Objective: This study aims to review the application of dobutamine stress cardiac magnetic resonance imaging (DSCMR) for patients with anomalous inter-arterial coronary arteries. Materials and Methods: Consecutive adult patients (≥18 years) with anomalous inter-arterial coronary arteries and DSCMR performed in a quaternary referral center from January 2020 to December 2024 were retrospectively reviewed. Examination details, including medication and complications, were reviewed. Radiological findings, such as wall motion abnormality, perfusion defect and late myocardial enhancement were evaluated. Post-examination management and outcomes were assessed. Results: A total of 31 patients (17 females [54.8%]; age 53.6±11.7 years) with anomalous inter-arterial coronary arteries were included. Most patients (n=25, 80.6%) had anomalous right coronary artery. There were significant differences in peak heart rate (p<0.001) and blood pressure (p<0.001) when compared to the baseline. Only one patient (3.2%) experienced minor adverse event with chest pain during the examination. Her cardiac enzymes and electrocardiogram were normal. All other patients (n=30, 96.8%) had no examination-related complications. Left ventricular stroke volume (78.3 [interquartile range, IQR 15.8] mL) and ejection fraction (63.2% [IQR 9.2%]) were normal. No wall motion abnormality, perfusion defect nor late myocardial enhancement were identified. Median follow-up after DSCMR was 21.0 (IQR 28.0) months. One patient underwent reimplantation of right coronary artery due to recurrent syncope. Conservative management was adopted for all other patients (n= 30, 96.8%). Most (n=28, 90.3%) were asymptomatic post-examination. No major adverse cardiovascular events were reported. Conclusion DSCMR can be safely performed for patients with anomalous inter-arterial coronary arteries and can help guide management plan.

OBJECTIVE: To evaluate the dynamic changes of glucocorticoid (GC) dose and the feasibility of GC discontinuation in rheumatoid arthritis (RA) patients under the background of Chinese medicine (CM). METHODS: This multicenter retrospective cohort study included 1,196 RA patients enrolled in the China Rheumatoid Arthritis Registry of Patients with Chinese Medicine (CERTAIN) from September 1, 2019 to December 4, 2023, who initiated GC therapy. Participants were divided into the Western medicine (WM) and integrative medicine (IM, combination of CM and WM) groups based on medication regimen. Follow-up was performed at least every 3 months to assess dynamic changes in GC dose. Changes in GC dose were analyzed by generalized estimator equation, the probability of GC discontinuation was assessed using Kaplan-Meier curve, and predictors of GC discontinuation were analyzed by Cox regression. Patients with <12 months of follow-up were excluded for the sensitivity analysis. RESULTS: Among 1,196 patients (85.4% female; median age 56.4 years), 880 (73.6%) received IM. Over a median 12-month follow-up, 34.3% (410 cases) discontinued GC, with significantly higher rates in the IM group (40.8% vs. 16.1% in WM; P<0.05). GC dose declined progressively, with IM patients demonstrating faster reductions (median 3.75 mg vs. 5.00 mg in WM at 12 months; P<0.05). Multivariate Cox analysis identified age <60 years [P<0.001, hazard ratios (HR)=2.142, 95% confidence interval (CI): 1.523-3.012], IM therapy (P=0.001, HR=2.175, 95% CI: 1.369-3.456), baseline GC dose ⩽7.5 mg (P=0.003, HR=1.637, 95% CI: 1.177-2.275), and absence of non-steroidal anti-inflammatory drugs use (P=0.001, HR=2.546, 95% CI: 1.432-4.527) as significant predictors of GC discontinuation. Sensitivity analysis (545 cases) confirmed these findings. CONCLUSIONS RA patients receiving CM face difficulties in following guideline-recommended GC discontinuation protocols. IM can promote GC discontinuation and is a promising strategy to reduce GC dependency in RA management. (Trial registration: ClinicalTrials.gov, No. NCT05219214).
Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Arthritis, Rheumatoid/drug therapy* ; Glucocorticoids/therapeutic use* ; Medicine, Chinese Traditional ; Retrospective Studies

[This corrects the article DOI: 10.1016/j.apsb.2018.08.009.].

The prefrontal cortex (PFC) plays a pivotal role in orchestrating higher-order emotional and cognitive processes, a function that depends on the precise modulation of synaptic activity. Although pharmacological studies have demonstrated that dopamine signaling through dopamine D1 receptor (DRD1) in the PFC is essential for these functions, the cell-type-specific and molecular mechanisms underlying the neuromodulatory effects remain elusive. Using cell-type-specific knockout mice and patch-clamp recordings, we investigated the regulatory role of DRD1 on neurons and astrocytes in synaptic transmission and plasticity. Furthermore, we explored the mechanisms by which DRD1 on astrocytes regulate synaptic transmission and plasticity at the cellular level, as well as emotional and cognitive functions at the behavioral level, through two-photon imaging, microdialysis, high-performance liquid chromatography, transcriptome sequencing, and behavioral testing. We found that conditional knockout of the Drd1 in astrocytes (CKO^AST) increased glutamatergic synaptic transmission and long-term potentiation (LTP) in the medial prefrontal cortex (mPFC), whereas Drd1 deletion in pyramidal neurons did not affect synaptic transmission. The elevated level of d-serine in the mPFC of CKO^AST mice increased glutamatergic transmission and LTP through NMDA receptors. In addition, CKO^AST mice exhibited abnormal emotional and cognitive function. Notably, these behavioral changes in CKO^AST mice could be reversed through the administration of d-serine degrease to the mPFC. These results highlight the critical role of the astrocytic DRD1 in modulating mPFC synaptic transmission and plasticity, as well as higher brain functions through d-serine, and may shed light on the treatment of mental disorders.

Identification of disease-specific cell subtypes (DSCSs) has profound implications for understanding disease mechanisms, preoperative diagnosis, and precision therapy. However, achieving unified annotation of DSCSs in heterogeneous single-cell datasets remains a challenge. In this study, we developed the gPRINT algorithm (generalized approach for cell subtype identification with single cell's voicePRINT). Inspired by the principles of speech recognition in noisy environments, gPRINT transforms gene position and gene expression information into voiceprints based on ordered and clustered gene expression phenomena, obtaining unique "gene print" patterns for each cell. Then, we integrated neural networks to mitigate the impact of background noise on cell identity label mapping. We demonstrated the reproducibility of gPRINT across different donors, single-cell sequencing platforms, and disease subtypes, and its utility for automatic cell subtype annotation across datasets. Moreover, gPRINT achieved higher annotation accuracy of 98.37% when externally validated based on the same tissue, surpassing other algorithms. Furthermore, this approach has been applied to fibrosis-associated diseases in multiple tissues throughout the body, as well as to the annotation of fibroblast subtypes in a single tissue, tendon, where fibrosis is prevalent. We successfully achieved automatic prediction of tendinopathy-specific cell subtypes, key targets, and related drugs. In summary, gPRINT provides an automated and unified approach for identifying DSCSs across datasets, facilitating the elucidation of specific cell subtypes under different disease states and providing a powerful tool for exploring therapeutic targets in diseases.
Humans ; Algorithms ; Single-Cell Analysis ; Databases, Genetic ; Molecular Sequence Annotation

The quest to decipher the determinants of human longevity has intensified with the rise in global life expectancy. Long-lived individuals (LLIs), who exceed the average life expectancy while delaying age-related diseases, serve as a unique model for studying human healthy aging and longevity. Longevity is a complex phenotype influenced by both genetic and non-genetic factors. This review paper delves into the genetic, epigenetic, metabolic, immune, and environmental factors underpinning the phenomenon of human longevity, with a particular focus on LLIs, such as centenarians. By integrating findings from human longevity studies, this review highlights a diverse array of factors influencing longevity, ranging from genetic polymorphisms and epigenetic modifications to the impacts of diet and physical activity. As life expectancy grows, understanding these factors is crucial for developing strategies that promote a healthier and longer life.
Humans ; Healthy Aging/physiology* ; Longevity/physiology* ; Epigenesis, Genetic ; Life Expectancy ; Exercise ; Aging/genetics* ; Diet ; Aged, 80 and over

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OBJECTIVES: To explore the relationship between white matter injury (WMI) and cerebral perfusion in preterm infants using arterial spin labeling (ASL). METHODS: A total of 293 preterm infants (gestational age <34 weeks) hospitalized at the Third Affiliated Hospital of Zhengzhou University between June 2022 and June 2024 were included. After achieving clinical stability, the infants underwent brain magnetic resonance imaging (MRI) and ASL. Based on MRI findings, infants were classified into WMI (n=66) and non-WMI (n=227) groups. Cerebral perfusion parameters were compared between groups, and the association between WMI and perfusion alterations was evaluated. RESULTS: The WMI group showed a higher incidence of mild intraventricular hemorrhage (IVH) than the non-WMI group (P<0.05). Significantly lower cerebral perfusion was observed in the WMI group across bilateral frontal, temporal, parietal, and occipital lobes, as well as the basal ganglia and thalamus (P<0.05). After adjusting for gestational age, corrected gestational age at ASL scan, and mild IVH, WMI remained significantly associated with reduced regional perfusion (P<0.05). CONCLUSIONS WMI in preterm infants correlates with localized cerebral hypoperfusion. ASL-detected perfusion abnormalities may provide novel insights into WMI pathogenesis.
Humans ; White Matter/blood supply* ; Infant, Newborn ; Spin Labels ; Infant, Premature ; Female ; Male ; Cerebrovascular Circulation ; Magnetic Resonance Imaging

Objective: To investigate the incidence of postoperative neurological complications among patients who underwent spinal deformity surgery and to determine the significant risk factors for postoperative neurological complications. Methods: Six databases PubMed, Web of Science, Scopus, MEDLINE, Embase, and Cochrane Library have been searched to identify observational studies from inception until January 2025. Inclusion criteria were patients aged ≥10 years with postoperative neurological complications after spinal deformity surgery. Stata/MP18.0 was used to conduct the meta-analysis in this review. The summary incidence estimates, proportion with 95% confidence intervals (CIs) and weights were pooled by the random-effects restricted maximum likelihood model. Results: The search strategy identified 53 articles with 40,958 patients for final review. Overall incidence of postoperative neurological complications was 7% (95% CI, 5.0%–9.0%; p < 0.001; I2 = 98.34%) in which incidence estimates for patients with adult spinal deformity and underwent 3-column spinal osteotomies were 12% (95% CI, 9%–16%; p < 0.001; I2 = 93.17%) and 18% (95% CI, 8%–31%; p < 0.001; I2 = 94.68%) respectively. Preoperative neurological deficit was the risk factor with highest overall odds ratio (OR, 2.86; 95% CI, 1.85–4.41; p = 0.01; I2 = 76.20%), followed by the presence of kyphosis (OR, 1.13; 95% CI, 0.75–1.70; p = 0.02; I2 = 81.80%) and age at surgery (OR, 1.04; 95% CI, 1.01–1.08; p = 0.04; I2 = 68.80%). Conclusion Preoperative neurological deficit, the presence of kyphosis and age at surgery were significant risk factors for postoperative neurological complications. Therefore, comprehensive preoperative assessment and surgical planning are crucial to minimize the risk of developing postoperative neurological complications or the deterioration of pre-existing neurologic deficits.