Suzhou Traditional Chinese Medicine Hospital

To evaluate serum homocysteine (Hcy) and small dense low-density lipoprotein cholesterol (sdLDL-C) as predictors of cardiovascular risk in obese patients and their incremental value for prediction models. A retrospective cohort study was conducted on obese patients. Baseline data and laboratory parameters, including Hcy, sdLDL-C, and traditional cardiovascular risk factors, were collected. Cardiovascular events were recorded during follow-up. Multivariable logistic regression was used to assess the independent associations of Hcy and sdLDL-C with cardiovascular risk. Model performance was assessed using receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis (DCA). Cardiovascular events were strongly associated with elevated Hcy and sdLDL-C. Hcy levels showed a dose-response relationship with event rates. After adjustment for age, sex, body mass index, smoking status, hypertension, diabetes, conventional lipid profiles, high-sensitivity C-reactive protein, and estimated glomerular filtration rate, serum homocysteine (Hcy) remained independently associated with cardiovascular risk (OR = 1.90, 95% CI: 1.54–2.35, P < 0.001). sdLDL-C also showed significant predictive value (OR = 1.21, 95% CI: 1.13–1.30, P < 0.001). The traditional model’s area under the ROC curve (AUC) was 0.849. Adding Hcy or sdLDL-C individually improved discrimination, while the combined model achieved a significantly higher AUC of 0.972 (95% CI: 0.953–0.991), with superior calibration and clinical net benefit. In obese patients, Hcy and sdLDL-C are independent risk markers for cardiovascular events. Their combined use significantly enhances risk prediction model performance, aiding refined risk stratification.

BackgroundWe analyzed the prevalence and clinical characteristics of children with plastic bronchitis (PB) caused by severe Mycoplasma pneumoniae (SMPP) and explored its risk factors.MethodsThis retrospective study included pediatric patients with SMPP who were admitted to the Respiratory Department of Children’s Hospital of Soochow University and underwent fiberoptic bronchoscopy (FB) treatment between January 1 and December 31, 2024. The SMPP patients were divided into a PB group and a non-PB group according to whether there was a plastic shape under FB. Epidemiological characteristics, general information, clinical manifestations, laboratory findings, imaging features, and treatment regimens were collected and compared between the two groups. Risk factors for PB were identified using logistic regression analysis, and their predictive value was assessed with receiver operating characteristic (ROC) curves.ResultsThis study incorporated a total of 510 children diagnosed with SMPP, with 60 and 450 assigned to the PB and non-PB groups, respectively. The epidemic peak of SMPP occurred in summer and autumn; the highest detection rate of PB was recorded in winter (19.30%), with the PB positivity rate peaking in December (32.26%). In the PB group, fever days, runny nose, diminished breath sounds, abnormal liver function, abnormal coagulation function, number of bronchoscopic interventions, neutrophil percentage, C-reactive protein (CRP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), D-dimer, atelectasis, and pleural effusion were all significantly higher compared to the non-PB group (P < 0.05). In the PB group, lymphocyte percentage and platelet count were significantly lower compared to the non-PB group (P < 0.05). Multivariate logistic regression analysis identified LDH, pleural effusion, and length of hospital stay as independent predictors of PB in children. The combination of these three indicators yielded a notably higher predictive value, with an area under the receiver operating characteristics curve (AUC) of 0.911 (95% CI: 0.868∼0.953).ConclusionLDH, pleural effusion, and length of hospital stay were independent risk factors for PB in SMPP children. For children suspected of PB, pediatricians should pay close attention to the above indicators, strive for early diagnosis and treatment, and improve prognosis.

Chikungunya virus (CHIKV) and Dengue virus (DENV) infections present with highly similar clinical symptoms but require distinct management strategies, highlighting an urgent need for rapid and accurate differential diagnostic methods. The current gold standard, reverse transcription quantitative real-time PCR (RT-qPCR), has significant limitations: it relies on expensive thermal cyclers, complex laboratory infrastructure, and specialized personnel, making it difficult to implement in resource-limited settings and for on-site screening. To address this technological bottleneck, this study developed a portable, instrument-independent rapid detection technology based on the CRISPR-Cas12a/Cas13a dual-enzyme cleavage system. By precisely designing specific crRNAs targeting the CHIKV E1 gene and the DENV 3′-UTR region, and integrating them with reverse transcription recombinase-aided amplification (RT-RAA) technology, we established an integrated reaction system that performs nucleic acid amplification and detection under isothermal conditions. The core mechanism of the technology is as follows: upon recognition of the corresponding viral targets, Cas12a (targeting CHIKV) and Cas13a (targeting DENV) become activated and cleave fluorescent reporters or lateral flow strip reporter probes, enabling visual detection. Gradient-diluted viral nucleic acid tests indicated that the lowest detectable concentration that generated a signal reached 10² copies/mL, which is comparable to qPCR. Clinical simulated sample validation showed 100% overall agreement with qPCR, and the system accurately distinguished single infections from co-infections.The CRISPR dual-enzyme cleavage technology established in this study effectively circumvents the reliance of qPCR on sophisticated equipment, providing a rapid, simple, and low-cost solution for CHIKV/DENV differential diagnosis. It holds significant practical value for the early prevention and control of arboviral diseases.

Acute Myeloid Leukemia (AML) is a heterogeneous hematologic malignancy driven by genetic and epigenetic alterations, where super-enhancers (SEs) play key oncogenic roles, representing promising therapeutic targets in AML. Through H3K27ac ChIP-seq profiling of 7 AML cell lines and 13 primary samples, we identified USP20 as the deubiquitinase that most frequently associated with super-enhancers. Public database analysis confirmed USP20 overexpression in AML and its correlation with adverse prognosis. Genetic knockdown of USP20 via shRNA significantly induced apoptosis and suppressed proliferation in AML cells in vitro, while in vivo depletion of USP20 attenuated leukemia development and improved overall survival. AS1517499, a novel USP20 inhibitor identified via virtual screening, recapitulated these anti-leukemic effects in vitro and in vivo with low toxicity. Mechanistically, USP20 interacts with CTNNB1 and stabilizes the CTNNB1 protein via deubiquitination. Cut&tag analysis indicated that USP20 co-localizes with CTNNB1 on the genome, where they jointly regulate target genes in AML. Collectively, our study identified USP20 as a super-enhancer-regulated oncogene maintaining AML cell survival and proliferation through CTNNB1 stabilization. Pharmacologic targeting of USP20 with AS1517499 presents a promising therapeutic strategy targeting the SE-USP20- CTNNB1 axis.

Neuroblastoma (NB) is a prevalent pediatric tumor, accounting for over 15% of cancer-related fatalities in children. Super-enhancers (SEs), as pivotal cis-regulatory elements known for driving oncogene expression across various tumors, may serve as an innovative strategy for deciphering NB pathogenesis. Here, we meticulously analyzed epigenomic and transcriptomic data to delineate the distinct SE landscape in NB. Our study identified a NB-specific and NB-common SE at the MAB21L2 locus. Functional analyses further underlined MAB21L2's oncogenic role in NB, linking its high expression to poor patient outcomes. MAB21L2 knockdown strikingly inhibited the growth of NB tumor cells in vitro and reduced their proliferation in vivo. Notably, through RNA-seq analysis and experimental verification, we demonstrated that MAB21L2 substantially enhanced the migratory capacity of NB cells. Collectively, these findings underscore the indispensable role of the super-enhancer-MAB21L2 axis in the pathogenesis of NB and provide mechanistic insights into NB progression.