Leverage Variational Graph Representation for Model Poisoning on Federated Learning.

This article puts forth a new training data-untethered model poisoning (MP) attack on federated learning (FL). The new MP attack extends an adversarial variational graph autoencoder (VGAE) to create malicious local models based solely on the benign local models overheard without any access to the training data of FL. Such an advancement leads to the VGAE-MP attack that is not only efficacious but also remains elusive to detection. VGAE-MP attack extracts graph structural correlations among the benign local models and the training data features, adversarially regenerates the graph structure, and generates malicious local models using the adversarial graph structure and benign models' features. Moreover, a new attacking algorithm is presented to train the malicious local models using VGAE and sub-gradient descent, while enabling an optimal selection of the benign local models for training the VGAE. Experiments demonstrate a gradual drop in FL accuracy under the proposed VGAE-MP attack and the ineffectiveness of existing defense mechanisms in detecting the attack, posing a severe threat to FL.

Water-Responsive Self-Contractive Silk-Based Skin Anti-Aging Tensioners with Customizable Biofunctions.

Skin anti-aging treatments have become increasingly popular. Currently, the prevalent treatment method involves implanting skin tension regulation threads (skin lifting threads) under the skin, and radiofrequency treatments. In this study, inspired by the natural supercontraction of spider silk, the molecular structure of silk fibroin fibers is modulated into an oriented configuration. This modification endows silk proteins with water-responsive self-contraction capabilities, leading to the development of innovative self-contracting silk-based skin tensioners (SSSTs). To align with clinical requirements, skin tension regulation materials are functionalized by testing for their self-contraction, near-infrared laser heating function, and bacteriostatic properties. The SSSTs exhibited remarkable self-contraction properties, drug-loading and sustained-release capabilities, notable antibacterial effects, controllable degradation, and good biocompatibility. Moreover, the near-infrared light heating function effectively increased subcutaneous temperature, demonstrating its potential for enhancing and prolonging skin lifting effects. Therefore, SSSTs can be applied for skin tension regulation to improve and delay skin aging. The results may pave the way for novel strategies in skin rejuvenation, with broad implications for the field of skin anti-aging.

Enhanced neural synchronization during social communications between dyads with high autistic traits.

Autism is characterized by atypical social communication styles. To investigate whether individuals with high autistic traits could still have effective social communication among each other, we compared the behavioral patterns and communication quality within 64 dyads of college students paired with both high, both low, and mixed high-low (HL) autistic traits, with their gender matched. Results revealed that the high-high (HH) autistic dyads exhibited atypical behavioral patterns during conversations, including reduced mutual gaze, communicational turns, and emotional sharing compared with the low-low and/or HL autistic dyads. However, the HH autistic dyads displayed enhanced interpersonal neural synchronization during social communications measured by functional near-infrared spectroscopy, suggesting an effective communication style. Besides, they also provided more positive subjective evaluations of the conversations. These findings highlight the potential for alternative pathways to effectively communicate with the autistic community, contribute to a deeper understanding of how high autistic traits influence social communication dynamics among autistic individuals, and provide important insights for the clinical practices for supporting autistic people.

HIF-1α and adaptor protein LIM and senescent cell antigen-like domains protein 1 axis promotes tubulointerstitial fibrosis by interacting with vimentin in angiotensin II-induced hypertension.

BACKGROUND AND PURPOSE: Activation of the renin-angiotensin system, as a hallmark of hypertension and chronic kidney diseases (CKD) is the key pathophysiological factor contributing to the progression of tubulointerstitial fibrosis. LIM and senescent cell antigen-like domains protein 1 (LIMS1) plays an essential role in controlling of cell behaviour through the formation of complexes with other proteins. Here, the function and regulation of LIMS1 in angiotensin II (Ang II)-induced hypertension and tubulointerstitial fibrosis was investigated. EXPERIMENTAL APPROACH: C57BL/6 mice were treated with Ang II to induce tubulointerstitial fibrosis. Hypoxia-inducible factor-1α (HIF-1α) renal tubular-specific knockout mice or LIMS1 knockdown AAV was used to investigate their effects on Ang II-induced renal interstitial fibrosis. In vitro, HIF-1α or LIMS1 was knocked down or overexpressed in HK2 cells after exposure to Ang II. KEY RESULTS: Increased expression of tubular LIMS1 was observed in human kidney with hypertensive nephropathy and in murine kidney from Ang II-induced hypertension model. Tubular-specific knockdown of LIMS1 ameliorated Ang II-induced tubulointerstitial fibrosis in mice. Furthermore, we demonstrated that LIMS1 was transcriptionally regulated by HIF-1α in tubular cells and that tubular HIF-1α knockout ameliorates LIMS1-mediated tubulointerstitial fibrosis. In addition, LIMS1 promotes Ang II-induced tubulointerstitial fibrosis by interacting with vimentin. CONCLUSION AND IMPLICATIONS: We conclude that HIF-1α transcriptionally regulated LIMS1 plays a central role in Ang II-induced tubulointerstitial fibrosis through interacting with vimentin. Our finding represents a new insight into the mechanism of Ang II-induced tubulointerstitial fibrosis and provides a novel therapeutic target for progression of CKD.

An Immune-Regulating Polysaccharide Hybrid Hydrogel with Mild Photothermal Effect and Anti-Inflammatory for Accelerating Infected Wound Healing.

Bacterial infections and excessive inflammation present substantial challenges for clinical wound healing. Hydrogels with mild photothermal (PTT) effects have emerged as promising agents owing to their dual actions: positive effects on cells and negative effects on bacteria. Here, an injectable self-healing hydrogel of oxidized konjac glucomannan/arginine-modified chitosan (OKGM/CS-Arg, OC) integrated with protocatechualdehyde-@Fe (PF) nanoparticles capable of effectively absorbing near-infrared radiation is synthesized successfully. The OC/PF hydrogels exhibit excellent mechanical properties, biocompatibility, and antioxidant activity. Moreover, in synergy with PTT, OC/PF demonstrates potent antibacterial effects while concurrently stimulating cell migration and new blood vessel formation. In methicillin-resistant Staphylococcus aureus-infected full-thickness mouse wounds, the OC/PF hydrogel displays remarkable antibacterial and anti-inflammatory activities, and accelerates wound healing by regulating the wound immune microenvironment and promoting M2 macrophage polarization. Consequently, the OC/PF hydrogel represents a novel therapeutic approach for treating multidrug-resistant bacterial infections and offers a technologically advanced solution for managing infectious wounds in clinical settings.

One-step in vivo gene knock-out in porcine embryos using recombinant adeno-associated viruses.

Introduction: Gene-edited pigs have become prominent models for studying human disease mechanisms, gene therapy, and xenotransplantation. CRISPR (clustered regularly interspaced short palindromic repeats)/CRISPR-associated 9 (CRISPR/Cas9) technology is a widely employed tool for generating gene-edited pigs. Nevertheless, delivering CRISPR/Cas9 to pre-implantation embryos has traditionally posed challenges due to its reliance on intricate micromanipulation equipment and specialized techniques, resulting in high costs and time-consuming procedures. This study aims to introduce a novel one-step approach for generating genetically modified pigs by transducing CRISPR/Cas9 components into pre-implantation porcine embryos through oviductal injection of recombinant adeno-associated viruses (rAAV). Methods: We first used rAAV-1, rAAV-6, rAAV-8, rAAV-9 expressing EGFP to screen for rAAV serotypes that efficiently target porcine embryos, and then, to achieve efficient expression of CRISPR/Cas9 in vivo for a short period, we packaged sgRNAs targeting the GHR genes to self-complementary adeno-associated virus (scAAV), and Cas9 proteins to single-stranded adeno-associated virus (ssAAV). The efficiency of porcine embryos -based editing was then validated in vitro. The feasibility of this one-step method to produce gene-edited pigs using rAAV-CRISPR/Cas9 oviductal injection into sows within 24 h of conception was then validated. Results: Our research firstly establishes the efficient delivery of CRISPR/Cas9 to pig zygotes, both in vivo and in vitro, using rAAV6. Successful gene editing in pigs was achieved through oviductal injection of rAAV-CRISPR/Cas9. Conclusion: This method circumvents the intricate procedures involved in in vitro embryo manipulation and embryo transfers, providing a straightforward and cost-effective approach for the production of gene-edited pigs.

Synergy between BRD9- and IKZF3-Targeting as a Therapeutic Strategy for Multiple Myeloma.

Progress in the treatment of multiple myeloma (MM) has resulted in improvement in the survival rate. However, there is still a need for more efficacious and tolerated therapies. We and others have shown that bromodomain-containing protein 9 (BRD9), a member of the non-canonical SWI/SNF chromatin remodeling complex, plays a role in MM cell survival, and targeting BRD9 selectively blocks MM cell proliferation and synergizes with IMiDs. We found that synergy in vitro is associated with the downregulation of MYC and Ikaros proteins, including IKZF3, and overexpression of IKZF3 or MYC could partially reverse synergy. RNA-seq analysis revealed synergy to be associated with the suppression of pathways associated with MYC and E2F target genes and pathways, including cell cycle, cell division, and DNA replication. Stimulated pathways included cell adhesion and immune and inflammatory response. Importantly, combining IMiD treatment and BRD9 targeting, which leads to the downregulation of MYC protein and upregulation of CRBN protein, was able to override IMiD resistance of cells exposed to iberdomide in long-term culture. Taken together, our results support the notion that combination therapy based on agents targeting BRD9 and IKZF3, two established dependencies in MM, represents a promising novel therapeutic strategy for MM and IMiD-resistant disease.

Taurine ameliorates sensorimotor function by inhibiting apoptosis and activating A2 astrocytes in mice after subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a form of severe acute stroke with very high mortality and disability rates. Early brain injury (EBI) and delayed cerebral ischemia (DCI) contribute to the poor prognosis of patients with SAH. Currently, some researchers have started to focus on changes in amino acid metabolism that occur in brain tissues after SAH. Taurine is a sulfur-containing amino acid that is semi-essential in animals, and it plays important roles in various processes, such as neurodevelopment, osmotic pressure regulation, and membrane stabilization. In acute stroke, such as cerebral hemorrhage, taurine plays a neuroprotective role. However, the role of taurine after subarachnoid hemorrhage has rarely been reported. In the present study, we established a mouse model of SAH. We found that taurine administration effectively improved the sensorimotor function of these mice. In addition, taurine treatment alleviated sensorimotor neuron damage and reduced the proportion of apoptotic cells. Furthermore, taurine treatment enhanced the polarization of astrocytes toward the neuroprotective phenotype while inhibiting their polarization toward the neurotoxic phenotype. This study is the first to reveal the relationship between taurine and astrocyte polarization and may provide a new strategy for SAH research and clinical treatment.

Low-Dimensional Vanadium-Based High-Voltage Cathode Materials for Promising Rechargeable Alkali-Ion Batteries.

Owing to their rich structural chemistry and unique electrochemical properties, vanadium-based materials, especially the low-dimensional ones, are showing promising applications in energy storage and conversion. In this invited review, low-dimensional vanadium-based materials (including 0D, 1D, and 2D nanostructures of vanadium-containing oxides, polyanions, and mixed-polyanions) and their emerging applications in advanced alkali-metal-ion batteries (e.g., Li-ion, Na-ion, and K-ion batteries) are systematically summarized. Future development trends, challenges, solutions, and perspectives are discussed and proposed. Mechanisms and new insights are also given for the development of advanced vanadium-based materials in high-performance energy storage and conversion.

Attenuation of neuronal ferroptosis in intracerebral hemorrhage by inhibiting HDAC1/2: Microglial heterogenization via the Nrf2/HO1 pathway.

AIM: The class I histone deacetylases (HDACs) implicate in microglial heterogenization and neuroinflammation following Intracerebral hemorrhage (ICH). Ferroptosis has also been reported in the ICH model. However, the relationship between HDAC1/2's role in microglial heterogenization and neuronal ferroptosis remains unclear. METHODS: In both in vivo and in vitro models of ICH, we used Romidepsin (FK228), a selective HDAC1/2 inhibitor, to investigate its effects on microglial heterogenization and neuronal ferroptosis. In the in vitro ICH model using Hemin, a transwell system was utilized to examine how microglia-driven inflammation and ICH-triggered neuronal ferroptosis interact. Immunostaining, Western blotting and RT-qPCR were used to evaluate the microglial heterogenization and neuronal ferroptosis. Microglial heterogenization, neuronal ferroptosis, and neurological dysfunctions were assessed in vivo ICH mice model performed by autologous blood injection. RESULTS: HDAC1/2 inhibition altered microglial heterogenization after ICH, as showing the reducing neuroinflammation and shifting microglia towards an anti-inflammatory phenotype by immunostaining and qPCR results. HDAC1/2 inhibition reduced ferroptosis, characterized by high ROS and low GPx4 expression in HT22 cells, and reduced iron and lipid deposition post-ICH in vivo. Additionally, the Nrf2/HO1 signaling pathway, especially acetyl-Nrf2, activated in the in vivo ICH model due to HDAC1/2 inhibition, plays a role in regulating microglial heterogenization. Furthermore, HDAC1/2 inhibition improved sensorimotor and histological outcomes post-ICH, offering a potential mechanism against ICH. CONCLUSION: Inhibition of HDAC1/2 reduces neuro-ferroptosis by modifying the heterogeneity of microglia via the Nrf2/HO1 pathway, with a particular focus on acetyl-Nrf2. Additionally, this inhibition aids in the faster removal of hematomas and lessens prolonged neurological impairments, indicating novel approach for treating ICH.

Windows of sensitivity for risk of adverse birth outcomes related to gestational PM2.5 exposure: Evidence from a natural experiment.

While numerous studies have associated maternal exposure to PM2.5 with adverse birth outcomes, findings remain inconsistent and difficult to generalize. We aimed to investigate the causal relationship and window of sensitivity between gestational exposure to PM2.5 and birth outcomes. We leveraged high-resolution satellite data to quantify gestational PM2.5 exposure at the individual level, along with a combined model to determine daily relative risks (RRs) of birth outcomes in COVID-19 prelockdown and lockdown groups. RRs between the two groups were further compared using a longitudinal pre-post non-experimental design to identify sensitivity windows of adverse birth outcomes. A total of 73,781 pregnant women from the COVID-19 prelockdown group and 6267 pregnant women from the lockdown group were included for analysis. The daily mean PM2.5 concentrations in the lockdown group decreased by 21.7% compared to the prelockdown group. During the first trimester, every 10 µg/m3 increase in PM2.5 significantly increased the risk of congenital abnormalities of major organs such as the cardiovascular system, gastrointestinal tract, nervous system, urinary system, and respiratory system. Moreover, gestational exposure to PM2.5 during the first trimester was associated with higher risks of premature delivery and term low birth weight. While PM2.5 exposure during the second trimester was positively correlated with macrosomia. Gestational exposure to PM2.5 is associated with increased risks of various adverse birth outcomes with specific sensitive windows. We demonstrated that gestational exposure to PM2.5 increased risks of various adverse birth outcomes with specific window of sensitivity through the natural experiment design. Our findings underscore the urgent need for policies and initiatives targeting PM2.5 reduction, especially during critical periods of pregnancy.

mTORC1 hyperactivation and resultant suppression of macroautophagy contribute to the induction of cardiomyocyte necroptosis by catecholamine surges.

Previous studies revealed a controversial role of mechanistic target of rapamycin complex 1 (mTORC1) and mTORC1-regulated macroautophagy in isoproterenol (ISO)-induced cardiac injury. Here we investigated the role of mTORC1 and potential underlying mechanisms in ISO-induced cardiomyocyte necrosis. Two consecutive daily injections of ISO (85 mg/kg, s.c.) or vehicle control (CTL) were administered to C57BL/6J mice with or without rapamycin (RAP, 5 mg/kg, i.p.) pretreatment. Western blot analyses showed that myocardial mTORC1 signaling and the RIPK1-RIPK3-MLKL necroptotic pathway were activated, mRNA expression analyses revealed downregulation of representative TFEB target genes, and Evan's blue dye uptake assays detected increased cardiomyocyte necrosis in ISO-treated mice. However, RAP pretreatment prevented or significantly attenuated the ISO-induced cardiomyocyte necrosis, myocardial inflammation, downregulation of TFEB target genes, and activation of the RIPK1-RIPK3-MLKL pathway. LC3-II flux assays confirmed the impairment of myocardial autophagic flux in the ISO-treated mice. In cultured neonatal rat cardiomyocytes, mTORC1 signaling was also activated by ISO, and inhibition of mTORC1 by RAP attenuated ISO-induced cytotoxicity. These findings suggest that mTORC1 hyperactivation and resultant suppression of macroautophagy play a major role in the induction of cardiomyocyte necroptosis by catecholamine surges, identifying mTORC1 inhibition as a potential strategy to treat heart diseases with catecholamine surges.

Tubule-specific cyclin-dependent kinase 12 knockdown potentiates kidney injury through transcriptional elongation defects.

Direct tubular injury caused by several medications, especially chemotherapeutic drugs, is a common cause of AKI. Inhibition or loss of cyclin-dependent kinase 12 (CDK12) triggers a transcriptional elongation defect that results in deficiencies in DNA damage repair, producing genomic instability in a variety of cancers. Notably, 10-25% of individuals developed AKI after treatment with a CDK12 inhibitor, and the potential mechanism is not well understood. Here, we found that CDK12 was downregulated in the renal tubular epithelial cells in both patients with AKI and murine AKI models. Moreover, tubular cell-specific knockdown of CDK12 in mice enhanced cisplatin-induced AKI through promotion of genome instability, apoptosis, and proliferative inhibition, whereas CDK12 overexpression protected against AKI. Using the single molecule real-time (SMRT) platform on the kidneys of CDK12RTEC+/- mice, we found that CDK12 knockdown targeted Fgf1 and Cast through transcriptional elongation defects, thereby enhancing genome instability and apoptosis. Overall, these data demonstrated that CDK12 knockdown could potentiate the development of AKI by altering the transcriptional elongation defect of the Fgf1 and Cast genes, and more attention should be given to patients treated with CDK12 inhibitors to prevent AKI.

Nitrogen-potassium balance improves leaf photosynthetic capacity by regulating leaf nitrogen allocation in apple.

Nitrogen (N) and potassium (K) are two important mineral nutrients in regulating leaf photosynthesis. However, the influence of N and K interaction on photosynthesis is still not fully understood. Using a hydroponics approach, we studied the effects of different N and K conditions on the physiological characteristics, N allocation and photosynthetic capacity of apple rootstock M9T337. The results showed that high N and low K conditions significantly reduced K content in roots and leaves, resulting in N/K imbalance, and allocated more N in leaves to non-photosynthetic N. Low K conditions increased biochemical limitation (BL), mesophyll limitation (MCL), and stomatal limitation (SL). By setting different N supplies, lowering N levels under low K conditions increased the proportion of water-soluble protein N (Nw) and sodium dodecyl sulfate-soluble proteins (Ns) by balancing N/K and increased the proportion of carboxylation N and electron transfer N. This increased the maximum carboxylation rate and mesophyll conductance, which reduced MCL and BL and alleviated the low K limitation of photosynthesis in apple rootstocks. In general, our results provide new insights into the regulation of photosynthetic capacity by N/K balance, which is conducive to the coordinated supply of N and K nutrients.

A Novel Method for Targeted Identification of Essential Proteins by Integrating Chemical Reaction Optimization and Naive Bayes Model.

Targeted identification of essential proteins is of great significance for species identification, drug manufacturing, and disease treatment. It is a challenge to analyze the binding mechanism between essential proteins and improve the identification speed while ensuring the accuracy of the identification. This paper proposes a novel method called EPCRO for identifying essential proteins, which incorporates the chemical reaction optimization (CRO) algorithm and the naive Bayes model to effectively detect essential proteins. In EPCRO, the naive Bayes model is employed to analyze the homogeneity between proteins. In order to improve the identification rate and speed of essential proteins, the protein homogeneity rate is integrated into the CRO algorithm to balance between local and global searches. EPCRO is experimentally compared with 17 existing methods (including, DC, SC, IC, EC, LAC, NC, PeC, WDC, EPD-RW, RWHN, TEGS, CFMM, BSPM, AFSO-EP, CVIM, RWEP, and EPPSODC) based on biological datasets. The results show that EPCRO is superior to the above methods in identification accuracy and speed.

CDK12 is a potential biomarker for diagnosis, prognosis and immunomodulation in pan-cancer.

Cell cycle-dependent protein kinase 12 (CDK12) plays a key role in a variety of carcinogenesis processes and represents a promising therapeutic target for cancer treatment. However, to date, there have been no systematic studies addressing its diagnostic, prognostic and immunological value across cancers. Here, we found that CDK12 was significantly upregulated in various types of cancers, and it expression increased with progression in ten cancer types, including breast cancer, cholangiocarcinoma and colon adenocarcinoma. Moreover, the ROC curves indicated that CDK12 showed diagnostic value in eight cancer types. High CDK12 expression was associated with poor prognosis in eight types of cancer, including low-grade glioma, mesothelioma, melanoma and pancreatic cancer. Furthermore, we conducted immunoassays to explore the exact mechanisms underlying CDK12-induced carcinogenesis, which revealed that increased expression of CDK12 allowed tumours to evade immune surveillance and upregulate immune checkpoint genes. Additionally, mutational studies have shown that amplification and missense mutations are the predominant mutational events affecting CDK12 across cancers. These findings establish CDK12 as a significant biological indicator of cancer diagnosis, prognosis, and immunotherapeutic targeting. Early surveillance and employment of CDK12 inhibitors, along with concomitant immunotherapy interventions, may enhance the clinical outcomes of cancer patients.

Low-intensity exercise training improves systolic function of heart during metastatic melanoma-induced cachexia in mice.

Cardiac dysfunction frequently emerges in the initial stages of cancer cachexia, posing a significant complication of the disease. Physical fitness is commonly recommended in these early stages of cancer cachexia due to its beneficial impacts on various aspects of the condition, including cardiac dysfunction. However, the direct functional impacts of exercise on the heart during cancer cachexia largely remain unexplored. In this study, we induced cancer cachexia in mice using a metastatic B16F10 melanoma model. Concurrently, these mice underwent a low-intensity exercise regimen to investigate its potential role in cardiac function during cachexia. Our findings indicate that exercise training can help prevent metastatic melanoma-induced muscle loss without significant alterations to body and fat weight. Moreover, exercise improved the melanoma-induced decline in left ventricular ejection fraction and fractional shortening, while also mitigating the increase in high-sensitive cardiac troponin T levels caused by metastatic melanoma in mice. Transcriptome analysis revealed that exercise significantly reversed the transcriptional alterations in the heart induced by melanoma, which were primarily enriched in pathways related to heart contraction. These results suggest that exercise can improve systolic heart function and directly influence the transcriptome of the heart during metastatic melanoma-induced cachexia.

Efficacy of H2O2 inactivated bovine virus diarrhoea virus (BVDV) type 1 vaccine in mice.

BACKGROUND: Bovine viral diarrhea (BVD) is an acute febrile infectious disease caused by the bovine viral diarrhea virus (BVDV), which has brought huge economic losses to the world's cattle industry. At present, commercial inactivated BVDV vaccines may cause some adverse reactions during use. This study aims to develop a safer and more efficient inactivated BVDV vaccine. METHODS: Here, we described the generation and preclinical efficacy of a hydrogen peroxide (H2O2) inactivated BVDV type 1 vaccine in mice, and administered it separately with commercial vaccine (formaldehyde inactivated) in mice to study its efficacy. RESULTS: The BVDV type 1 IgG, IFN- γ, IL-4 and neutralizing antibody in the serum of the H2O2 inactivated vaccine group can be maintained in mice for 70 days. The IgG level reached its maximum value of 0.67 on the 42nd day, significantly higher than the commercial formaldehyde inactivated BVDV type 1 vaccine. IFN- γ and IL-4 reached their maximum values on the 28th day after immunization, at 123.16 pg/ml and 143.80 pg/ml, respectively, slightly higher than commercial vaccines, but the effect was not significant. At the same time the BVDV-1 neutralizing antibody titer reached a maximum of 12 Nu on the 42nd day post vaccination. CONCLUSIONS: The H2O2 inactivated BVDV vaccine has good safety and immunogenicity, which provides a potential solution for the further development of an efficient and safe BVDV vaccine.

Enhancing the Efficiency of a Radiation Oncology Department Using Electronic Medical Records: Protocol for Preparing Radiotherapy.

BACKGROUND: Electronic medical records (EMRs) streamline medical processes, improve quality control, and facilitate data sharing among hospital departments. They also reduce maintenance costs and storage space needed for paper records, while saving time and providing structured data for future research. OBJECTIVE: This study aimed to investigate whether the integration of the radiation oncology information system and the hospital information system enhances the efficiency of the department of radiation oncology. METHODS: We held multidisciplinary discussions among physicians, physicists, medical radiation technologists, nurses, and engineers. We integrated paper records from the radiation oncology department into the existing hospital information system within the hospital. A new electronic interface was designed. A comparison was made between the time taken to retrieve information from either the paper records or the EMRs for radiation preparation. A total of 30 cases were randomly allocated in both the old paper-based system and the new EMR system. The time spent was calculated manually at every step during the process, and we performed an independent 1-tailed t test to evaluate the difference between the 2 systems. RESULTS: Since the system was launched in August 2020, more than 1000 medical records have been entered into the system, and this figure continues to increase. The total time needed for the radiation preparation process was reduced from 286.8 minutes to 154.3 minutes (P<.001)-a reduction of 46.2%. There was no longer any need to arrange for a nurse to organize the radiotherapy paper records, saving a workload of 16 hours per month. CONCLUSIONS: The implementation of the integrated EMR system has resulted in a significant reduction in the number of steps involved in radiotherapy preparation, as well as a decrease in the amount of time required for the process. The new EMR system has provided numerous benefits for the department, including a decrease in workload, a simplified workflow, and conserving more patient data within a confined space.

Advancing Understanding of Childhood Asthma: Lessons Learned from Birth Cohort Studies.

Asthma and allergies are some of the most common chronic disorders affecting children, the prevalence of which has been increasing in countries and regions undergoing rapid development like China. To curb the rising tide of allergies and safeguard the health of future generations, it is of critical importance to understand how asthma inception is influenced by factors acting at different life stages. Birth cohorts represent a powerful tool to investigate the temporal sequence of exposures along the natural course of asthma. We examined recent evidence on birth cohort studies of asthma and allergic diseases and evaluated their strengths and weaknesses. Essential elements for a successful birth cohort are proposed to further elucidate asthma etiology and pathogenies. Initiating new cohorts in understudied populations with the application of advanced analytical approaches will be needed. Moreover, fostering collaborative networks using standardized methodologies should be prioritized to enable integration of findings across diverse cohorts. There remains an urgent and unmet need to further translate the seminal findings from asthma birth cohort studies into targeted primary prevention strategies to eradicate the disease.