Structural basis of pre-tRNA intron removal by human tRNA splicing endonuclease.

Removal of the intron from precursor-tRNA (pre-tRNA) is essential in all three kingdoms of life. In humans, this process is mediated by the tRNA splicing endonuclease (TSEN) comprising four subunits: TSEN2, TSEN15, TSEN34, and TSEN54. Here, we report the cryo-EM structures of human TSEN bound to full-length pre-tRNA in the pre-catalytic and post-catalytic states at average resolutions of 2.94 and 2.88 Å, respectively. Human TSEN features an extended surface groove that holds the L-shaped pre-tRNA. The mature domain of pre-tRNA is recognized by conserved structural elements of TSEN34, TSEN54, and TSEN2. Such recognition orients the anticodon stem of pre-tRNA and places the 3'-splice site and 5'-splice site into the catalytic centers of TSEN34 and TSEN2, respectively. The bulk of the intron sequences makes no direct interaction with TSEN, explaining why pre-tRNAs of varying introns can be accommodated and cleaved. Our structures reveal the molecular ruler mechanism of pre-tRNA cleavage by TSEN.

Mechanism of exon ligation by human spliceosome.

Pre-mRNA splicing involves two sequential reactions: branching and exon ligation. The C complex after branching undergoes remodeling to become the C∗ complex, which executes exon ligation. Here, we report cryo-EM structures of two intermediate human spliceosomal complexes, pre-C∗-I and pre-C∗-II, both at 3.6 Å. In both structures, the 3' splice site is already docked into the active site, the ensuing 3' exon sequences are anchored on PRP8, and the step II factor FAM192A contacts the duplex between U2 snRNA and the branch site. In the transition of pre-C∗-I to pre-C∗-II, the step II factors Cactin, FAM32A, PRKRIP1, and SLU7 are recruited. Notably, the RNA helicase PRP22 is positioned quite differently in the pre-C∗-I, pre-C∗-II, and C∗ complexes, suggesting a role in 3' exon binding and proofreading. Together with information on human C and C∗ complexes, our studies recapitulate a molecular choreography of the C-to-C∗ transition, revealing mechanistic insights into exon ligation.

GARP-mediated active TGF-ß1 induces bone marrow NK cell dysfunction in AML patients with early relapse post-allo-HSCT.

Relapse is a leading cause of death after allogeneic hematopoietic stem cell transplantation (allo-HSCT) for acute myeloid leukemia (AML). However, the underlying mechanisms remain poorly understood. Natural killer (NK) cells play a crucial role in tumor surveillance and cancer immunotherapy, and NK cell dysfunction has been observed in various tumors. Here, we performed ex vivo experiments to systematically characterize the mechanisms underlying the dysfunction of bone marrow-derived NK (BMNK) cells isolated from AML patients experiencing early relapse after allo-HSCT. We demonstrated that higher levels of active transforming growth factor ß1 (TGF-ß1) were associated with impaired effector function of BMNK cells in these AML patients. TGF-ß1 activation was induced by the overexpression of glycoprotein A repetitions predominant on the surface of CD4+ T cells. Active TGF-ß1 significantly suppressed mTORC1 activity, mitochondrial oxidative phosphorylation, the proliferation, and cytotoxicity of BMNK cells. Furthermore, pretreatment with the clinical stage TGF-ß1 pathway inhibitor, galunisertib, significantly restored mTORC1 activity, mitochondrial homeostasis, and cytotoxicity. Importantly, the blockade of the TGF-ß1 signaling improved the antitumor activity of NK cells in a leukemia xenograft mouse model. Thus, our findings reveal a mechanism explaining BMNK cell dysfunction and suggest that targeted inhibition of TGF-ß1 signaling may represent a potential therapeutic intervention to improve outcomes in AML patients undergoing allo-HSCT or NK cell-based immunotherapy.

Non-Line-of-Sight Imaging and Vibrometry Using a Comb-Calibrated Coherent Sensor.

Non-line-of-sight (NLOS) imaging has the ability to reconstruct hidden objects, allowing a wide range of applications. Existing NLOS systems rely on pulsed lasers and time-resolved single-photon detectors to capture the information encoded in the time of flight of scattered photons. Despite remarkable advances, the pulsed time-of-flight LIDAR approach has limited temporal resolution and struggles to detect the frequency-associated information directly. Here, we propose and demonstrate the coherent scheme-frequency-modulated continuous wave calibrated by optical frequency comb-for high-resolution NLOS imaging, velocimetry, and vibrometry. Our comb-calibrated coherent sensor presents a system temporal resolution at subpicosecond and its superior signal-to-noise ratio permits NLOS imaging of complex scenes under strong ambient light. We show the capability of NLOS localization and 3D imaging at submillimeter scale and demonstrate NLOS vibrometry sensing at an accuracy of dozen Hertz. Our approach unlocks the coherent LIDAR techniques for widespread use in imaging science and optical sensing.

Twin-Field Quantum Key Distribution without Phase Locking.

Twin-field quantum key distribution (TF-QKD) has emerged as a promising solution for practical quantum communication over long-haul fiber. However, previous demonstrations on TF-QKD require the phase locking technique to coherently control the twin light fields, inevitably complicating the system with extra fiber channels and peripheral hardware. Here, we propose and demonstrate an approach to recover the single-photon interference pattern and realize TF-QKD without phase locking. Our approach separates the communication time into reference frames and quantum frames, where the reference frames serve as a flexible scheme for establishing the global phase reference. To do so, we develop a tailored algorithm based on fast Fourier transform to efficiently reconcile the phase reference via data postprocessing. We demonstrate no-phase-locking TF-QKD from short to long distances over standard optical fibers. At 50-km standard fiber, we produce a high secret key rate (SKR) of 1.27 Mbit/s, while at 504-km standard fiber, we obtain the repeaterlike key rate scaling with a SKR of 34 times higher than the repeaterless secret key capacity. Our work provides a scalable and practical solution to TF-QKD, thus representing an important step towards its wide applications.

Opportunistic osteoporosis screening using chest CT with artificial intelligence.

Osteoporosis has a high incidence and a low detection rate. If it is not detected in time, it will cause osteoporotic fracture and other serious consequences. This study showed that the attenuation values of vertebrae on chest CT could be used for opportunistic screening of osteoporosis. This will be beneficial to improve the detection rate of osteoporosis and reduce the incidence of adverse events caused by osteoporosis. INTRODUCTION: To explore the value of the attenuation values of all thoracic vertebrae and the first lumbar vertebra measured by artificial intelligence on non-enhanced chest CT to do osteoporosis screening. METHODS: On base of images of chest CT, using artificial intelligence (AI) to measure the attenuation values (HU) of all thoracic and the first vertebrae of patients who underwent CT examination for lung cancer screening and dual-energy X-ray absorptiometry (DXA) examination during the same period. The patients were divided into three groups: normal group, osteopenia group, and osteoporosis group according to the results of DXA. Clinical baseline data and attenuation values were compared among the three groups. The correlation between attenuation values and BMD values was analyzed, and the predictive ability and diagnostic efficacy of attenuation values of thoracic and first lumbar vertebrae on osteopenia or osteoporosis risk were further evaluated. RESULTS: CT values of each thoracic vertebrae and the first lumbar vertebrae decreased with age, especially in menopausal women and presented high predictive ability and diagnostic efficacy for osteopenia or osteoporosis. After clinical data correction, with every 10 HU increase of CT values, the risk of osteopenia or osteoporosis decreased by 32 ~ 44% and 61 ~ 80%, respectively. And the combined diagnostic efficacy of all thoracic vertebrae was higher than that of a single vertebra. The AUC of recognizing osteopenia or osteoporosis from normal group was 0.831and 0.972, respectively. CONCLUSIONS: The routine chest CT with AI is of great value in opportunistic screening for osteopenia or osteoporosis, which can quickly screen the population at high risk of osteoporosis without increasing radiation dose, thus reducing the incidence of osteoporotic fracture.

Chromatin accessibility landscapes of immune cells in rheumatoid arthritis nominate monocytes in disease pathogenesis.

BACKGROUND: Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease that involves a variety of cell types. However, how the epigenetic dysregulations of peripheral immune cells contribute to the pathogenesis of RA still remains largely unclear. RESULTS: Here, we analysed the genome-wide active DNA regulatory elements of four major immune cells, namely monocytes, B cells, CD4+ T cells and CD8+ T cells, in peripheral blood of RA patients, osteoarthritis (OA) patients and healthy donors using Assay of Transposase Accessible Chromatin with sequencing (ATAC-seq). We found a strong RA-associated chromatin dysregulation signature in monocytes, but no other examined cell types. Moreover, we found that serum C-reactive protein (CRP) can induce the RA-associated chromatin dysregulation in monocytes via in vitro experiments. And the extent of this dysregulation was regulated through the transcription factor FRA2. CONCLUSIONS: Together, our study revealed a CRP-induced pathogenic chromatin dysregulation signature in monocytes from RA patients and predicted the responsible signalling pathway as potential therapeutic targets for the disease.

ATAC-pipe: general analysis of genome-wide chromatin accessibility.

Assay of Transposase-Accessible Chromatin by deep sequencing (ATAC-seq) has been widely used to profile the chromatin accessibility genome-wide. For the absence of an integrated scheme for deep data mining of specific biological issues, here we present ATAC-pipe, an efficient pipeline for general analysis of chromatin accessibility data obtained from ATAC-seq experiments. ATAC-pipe captures information includes not only the quality of original data and genome-wide chromatin accessibility but also signatures of significant differential peaks, transcription factor (TF) occupancy and nucleosome positions around regulatory sites. In addition, ATAC-pipe automatically converts statistic results into intuitive plots at publication quality, such as the read length distribution, heatmaps of sample clustering and cell-type-specific regulatory elements, enriched TF occupancy with motifs footprints and TF-driven regulatory networks. ATAC-pipe provides convenient workflow for researchers to study chromatin accessibility and gene regulation. Availability https://github.com/QuKunLab/ATAC-pipe.

Profilin 1 Protein and Its Implications for Cancers.

Profilin 1 (PFN1) is a ubiquitous small-molecule protein that exists in all eukaryotes. PFN1 was first identified as a G-actin sequestering molecule, and subsequently, its true functions in actin polymerization and F-actin dynamics were revealed. In the following decades, the structure of PFN1 was recognized to have 3 domains: an actin-binding domain, a poly-L-proline (PLP)-binding domain, and a phosphoinositide-binding domain. PFN1 plays a vital role in many cell functions, including membrane trafficking, endocytosis, cell cycle, motility, proliferation, cell survival, transcription, stemness, and autophagy (Figure 1). Abnormal expression or deletion of PFN1 can affect the normal physiological activity of cells and lead to disease development. PFN1 has been deeply studied in a variety of diseases, some genetic (eg, amyotrophic lateral sclerosis) and some chronic (eg, hypertension). In the past 10 years, PFN1's role in cancer has received increasing attention. In this review, we summarize the studies of PFN1 in cancer that have been completed in recent years, discuss the roles of PFN1 in cancer, and discuss the implications for tumor diagnosis and therapy in the future.

Surface Acoustic Wave Sensor for C-Reactive Protein Detection.

A surface acoustic wave (SAW) sensor was investigated for its application in C-reactive protein (CRP) detection. Piezoelectric lithium niobate (LiNbO3) substrates were used to study their frequency response characteristics in a SAW sensor with a CRP sensing area. After the fabrication of the SAW sensor, the immobilization process was performed for CRP/anti-CRP interaction. The CRP/anti-CRP interaction can be detected as mass variations in the sensing area. These mass variations may produce changes in the amplitude of sensor response. It was clearly observed that a CRP concentration of 0.1 µg/mL can be detected in the proposed SAW sensor. A good fitting linear relationship between the detected insertion loss (amplitude) and the concentrations of CRP from 0.1 µg/mL to 1 mg/mL was obtained. The detected shifts in the amplitude of insertion loss in SAW sensors for different CRP concentrations may be useful in the diagnosis of risk of cardiovascular diseases.

High NEK2 confers to poor prognosis and contributes to cisplatin-based chemotherapy resistance in nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is a common malignant tumor in southern China and Southeast Asia, but the molecular mechanism of its pathogenesis is poorly understood. Our previous work demonstrated that NEK2 is overexpressed in multiple cancers. However, how NEK2 involves in NPC development remains to be elucidated. In this study, we firstly identified NEK2, located at +1q32-q33, a late event in NPC pathogenesis, overexpressed in the stage III-IV and paired sequential recurrent patients with NPC by immunohistochemistry. Furthermore, Kaplan-Meier analysis indicated high NEK2 conferred an inferior overall survival in NPC. In addition, cisplatin experiments with cell counting kit-8, colony formation, and a xenograft mice model of NPC demonstrated that NEK2 contributed to proliferation and cisplatin resistance in vitro and in vivo. On the contrary, downregulation of NEK2 by short hairpin RNA inhibited NPC cell growth and increased the sensitivity of cisplatin treatment in vitro. Thus, increased expression of NEK2 protein could not be predicted for poor survival but used as a novel biomarker for recurrence of NPC. Targeting NEK2 has the potential to eradicate the cisplatin-based chemotherapy resistant NPC cells.

Sustained Specific and Cross-Reactive T Cell Responses to Zika and Dengue Virus NS3 in West Africa.

Recent studies on the role of T cells in Zika virus (ZIKV) infection have shown that T cell responses to Asian ZIKV infection are important for protection, and that previous dengue virus (DENV) exposure amplifies the protective T cell response to Asian ZIKV. Human T cell responses to African ZIKV infection, however, remain unexplored. Here, we utilized the modified anthrax toxin delivery system to develop a flavivirus enzyme-linked immunosorbent spot (ELISPOT) assay. Using human ZIKV and DENV samples from Senegal, West Africa, our results demonstrate specific and cross-reactive T cell responses to nonstructural protein 3 (NS3). Specifically, we found that T cell responses to NS3 protease are ZIKV and DENV specific, but responses to NS3 helicase are cross-reactive. Sequential sample analyses revealed immune responses sustained many years after infection. These results have important implications for African ZIKV/DENV vaccine development, as well as for potential flavivirus diagnostics based on T cell responses.IMPORTANCE The recent Zika virus (ZIKV) epidemic in Latin America and the associated congenital microcephaly and Guillain-Barré syndrome have raised questions as to why we have not recognized these distinct clinical diseases in Africa. The human immunologic response to ZIKV and related flaviviruses in Africa represents a research gap that may shed light on the mechanisms contributing to protection. The goal of our study was to develop an inexpensive assay to detect and characterize the T cell response to African ZIKV and DENV. Our data show long-term specific and cross-reactive human immune responses against African ZIKV and DENV, suggesting the usefulness of a diagnostic based on the T cell response. Additionally, we show that prior flavivirus exposure influences the magnitude of the T cell response. The identification of immune responses to African ZIKV and DENV is of relevance to vaccine development.

Chronocoulometric aptamer based assay for staphylococcal enterotoxin B by target-triggered assembly of nanostructured dendritic nucleic acids on a gold electrode.

A rapid and ultrasensitive method is described for the detection of staphylococcal enterotoxin B (SEB). It is based on the formation of a dendritic DNA superstructure by integrating (a) target-induced triggering of DNA release with (b) signal amplification by a hybridization chain reaction. Partially complementary pairing of aptamer and trigger DNA forms a duplex structure. The capture DNA is then placed on the surface of a gold electrode through gold-thiol chemistry. In the presence of SEB, the aptamer-target conjugate is compelled to form. This causes the release of trigger DNA owing to a strong competition with SEB. The trigger DNA is subsequently hybridized with the partial complementary sequences of the capture DNA to trigger HCR with three auxiliary DNA sequances (referred to as H1, H2, H3). Finally, the dendritic DNA superstructure is bound to hexaammineruthenium(III) cation by electrostatic adsorption and assembled onto the modified gold electrode. This produces an amplified electrochemical signal that is measured by chronocoulometry. Under optimal conditions, the charge difference increases linearly with the logarithm of the SEB concentrations in the range from 5 pg·mL-1 to 100 ng·mL-1 with a detection limit as low as 3 pg·mL-1 (at S/N = 3). Graphical abstract An electrochemical switching strategy is presented for the sensitive detection of Staphylococcus enterotoxin B based on target-triggered assembly of dendritic nucleic acid nanostructures.

Impact of Tissue Factor Localization on Blood Clot Structure and Resistance under Venous Shear.

The structure and growth of a blood clot depend on the localization of tissue factor (TF), which can trigger clotting during the hemostatic process or promote thrombosis when exposed to blood under pathological conditions. We sought to understand how the growth, structure, and mechanical properties of clots under flow are shaped by the simultaneously varying TF surface density and its exposure area. We used an eight-channel microfluidic device equipped with a 20- or 100-µm-long collagen surface patterned with lipidated TF of surface densities ∼0.1 and ∼2 molecules/µm2. Human whole blood was perfused at venous shear, and clot growth was continually measured. Using our recently developed computational model of clot formation, we performed simulations to gain insights into the clot's structure and its resistance to blood flow. An increase in TF exposure area resulted not only in accelerated bulk platelet, thrombin, and fibrin accumulation, but also in increased height of the platelet mass and increased clot resistance to flow. Moreover, increasing the TF surface density or exposure area enhanced platelet deposition by approximately twofold, and thrombin and fibrin generation by greater than threefold, thereby increasing both clot size and its viscous resistance. Finally, TF effects on blood flow occlusion were more pronounced for the longer thrombogenic surface than for the shorter one. Our results suggest that TF surface density and its exposure area can independently enhance both the clot's occlusivity and its resistance to blood flow. These findings provide, to our knowledge, new insights into how TF affects thrombus growth in time and space under flow.

Profilin 1 induces drug resistance through Beclin1 complex-mediated autophagy in multiple myeloma.

Autophagy plays an important role in multiple myeloma (MM) for homeostasis, survival and drug resistance, but which genes participate in this process is unclear. We identified several cytoskeleton genes upregulated in MM patients by gene expression profiling (GEP) datasets; in particular, patients with high profilin 1 (PFN1) expression had poor prognosis in MM. In vitro, overexpressed PFN1 promotes proliferation and bortezomib (BTZ) resistance in MM cells. Further study indicated overexpression of PFN1 significantly promoted the process of autophagy and induced BTZ resistance in MM. Otherwise, knockdown of PFN1 blocked autophagy and sensitized MM to BTZ. Co-immunoprecipitation in MM cells indicated that PFN1 could bind Beclin1 complex and promote the initiation of autophagy. Inhibition of autophagy by blocking the formation of Beclin1 complex could reverse the phenotype of BTZ resistance in MM. Our findings suggested that PFN1 could promote autophagy through taking part in Beclin1 complex and contribute to BTZ resistance, which may become a novel molecular target in the therapy of MM.

Ultra-low Impedance Graphene Microelectrodes with High Optical Transparency for Simultaneous Deep 2-photon Imaging in Transgenic Mice.

The last decades have witnessed substantial progress in optical technologies revolutionizing our ability to record and manipulate neural activity in genetically modified animal models. Meanwhile, human studies mostly rely on electrophysiological recordings of cortical potentials, which cannot be inferred from optical recordings, leading to a gap between our understanding of dynamics of microscale populations and brain-scale neural activity. By enabling concurrent integration of electrical and optical modalities, transparent graphene microelectrodes can close this gap. However, the high impedance of graphene constitutes a big challenge towards the widespread use of this technology. Here, we experimentally demonstrate that this high impedance of graphene microelectrodes is fundamentally limited by quantum capacitance. We overcome this quantum capacitance limit by creating a parallel conduction path using platinum nanoparticles. We achieve a 100 times reduction in graphene electrode impedance, while maintaining the high optical transparency crucial for deep 2-photon microscopy. Using a transgenic mouse model, we demonstrate simultaneous electrical recording of cortical activity with high fidelity while imaging calcium signals at various cortical depths right beneath the transparent microelectrodes. Multimodal analysis of Ca2+ spikes and cortical surface potentials offers unique opportunities to bridge our understanding of cellular dynamics and brain-scale neural activity.

Enhancement of photocurrent extraction and electron injection in dual-functional CH3NH3PbBr3 perovskite-based optoelectronic devices via interfacial engineering.

Photocurrent extraction and electron injection in CH3NH3PbBr3 (MAPbBr3) perovskite-based optoelectronic devices are both significantly increased by improving the contact at the PCBM/MAPbBr3 interface with an extended solvent annealing (ESA) process. Photoluminescence quenching and x-ray diffraction experiments show that the ESA not only improves the contact at the PCBM/MAPbBr3 interface but also increases the crystallinity of the MAPbBr3 thin films. The optimized dual-functional PCBM-MAPbBr3 heterojunction based optoelectronic device has a high power conversion efficiency of 4.08% and a bright visible luminescence of 1509 cd m-2. In addition, the modulation speed of the MAPbBr3 based light-emitting diodes is larger than 14 MHz, which indicates that the defect density in the MAPbBr3 thin film can be effectively reduced by using the ESA process.

Impedimetric determination of Staphylococcal enterotoxin B using electrochemical switching with DNA triangular pyramid frustum nanostructure.

An electrochemical switching strategy is presented for the sensitive determination of Staphylococcus enterotoxin B (SEB). It is based on the use of DNA triangular pyramid frustum nanostructure (TPFDNA) consisting of (a) three thiolated probes, (b) one auxiliary probe, and (c) an aptamer against SEB. The TPFDNA was assembled on the gold electrode, with the SEB aptamer designed on top of the TPFDNA. The electron transfer to hexacyanoferrate acting as an electrochemical probe is strongly inhibited in the TPFDNA-modified electrode. This is assumed to be due to the formation of a 3D TPFDNA structure that limits access of hexacyanoferrate to the electrode. Therefore, the Faradaic impedance is large. However, in the presence of SEB, it will bind to the aptamer and dehybridize the hybrid formed between aptamer and its complementary sequence. As a result, the TPFDNA nanostructure changes to an equilateral triangle DNA nanostructure. This results in a more efficient electron transfer and a smaller Faradaic impedance. The method has a detection limit of 0.17 ng mL-1 of SEB (at an S/N of 3) and a dynamic range that covers the 0.2-1000 ng mL-1 concentration range. The applicability and reliability of the method was demonstrated by anayzing (spiked) milk samples, and the results were compared to those obtained with an ELISA kit. The relative standard deviations between the two methods range between -6.59 and 9.33%. Graphical abstract An electrochemical switching strategy is presented for the sensitive detection of Staphylococcus enterotoxin B based on 3D DNA structure conversion of nanostructure from triangular pyramid frustum to equilateral triangle.

Dynamics of Thrombin Generation and Flux from Clots during Whole Human Blood Flow over Collagen/Tissue Factor Surfaces.

Coagulation kinetics are well established for purified blood proteases or human plasma clotting isotropically. However, less is known about thrombin generation kinetics and transport within blood clots formed under hemodynamic flow. Using microfluidic perfusion (wall shear rate, 200 s-1) of corn trypsin inhibitor-treated whole blood over a 250-µm long patch of type I fibrillar collagen/lipidated tissue factor (TF; ∼1 TF molecule/µm2), we measured thrombin released from clots using thrombin-antithrombin immunoassay. The majority (>85%) of generated thrombin was captured by intrathrombus fibrin as thrombin-antithrombin was largely undetectable in the effluent unless Gly-Pro-Arg-Pro (GPRP) was added to block fibrin polymerization. With GPRP present, the flux of thrombin increased to ∼0.5 × 10-12 nmol/µm2-s over the first 500 s of perfusion and then further increased by ∼2-3-fold over the next 300 s. The increased thrombin flux after 500 s was blocked by anti-FXIa antibody (O1A6), consistent with thrombin-feedback activation of FXI. Over the first 500 s, ∼92,000 molecules of thrombin were generated per surface TF molecule for the 250-µm-long coating. A single layer of platelets (obtained with αIIbß3 antagonism preventing continued platelet deposition) was largely sufficient for thrombin production. Also, the overall thrombin-generating potential of a 1000-µm-long coating became less efficient on a per µm2 basis, likely due to distal boundary layer depletion of platelets. Overall, thrombin is robustly generated within clots by the extrinsic pathway followed by late-stage FXIa contributions, with fibrin localizing thrombin via its antithrombin-I activity as a potentially self-limiting hemostatic mechanism.

[Exploration of Recent Mobile Technologies Applied in Nursing Education].

The development of science and technology has fundamentally changed people's lives and the way that medical systems function. Increasingly, mobile technologies are being introduced and integrated into classroom teaching and clinical applications, resulting in healthcare providers introducing innovative applications into health education. These applications enhance the clinical, education, and research expertise of medical staffs and nurses, while improving quality of care and providing new experiences for patients. In order to understand the current situation and trends in nursing education, the present study adopted literature analysis to explore the influence and effect of mobile technologies that have been introduced into nursing education from the school and clinical environments. The results found that students hold positive attitudes toward introducing these technologies into their curricula. Although these technologies may increase the work efficiency of nurses in the workplace, questions remain user perceptions and professional expression. Therefore, securing patient agreement and healthcare system approval were major turning points in the introduction of mobile technologies into nursing education. In the future, adapting mobile technologies for use in teaching materials and courses may be further developed. Moreover, empirical studies may be used in future research in order to facilitate the increasingly successful integration of relevant technologies into nursing education.