphatic vessels and that activating Piezo1 through transgenic overexpression or treatment with the chemical agonist Yoda1 is sufficient to increase cerebrospinal fluid (CSF) outflow by improving lymphatic absorption and transport. The abnormal accumulation of CSF, which often leads to hydrocephalus and ventriculomegaly, currently lacks effective treatments. We discovered that meningeal lymphatics in mouse models of Down syndrome were incompletely developed and abnormally formed. Selective overexpression of Piezo1 in lymphatics or systemic administration of Yoda1 in mice with hydrocephalus or Down syndrome resulted in a notable decrease in pathological CSF accumulation, ventricular enlargement and other associated disease symptoms. Together, our study highlights the importance of Piezo1-mediated lymphatic mechanotransduction in maintaining brain fluid drainage and identifies Piezo1 as a promising therapeutic target for treating excessive CSF accumulation and ventricular enlargement.

Hijacking of nucleotide biosynthesis and deamidation-mediated glycolysis by an oncogenic herpesvirus.

Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma (KS) and multiple types of B cell malignancies. Emerging evidence demonstrates that KSHV reprograms host-cell central carbon metabolic pathways, which contributes to viral persistence and tumorigenesis. However, the mechanisms underlying KSHV-mediated metabolic reprogramming remain poorly understood. Carbamoyl-phosphate synthetase 2, aspartate transcarbamoylase, and dihydroorotase (CAD) is a key enzyme of the de novo pyrimidine synthesis, and was recently identified to deamidate the NF-κB subunit RelA to promote aerobic glycolysis and cell proliferation. Here we report that KSHV infection exploits CAD for nucleotide synthesis and glycolysis. Mechanistically, KSHV vCyclin binds to and hijacks cyclin-dependent kinase CDK6 to phosphorylate Ser-1900 on CAD, thereby activating CAD-mediated pyrimidine synthesis and RelA-deamidation-mediated glycolytic reprogramming. Correspondingly, genetic depletion or pharmacological inhibition of CDK6 and CAD potently impeded KSHV lytic replication and thwarted tumorigenesis of primary effusion lymphoma (PEL) cells in vitro and in vivo. Altogether, our work defines a viral metabolic reprogramming mechanism underpinning KSHV oncogenesis, which may spur the development of new strategies to treat KSHV-associated malignancies and other diseases.

Schottky barrier height engineering on MoS2 field-effect transistors using a polymer surface modifier on a contact electrode.

Two-dimensional (2D) materials are highly sought after for their superior semiconducting properties, making them promising candidates for next-generation electronic and optoelectronic devices. Transition-metal dichalcogenides (TMDCs), such as molybdenum disulfide (MoS2) and tungsten diselenide (WSe2), are promising alternative 2D materials. However, the devices based on these materials experience performance deterioration due to the formation of a Schottky barrier between metal contacts and semiconducting TMDCs. Here, we performed experiments to reduce the Schottky barrier height of MoS2 field-effect transistors (FETs) by lowering the work function (Фm = Evacuum - EF,metal) of the contact metal. We chose polyethylenimine (PEI), a polymer containing simple aliphatic amine groups (-NH2), as a surface modifier of the Au (ФAu = 5.10 eV) contact metal. PEI is a well-known surface modifier that lowers the work function of various conductors such as metals and conducting polymers. Such surface modifiers have thus far been utilized in organic-based devices, including organic light-emitting diodes, organic solar cells, and organic thin-film transistors. In this study, we used the simple PEI coating to tune the work function of the contact electrodes of MoS2 FETs. The proposed method is rapid, easy to implement under ambient conditions, and effectively reduces the Schottky barrier height. We expect this simple and effective method to be widely used in large-area electronics and optoelectronics due to its numerous advantages.

Leader Boundary-Spanning Behavior and Employee Voice Behavior: The Job Demands-Resources Perspective.

Drawing on the job demands-resources model, we suggest and test a motivational mechanism that underlies the relationship between leader boundary-spanning behavior and employee voice behavior. Based on the field survey data of 383 leader-employee pairs collected from various organizations in South Korea, the results of our mediation model showed that leader boundary-spanning behavior, as a potential job resource, enhances employee voice behavior by increasing employee self-efficacy. The results of our moderated mediation model also showed that the focal leader's abusive supervision, as a potential job demand, could attenuate the beneficial effect of leader boundary-spanning behavior on employee voice behavior by diminishing employee self-efficacy. These findings highlight the importance of leader boundary-spanning behavior in enhancing employee voice behavior, the roles of employee self-efficacy as a key mediating mechanism, and the focal leader's abusive supervision as a preventable boundary condition within these relationships. Theoretical and practical implications are discussed.

Cancel cancer: The immunotherapeutic potential of CD200/CD200R blockade.

Immune checkpoint molecules function to inhibit and regulate immune response pathways to prevent hyperactive immune activity from damaging healthy tissues. In cancer patients, targeting these key molecules may serve as a valuable therapeutic mechanism to bolster immune function and restore the body's natural defenses against tumors. CD200, an immune checkpoint molecule, is a surface glycoprotein that is widely but not ubiquitously expressed throughout the body. By interacting with its inhibitory receptor CD200R, CD200 suppresses immune cell activity within the tumor microenvironment, creating conditions that foster tumor growth. Targeting the CD200/CD200R pathway, either through the use of monoclonal antibodies or peptide inhibitors, has shown to be effective in boosting anti-tumor immune activity. This review will explore CD200 and the protein's expression and role within the tumor microenvironment, blood endothelial cells, and lymph nodes. This paper will also discuss the advantages and challenges of current strategies used to target CD200 and briefly summarize relevant preclinical/clinical studies investigating the immunotherapeutic efficacy of CD200/CD200R blockade.

Experiences of Nursing Instructors Related to Safety Issues Using Students as Practice Models in Laboratories: A Focus Group Study.

AIM: Nursing school students perform invasive (i.e., injection, venipuncture) and/or non-invasive procedures (i.e., giving a bed bath and back massage) on each other to master these skills, and nursing instructors reported related safety issues. This study aimed to explore nursing instructors' experiences concerning their students' psychological and physical safety when using students as practice models in nursing skills laboratories. METHODS: A qualitative design using focus group interviews and thematic analysis was employed. Two semi-structured focus group interviews were conducted with a purposive sample of eight instructors with experience in teaching nursing skills in laboratories. This study was evaluated by the Institutional Review Board at Eulji University (EU18-51) in the Republic of Korea. RESULTS: Three main themes emerged to describe nursing instructors' safety-related experiences when using students as practice models in nursing skills laboratories: (1) a dilemma between the experimental learning of students and the need to keep students safe, (2) perception related to psychological safety, and (3) an inadequate safety reporting system. CONCLUSIONS: When instructors consider using students' bodies to practice nursing skills, they experience a dilemma between the students' experimental learning and the need to keep them safe. Thus, methods to maximize student learning and student safety guidelines should be developed.

Subconjunctival Lymphatics Respond to VEGFC and Anti-Metabolites in Rabbit and Mouse Eyes.

Purpose: To characterize and pharmacologically influence subconjunctival lymphatics in rabbit and mouse eyes. Methods: Rabbits received subconjunctival injections of trypan blue or fixable fluorescent dextrans. Bleb-related outflow pathways were quantified. Immunofluorescence for vessel-specific markers (lymphatics [podoplanin and LYVE-1] and blood vessels [CD31]) were performed in native rabbit conjunctiva and after fixable fluorescent dextran injection. Vascular endothelial cell growth factor-C (VEGFC) was injected subconjunctivally in rabbits. mRNA and protein were assessed for the above markers using RT-PCR and Western blot. Alternatively, mouse studies used Prox1-tdTomato transgenic reporter mice. Subconjunctival injection conditions included: no injection, balanced salt solution (BSS), VEGFC, 5-fluorouracil (5FU) and two concentrations of mitomycin-C (MMC). Two mouse injection protocols (short and long) with different follow-up times and number of injections were performed. Mouse eyes were enucleated, flat mounts created, and subconjunctival branching and length assessed. Results: Rabbit eyes demonstrated clear bleb-related subconjunctival outflow pathways that were distinct from blood vessels and were without nasal/temporal predilection. Immunofluorescence against vessel-specific markers showed lymphatics and blood vessels in rabbit conjunctiva, and these lymphatics overlapped with bleb-related subconjunctival outflow pathways. Subconjunctival VEGFC increased lymphatic (P = 0.004-0.04) but not blood vessel (P = 0.77-0.84) mRNA or protein in rabbits. Prox1-tdTomato transgenic reporter mice demonstrated natively fluorescent lymphatics. Subconjunctival VEGFC increased murine lymphatic branching and length (P ≤ 0.001-0.004) while antimetabolites (P ≤ 0.001-0.043) did the opposite for the long protocol. Discussion: Subconjunctival lymphatics are pharmacologically responsive to both VEGFC and antimetabolites in two animal models studied using different methodologies. These results may be important for bleb-forming glaucoma surgeries or ocular drug delivery.

The ambivalent nature of the relationship between lymphatics and cancer.

Do lymphatic vessels support cancer cells? Or are they vessels that help suppress cancer development? It is known that the lymphatic system is a vehicle for tumor metastasis and that the lymphangiogenic regulator VEGF-C supports the tumor. One such role of VEGF-C is the suppression of the immune response to cancer. The lymphatic system has also been correlated with an increase in interstitial fluid pressure of the tumor microenvironment. On the other hand, lymphatic vessels facilitate immune surveillance to mount an immune response against tumors with the support of VEGF-C. Furthermore, the activation of lymphatic fluid drainage may prove to filter and decrease tumor interstitial fluid pressure. In this review, we provide an overview of the dynamic between lymphatics, cancer, and tumor fluid pressure to suggest that lymphatic vessels may be used as an antitumor therapy due to their capabilities of immune surveillance and fluid pressure drainage. The application of this potential may help to prevent tumor proliferation or increase the efficacy of drugs that target cancer.

Piezo1-Regulated Mechanotransduction Controls Flow-Activated Lymphatic Expansion.

BACKGROUND: Mutations in PIEZO1 (Piezo type mechanosensitive ion channel component 1) cause human lymphatic malformations. We have previously uncovered an ORAI1 (ORAI calcium release-activated calcium modulator 1)-mediated mechanotransduction pathway that triggers lymphatic sprouting through Notch downregulation in response to fluid flow. However, the identity of its upstream mechanosensor remains unknown. This study aimed to identify and characterize the molecular sensor that translates the flow-mediated external signal to the Orai1-regulated lymphatic expansion. METHODS: Various mutant mouse models, cellular, biochemical, and molecular biology tools, and a mouse tail lymphedema model were employed to elucidate the role of Piezo1 in flow-induced lymphatic growth and regeneration. RESULTS: Piezo1 was found to be abundantly expressed in lymphatic endothelial cells. Piezo1 knockdown in cultured lymphatic endothelial cells inhibited the laminar flow-induced calcium influx and abrogated the flow-mediated regulation of the Orai1 downstream genes, such as KLF2 (Krüppel-like factor 2), DTX1 (Deltex E3 ubiquitin ligase 1), DTX3L (Deltex E3 ubiquitin ligase 3L,) and NOTCH1 (Notch receptor 1), which are involved in lymphatic sprouting. Conversely, stimulation of Piezo1 activated the Orai1-regulated mechanotransduction in the absence of fluid flow. Piezo1-mediated mechanotransduction was significantly blocked by Orai1 inhibition, establishing the epistatic relationship between Piezo1 and Orai1. Lymphatic-specific conditional Piezo1 knockout largely phenocopied sprouting defects shown in Orai1- or Klf2- knockout lymphatics during embryo development. Postnatal deletion of Piezo1 induced lymphatic regression in adults. Ectopic Dtx3L expression rescued the lymphatic defects caused by Piezo1 knockout, affirming that the Piezo1 promotes lymphatic sprouting through Notch downregulation. Consistently, transgenic Piezo1 expression or pharmacological Piezo1 activation enhanced lymphatic sprouting. Finally, we assessed a potential therapeutic value of Piezo1 activation in lymphatic regeneration and found that a Piezo1 agonist, Yoda1, effectively suppressed postsurgical lymphedema development. CONCLUSIONS: Piezo1 is an upstream mechanosensor for the lymphatic mechanotransduction pathway and regulates lymphatic growth in response to external physical stimuli. Piezo1 activation presents a novel therapeutic opportunity for preventing postsurgical lymphedema. The Piezo1-regulated lymphangiogenesis mechanism offers a molecular basis for Piezo1-associated lymphatic malformation in humans.

Prolymphangiogenic Effects of 9-cis Retinoic Acid Are Enhanced at Sites of Lymphatic Injury and Dependent on Treatment Duration in Experimental Postsurgical Lymphedema.

Background: Patients undergoing surgical treatment for solid tumors are at risk for development of secondary lymphedema due to intraoperative lymphatic vessel injury. The damaged lymphatic vessels fail to adequately regenerate and lymphatic obstruction leads to fluid and protein accumulation in the interstitial space and chronic lymphedema develops as a result. There are currently no effective pharmacological agents that reduce the risk of developing lymphedema or treat pre-existing lymphedema, and management is largely palliative. The present study investigated the efficacy of various 9-cis retinoic acid (9-cis RA) dosing strategies in reducing postsurgical lymphedema by utilizing a well-established mouse tail lymphedema model. Methods and Results: Short-duration treatment with 9-cis RA did not demonstrate a significant reduction in postoperative tail volume, nor an improvement in lymphatic clearance. However, long-term treatment with 9-cis RA resulted in decreased overall tail volume, dermal thickness, and epidermal thickness, with an associated increase in functional lymphatic clearance and lymphatic vessel density, assessed by LYVE-1 immunostaining, compared with control. These effects were seen at the site of lymphatic injury, with no significant changes observed in uninjured sites such as ear skin and the diaphragm. Conclusions: Given the reported results indicating that 9-cis RA is a potent promoter of lymphangiogenesis and improved lymphatic clearance at sites of lymphatic injury, investigation of postoperative 9-cis RA administration to patients at high risk of developing lymphedema may demonstrate positive efficacy and reduced rates of postsurgical lymphedema.

Leader Humor and Followers' Change-Oriented Organizational Citizenship Behavior: The Role of Leader Machiavellianism.

The purpose of this study is to explore the mechanisms by which leader humor affects followers' change-oriented organizational citizenship behavior. Specifically, we examine the mediation effect of team commitment in the leader humor-change-oriented organizational citizenship behavior link and whether it varied by leader Machiavellianism. Using multi-sourced data from the four battalions of the Republic of Korean Army, our findings show that team commitment mediated the positive relationship between leaders' affiliative humor and followers' change-oriented organizational citizenship behavior. Furthermore, the mediated relationship was stronger when leader Machiavellianism was lower. On the other hand, we found no support for the negative relationship between leaders' aggressive humor and followers' change-oriented organizational citizenship behavior. Theoretical and practical implications are discussed.

Interface Engineering of Magnetic Anisotropy in van der Waals Ferromagnet-based Heterostructures.

Interface engineering is an effective approach to tune the magnetic properties of van der Waals (vdW) magnets and their heterostructures. The prerequisites for the practical utilization of vdW magnets and heterostructures are a quantitative analysis of their magnetic anisotropy and the ability to modulate their interfacial properties, which have been challenging to achieve with conventional methods. Here we characterize the magnetic anisotropy of Fe3GeTe2 layers by employing the magnetometric technique based on anomalous Hall measurements and confirm its intrinsic nature. In addition, on the basis of the thickness dependences of the anisotropy field, we identify the interfacial and bulk contributions. Furthermore, we demonstrate that the interfacial anisotropy in Fe3GeTe2-based heterostructures is locally controlled by adjacent layers, leading to the realization of multiple magnetic behaviors in a single channel. This work proposes that the magnetometric technique is a useful platform for investigating the intrinsic properties of vdW magnets and that functional devices can be realized by local interface engineering.

YAP and TAZ maintain PROX1 expression in the developing lymphatic and lymphovenous valves in response to VEGF-C signaling.

Lymphatic vasculature is an integral part of digestive, immune and circulatory systems. The homeobox transcription factor PROX1 is necessary for the development of lymphatic vessels, lymphatic valves (LVs) and lymphovenous valves (LVVs). We and others previously reported a feedback loop between PROX1 and vascular endothelial growth factor-C (VEGF-C) signaling. PROX1 promotes the expression of the VEGF-C receptor VEGFR3 in lymphatic endothelial cells (LECs). In turn, VEGF-C signaling maintains PROX1 expression in LECs. However, the mechanisms of PROX1/VEGF-C feedback loop remain poorly understood. Whether VEGF-C signaling is necessary for LV and LVV development is also unknown. Here, we report for the first time that VEGF-C signaling is necessary for valve morphogenesis. We have also discovered that the transcriptional co-activators YAP and TAZ are required to maintain PROX1 expression in LVs and LVVs in response to VEGF-C signaling. Deletion of Yap and Taz in the lymphatic vasculature of mouse embryos did not affect the formation of LVs or LVVs, but resulted in the degeneration of these structures. Our results have identified VEGF-C, YAP and TAZ as a crucial molecular pathway in valve development.

Lymphatic Proliferation Ameliorates Pulmonary Fibrosis after Lung Injury.

Despite many reports about pulmonary blood vessels in lung fibrosis, the contribution of lymphatics to fibrosis is unknown. We examined the mechanism and consequences of lymphatic remodeling in mice with lung fibrosis after bleomycin injury or telomere dysfunction. Widespread lymphangiogenesis was observed after bleomycin treatment and in fibrotic lungs of prospero homeobox 1-enhanced green fluorescent protein (Prox1-EGFP) transgenic mice with telomere dysfunction. In loss-of-function studies, blocking antibodies revealed that lymphangiogenesis 14 days after bleomycin treatment was dependent on vascular endothelial growth factor (Vegf) receptor 3 signaling, but not on Vegf receptor 2. Vegfc gene and protein expression increased specifically. Extensive extravasated plasma, platelets, and macrophages at sites of lymphatic growth were potential sources of Vegfc. Lymphangiogenesis peaked at 14 to 28 days after bleomycin challenge, was accompanied by doubling of chemokine (C-C motif) ligand 21 in lung lymphatics and tertiary lymphoid organ formation, and then decreased as lung injury resolved by 56 days. In gain-of-function studies, expansion of the lung lymphatic network by transgenic overexpression of Vegfc in club cell secretory protein (CCSP)/VEGF-C mice reduced macrophage accumulation and fibrosis and accelerated recovery after bleomycin treatment. These findings suggest that lymphatics have an overall protective effect in lung injury and fibrosis and fit with a mechanism whereby lung lymphatic network expansion reduces lymph stasis and increases clearance of fluid and cells, including profibrotic macrophages.

Organogenesis and distribution of the ocular lymphatic vessels in the anterior eye.

Glaucoma surgeries, such as trabeculectomy, are performed to lower intraocular pressure to reduce risk of vision loss. These surgeries create a new passage in the eye that reroutes the aqueous humor outflow to the subconjunctival space, where the fluid is presumably absorbed by the conjunctival lymphatics. Here, we characterized the development and function of the ocular lymphatics using transgenic lymphatic reporter mice and rats. We found that the limbal and conjunctival lymphatic networks are progressively formed from a primary lymphatic vessel that grows from the nasal-side medial canthus region at birth. This primary lymphatic vessel immediately branches out, invades the limbus and conjunctiva, and bidirectionally encircles the cornea. As a result, the distribution of the ocular lymphatics is significantly polarized toward the nasal side, and the limbal lymphatics are directly connected to the conjunctival lymphatics. New lymphatic sprouts are produced mainly from the nasal-side limbal lymphatics, posing the nasal side of the eye as more responsive to fluid drainage and inflammatory stimuli. Consistent with this polarized distribution of the ocular lymphatics, a higher drainage efficiency was observed in the nasal side than the temporal side of the eye when injected with a fluorescent tracer. In contrast, blood vessels are evenly distributed at the anterior surface of the eyes. Also, we found that these distinct vascular distribution patterns were conserved in human eyes. Together, our study demonstrated that the ocular surface lymphatics are more densely present in the nasal side and uncovered the potential clinical benefits in selecting the nasal side as a glaucoma surgery site to improve fluid drainage.

The Lymphatic Cell Environment Promotes Kaposi Sarcoma Development by Prox1-Enhanced Productive Lytic Replication of Kaposi Sarcoma Herpes Virus.

Kaposi sarcoma is the most common cancer in human immunodeficiency virus-positive individuals and is caused by Kaposi sarcoma-associated herpesvirus (KSHV). It is believed that a small number of latently infected Kaposi sarcoma tumor cells undergo spontaneous lytic reactivation to produce viral progeny for infection of new cells. Here, we use matched donor-derived human dermal blood and lymphatic endothelial cells (BEC and LEC, respectively) to show that KSHV-infected BECs progressively lose viral genome as they proliferate. In sharp contrast, KSHV-infected LECs predominantly entered lytic replication, underwent cell lysis, and released new virus. Continuous lytic cell lysis and de novo infection allowed LEC culture to remain infected for a prolonged time. Because of the strong propensity of LECs toward lytic replication, LECs maintained virus as a population, despite the death of individual host cells from lytic lysis. The master regulator of lymphatic development, Prox1, bound the promoter of the RTA gene to upregulate its expression and physically interacted with RTA protein to coregulate lytic genes. Thus, LECs may serve as a proficient viral reservoir that provides viral progeny for continuous de novo infection of tumor origin cells, and potentially BECs and mesenchymal stem cells, which give rise to Kaposi sarcoma tumors. Our study reveals drastically different host cell behaviors between BEC and LEC and defines the underlying mechanisms of the lymphatic cell environment supporting persistent infection in Kaposi sarcoma tumors. SIGNIFICANCE: This study defines the mechanism by which Kaposi's sarcoma could be maintained by virus constantly produced by lymphatic cells in HIV-positive individuals.

S1PR1 regulates the quiescence of lymphatic vessels by inhibiting laminar shear stress-dependent VEGF-C signaling.

During the growth of lymphatic vessels (lymphangiogenesis), lymphatic endothelial cells (LECs) at the growing front sprout by forming filopodia. Those tip cells are not exposed to circulating lymph, as they are not lumenized. In contrast, LECs that trail the growing front are exposed to shear stress, become quiescent, and remodel into stable vessels. The mechanisms that coordinate the opposed activities of lymphatic sprouting and maturation remain poorly understood. Here, we show that the canonical tip cell marker Delta-like 4 (DLL4) promotes sprouting lymphangiogenesis by enhancing VEGF-C/VEGF receptor 3 (VEGFR3) signaling. However, in lumenized lymphatic vessels, laminar shear stress (LSS) inhibits the expression of DLL4, as well as additional tip cell markers. Paradoxically, LSS also upregulates VEGF-C/VEGFR3 signaling in LECs, but sphingosine 1-phosphate receptor 1 (S1PR1) activity antagonizes LSS-mediated VEGF-C signaling to promote lymphatic vascular quiescence. Correspondingly, S1pr1 loss in LECs induced lymphatic vascular hypersprouting and hyperbranching, which could be rescued by reducing Vegfr3 gene dosage in vivo. In addition, S1PR1 regulates lymphatic vessel maturation by inhibiting RhoA activity to promote membrane localization of the tight junction molecule claudin-5. Our findings suggest a potentially new paradigm in which LSS induces quiescence and promotes the survival of LECs by downregulating DLL4 and enhancing VEGF-C signaling, respectively. S1PR1 dampens LSS/VEGF-C signaling, thereby preventing sprouting from quiescent lymphatic vessels. These results also highlight the distinct roles that S1PR1 and DLL4 play in LECs when compared with their known roles in the blood vasculature.

Fast Magneto-Ionic Switching of Interface Anisotropy Using Yttria-Stabilized Zirconia Gate Oxide.

Voltage control of interfacial magnetism has been greatly highlighted in spintronics research for many years, as it might enable ultralow power technologies. Among a few suggested approaches, magneto-ionic control of magnetism has demonstrated large modulation of magnetic anisotropy. Moreover, the recent demonstration of magneto-ionic devices using hydrogen ions presented relatively fast magnetization toggle switching, tsw ∼ 100 ms, at room temperature. However, the operation speed may need to be significantly improved to be used for modern electronic devices. Here, we demonstrate that the speed of proton-induced magnetization toggle switching largely depends on proton-conducting oxides. We achieve ∼1 ms reliable (>103 cycles) switching using yttria-stabilized zirconia (YSZ), which is ∼100 times faster than the state-of-the-art magneto-ionic devices reported to date at room temperature. Our results suggest that further engineering of the proton-conducting materials could bring substantial improvement that may enable new low-power computing scheme based on magneto-ionics.

Comparison of high-flow nasal cannula oxygen therapy and conventional reserve-bag oxygen therapy in carbon monoxide intoxication: A pilot study.

BACKGROUND: High-flow nasal cannula oxygen (HFNC) creates a positive pressure effect through high-flow rates compared to conventional oxygen therapy. The purpose of this human pilot study is to compare the effects of HFNC and conventional oxygen therapy on the rate of carbon monoxide (CO) clearance from the blood in patients with mild to moderate CO poisoning. METHODS: CO-poisoned Patients randomly received 100% oxygen from a rebreathing reserve mask (NBO2, flow of 15 L/min) or HFNC (flow of 60 L/min). The fraction of COHb value (fCOHb) was measured in 30-min intervals until it fell to under 10%. We determined the Half-life time of fCOHb (fCOHb t1/2). RESULTS: A total of 22 patients had fCOHb levels ≥ 10% at the time of ED arrival, with 9 of them having fCOHb level ranging between 25% and 50%. There was no significant difference in the fCOHbt1/2 between the HFNC group and NBO2 group. However, the mean fCOHbt1/2 in the HFNC group (48.5 ±â€¯12.4 min) has a smaller standard deviation than that in the NBO2 group (99.3 ±â€¯93.38 min). There were significant between-group differences in the mean COHbt1/2 among the patients with fCOHb levels less than 25% (HFNC 43.6 ±â€¯10.6 vs. NBO2 134.2 ±â€¯111.3). CONCLUSIONS: In this pilot randomized controlled trial study, HFNC therapy did not reduce fCOHbt1/2 compared to NBO2 therapy but could be beneficial in maintaining a constant fCOHbt1/2 as well as in reducing fCOHbt1/2 in mild CO poisoning patients compared to conventional NBO2 therapy. However, further studies with a larger number of patients are needed to establish HFNC therapy as an alternative therapy for CO poisoning patients.