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Inner-shell electrons naturally sense the electric field close to the nucleus, which can reach extreme values beyond 10 15  V cm −1 for the innermost electrons 1 . Especially in few-electron, highly charged ions, the interaction with the electromagnetic fields can be accurately calculated within quantum electrodynamics (QED), rendering these ions good candidates to test the validity of QED in strong fields. Consequently, their Lamb shifts were intensively studied in the past several decades 2 , 3 . Another approach is the measurement of gyromagnetic factors ( g factors) in highly charged ions 4 – 7 . However, so far, either experimental accuracy or small field strength in low- Z ions 5 , 6 limited the stringency of these QED tests. Here we report on our high-precision, high-field test of QED in hydrogen-like 118 Sn 49+ . The highly charged ions were produced with the Heidelberg electron beam ion trap (EBIT) 8 and injected into the ALPHATRAP Penning-trap setup 9 , in which the bound-electron g factor was measured with a precision of 0.5 parts per billion (ppb). For comparison, we present state-of-the-art theory calculations, which together test the underlying QED to about 0.012%, yielding a stringent test in the strong-field regime. With this measurement, we challenge the best tests by means of the Lamb shift and, with anticipated advances in the g -factor theory, surpass them by more than an order of magnitude. A high-precision, high-field test of quantum electrodynamics measuring the bound-electron g factor in hydrogen-like tin is described, which—together with state-of-the-art theory calculations—yields a stringent test in the strong-field regime.

Gravitational‐wave high‐energy Electromagnetic Counterpart All‐sky Monitor (GECAM) is a space‐borne instrument dedicated to monitoring high‐energy transients, including Terrestrial Gamma‐ray Flashes (TGFs) and Terrestrial Electron Beams (TEBs). We implemented a TGF/TEB search algorithm for GECAM, with which 147 bright TGFs, 2 typical TEBs and 2 special TEB‐like events are identified during an effective observation time of ∼9 months. We show that, with gamma‐ray and charged particle detectors, GECAM can effectively identify and distinguish TGFs and TEBs, and measure their temporal and spectral properties in detail. A very high TGF‐lightning association rate of ∼80% is obtained between GECAM and GLD360 in east Asia region. Plain Language Summary Terrestrial gamma‐ray flashes (TGFs) and Terrestrial Electron Beams (TEBs) represent the most energetic radioactive phenomena in the atmosphere of the Earth. They reflect a natural particle accelerator that can boost electrons up to at least several tens of mega electron volts and produce gamma‐ray radiation. With novel detection technologies, Gravitational‐wave high‐energy Electromagnetic Counterpart All‐sky Monitor (GECAM) is a new powerful instrument to observe TGFs and TEBs, as well as study their properties. For example, it is difficult for most space‐borne high‐energy instruments to distinguish between TGFs and TEBs. However, we show here that, with the joint observation of gamma‐ray and charged particle detectors, GECAM can effectively identify TGFs and TEBs. GECAM can also reveal their fine features in the light curves and spectra. Key Points During 9‐month observation, Gravitational‐wave high‐energy Electromagnetic Counterpart All‐sky Monitor (GECAM) has detected 147 bright Terrestrial Gamma‐ray Flashes (TGFs), 2 typical Terrestrial Electron Beams (TEBs), and 2 special TEB‐like events With novel detector design, GECAM can effectively classify TGFs and TEBs, and reveal their fine temporal features We obtained a very high TGF‐lightning association rate (∼80%) between GECAM and GLD360 in east Asia region

To explore the molecular mechanism by which andrographolide (ADR) inhibits static mechanical pressure-induced apoptosis in nucleus pulposus cells (NPCs) and to assess the role of ADR in inhibiting IDD. Hematoxylin-eosin (HE), toluidine blue, and immunofluorescence staining were used to identify NPCs. An NPC apoptosis model was constructed using a homemade cell pressurization device. The proliferation activity, reactive oxygen species (ROS) content, and apoptosis rate were detected using kits. The expression of related proteins was detected using Western blot. A rat tailbone IDD model was constructed using a homemade tailbone stress device. HE staining and safranine O-fast green FCF cartilage staining were used to observe the degeneration degree of the intervertebral disk. ADR inhibits static mechanical pressure-induced apoptosis and ROS accumulation in NPCs and improves cell viability. ADR can promote the expression of Heme oxygenase-1 (HO-1), p-Nrf2, p-p38, p-Erk1/2, p-JNK, and other proteins, and its effects can be blocked by inhibitors of the above proteins. ADR can inhibit IDD by activating the MAPK/Nrf2/HO-1 signaling pathway and suppressing static mechanical pressure-induced ROS accumulation in the NPCs.

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1134/S1810232823020157

Pregnant women face a higher risk of developing gestational diabetes mellitus (GDM) due to the poor dietary habits. GDM can influence the health of both mothers and child. As food processing develops, pregnant women inevitably consume artificial sweeteners, among with the three most common are sucralose, aspartame, and sodium saccharin. It is a concern whether artificial sweeteners consumed during pregnancy increases GDM risk. To analyze the association between artificial sweetener consumption during pregnancy and the incidence of GDM. 422 pregnant women from a Guangdong hospital were surveyed through convenience sampling. The questionnaire collected general information, artificial sweeteners consumption and other GDM related factors. According to the International Association of Diabetes and Pregnancy Study Groups (IADPSG), GDM was diagnosed was met the 75g oral glucose tolerance test (OGTT) at any time of pregnancy. The consumption of artificial sweeteners was categorized into low and high-consumption groups according to a four-point scale. A multifactorial logistic regression model was used to control for confounders and analyze the association between artificial sweetener consumption andGDM. This study included 422 pregnant women with a mean age of (32 ± 3.73) years and a GDM incidence of 13.74%. The GDM incidence was higher in the high artificial sweeteners consumption group (56.90%), than in the low consumption group (43.10%) (p < 0.05). Increased artificial sweetener consumption was linked to a higher GDM risk (OR=2.66,95% CI: 1.48-1.78). High artificial sweeteners consumption was a GDM risk factor in BMI-stratified analyses. High consumption of artificial sweeteners, like sucralose, aspartame, and sodium saccharin, is linked to increased risk of GDM in pregnant women. Further research is required to confirm results and explore mechanism, guiding healthy eating habits during pregnancy.

G protein-gated inwardly rectifying potassium (GIRK) channels are involved in the regulation of neuronal excitability. Four GIRK subunits (GIRK1-4) are expressed in rat dorsal root ganglia (DRGs). Recently, we have characterized the expression of GIRK1 and -2, and both are downregulated in rat DRGs and spinal cord after a complete sciatic nerve transection (axotomy). Here, we aimed to study the neurochemical characteristics of GIRK3, and its regulation in rat DRGs and spinal cord induced by nerve injury. A sciatic nerve axotomy was performed to study the influences of injury on GIRK3 expression in DRGs and spinal cord. A dorsal root rhizotomy and a sciatic nerve crush were employed to study the axonal transport of GIRK3 protein, respectively. Immunohistochemistry analysis was employed for investigating the neurochemical characteristics of GIRK3. In control DRGs, ~18% of neuron profiles (NPs) were GIRK3-positive ( ), and ~41%, ~48% and ~45% of GIRK3 NPs were CGRP , IB4 and NF200 , respectively. GIRK3-like immunoreactivity was observed in glabrous skin of hind paws and axons originating from DRG neurons. Fourteen days after axotomy, more than one-third of DRG NPs were GIRK3 , and among these ~51% and ~56% coexpressed galanin and neuropeptide Y, respectively. In control animals, a small group of interneurons found in the dorsal horn was GIRK3 . In addition, GIRK3 processes could be observed in superficial laminae of spinal dorsal horn. After nerve injury, the intensity of GIRK3-like immunoreactivity in the superficial layers was increased. Evidence based on rhizotomy and sciatic nerve crush indicated both anterograde and retrograde transport of GIRK3. Our study demonstrates that GIRK3 is expressed in sensory neurons and spinal cord. GIRK3 has both anterograde and retrograde axonal transport. GIRK3 expression can be regulated by peripheral nerve injury.

Nerve injury may induce neuropathic pain. In studying the mechanisms of orofacial neuropathic pain, attention has been paid to the plastic changes that occur in the trigeminal ganglia (TGs) and nucleus in response to an injury of the trigeminal nerve branches. Previous studies have explored the impact of sciatic nerve injury on dorsal root ganglia (DRGs) and it has shown dramatic changes in the expression of multiple biomarkers. In large, the changes in biomarker expression in TGs after trigeminal nerve injury are similar to that in DRGs after sciatic nerve injury. However, important differences exist. Therefore, there is a need to study the plasticity of biomarkers in TGs after nerve injury in the context of the development of neuropathic pain-like behaviors. The aim of this study was to investigate the plasticity of biomarkers associated with chronic persistent pain in TGs after trigeminal nerve injury. To mimic the chronic nature of the disorder, we used an intraoral procedure to access the infraorbital nerve (ION) and induced a nerve injury in mice. Immunohistochemistry and quantification were used for revealing the expression level of each biomarker in TGs after nerve injury. Two weeks after partial ION injury, immunohistochemistry results showed strongly upregulated expressions of activating transcription factor 3 and neuropeptide Y (NPY) in the ipsilateral TGs. Microglial cells were also activated after nerve injury. In regard to positive neuronal profile counting, however, no significant difference in expression was observed in galanin, substance P, calcitonin gene-related peptide, neuronal nitric oxide synthase, phosphorylated AKT, or P2X3 in ipsilateral TGs when compared to contralateral TGs. In this study, the expression and regulation of biomarkers in TGs have been observed in response to trigeminal nerve injury. Our results suggest that NPY and Iba1 might play crucial roles in the pathogenesis of orofacial neuropathic pain following this type of injury. Further investigations on the relevance of these changes may help to target suitable treatment possibilities for trigeminal neuralgia.

Cardiovascular disease is a leading cause of death in systemic lupus erythematosus (SLE). Early prediction of cardiac involvement is critical for improving patient outcomes. This study aimed to identify key factors associated with cardiac involvement in SLE and to develop an interpretable machine learning (ML) model for risk prediction. We conducted a retrospective analysis of 1,023 SLE patients hospitalized in Shenzhen People's Hospital between January 2000 and December 2021, with a median age of 31 years at hospitalization (IQR: 25-39 years), 92.1% being female, and 18.77% developing cardiovascular involvement during a median follow-up of 3,737 days (IQR: 1,920-5,246). The most predictive features were selected through the intersection of three feature selection techniques: Random Forest, LASSO, and XGBoost. Models were trained on 70% of the dataset and tested on the remaining 30%. Among seven evaluated algorithms, the Gradient Boosting Machine (GBM) demonstrated the best performance on the test set. Model interpretability was assessed using the DALEX package, which generated feature importance plots and instance-level breakdown profiles to visualize decision-making logic. Over a median follow-up of 3737 days, 192 (18.77%) patients developed cardiac involvement. Seven key predictors-arthritis, hypertension, HDL-C, LDL-C, total cholesterol, CRP, and ESR- were identified from 51 clinical and biological variables at admission. The Gradient Boosting Machine (GBM) model (AUC: 0.748, Accuracy: 0.779, Precision: 0.605, F1 score: 0.433, recall 0.338) performed the best of the seven models. This study is the first to develop an interpretable ML model to predict the risk of cardiac involvement in SLE. Notably, the GBM model showed optimal performance, and its interpretability allowed clinicians to visualize decision-making processes, facilitating early identification of high-risk patients.

The proapoptotic molecule BAX, plays an important role in mitochondrial apoptotic pathway. Dorsal root ganglion (DRG) neurons depend on neurotrophic factors for survival at early developmental stages. Withdrawal of neurotrophic factors will induce apoptosis in DRG neurons, but this type of cell death can be delayed or prevented in neonatal knockout (KO) mice. In adult animals, evidence also shows that DRG neurons are less dependent upon neurotrophic factors for survival. However, little is known about the effect of deletion on the survival of normal and denervated DRG neurons in adult mice. A unilateral sciatic nerve transection was performed in adult KO mice and wild-type (WT) littermates. Stereological method was employed to quantify the number of lumbar-5 DRG neurons 1 month post-surgery. Nerve injury-induced autotomy behavior was also examined on days 1, 3, and 7 post-surgery. There were significantly more neurons in contralateral DRGs of KO mice as compared with WT mice. The number of neurons was reduced in ipsilateral DRGs in both KO and WT mice. No changes in size distributions of DRG neuron profiles were detected before or after nerve injury. Injury-induced autotomy behavior developed much earlier and was more serious in KO mice. Although postnatal death or loss of DRG neurons is partially prevented by deletion, this effect cannot interfere with long-term nerve injury-induced neuronal loss. The exaggerated self-amputation behavior observed in the mutant mice indicates that deficiency may enhance the development of spontaneous pain following nerve injury.

The objective of this study was to evaluate the efficacy and safety of micafungin for the prevention of invasive fungal infection (IFI) during the neutropenic phase of allogeneic hematopoietic SCT (allo-HSCT) in children and adolescents. This was a prospective, multicenter, open-label, single-arm study. Micafungin was administered i.v. at a dose of 1 mg/kg/day (max 50 mg) from the beginning of conditioning until neutrophil engraftment. Treatment success was defined as the absence of proven, probable, possible or suspected IFI through to 4 weeks after therapy. From April 2010 to December 2011, 155 patients were enrolled from 11 institutions in Korea, and 147 patients were analyzed. Of the 147 patients, 121 (82.3%) completed the protocol without premature interruption. Of the 132 patients in whom micafungin efficacy could be evaluated, treatment success was achieved in 119 patients (90.2%). There was no proven fungal infection in any patient. The number of patients with probable, possible and suspected IFI was two, two and nine, respectively. Thirty-five patients (23.8%) experienced 109 adverse events (AEs) possibly related to micafungin. No patients experienced grade IV AEs. Two patients (1.4%) discontinued micafungin administration due to adverse effects. None of the deaths were related to the study drug.