To analyze the disease burden of acute lymphoid leukemia(ALL) and its changing trends in China and globally from 1990 to 2021, aiming to provide a theoretical basis for disease prevention, treatment, and policy formulation.

ObjectiveTaking Aurantii Fructus Immaturus juice（AFI）-processed Atractylodis Macrocephalae Rhizoma（AMR） as an example， this study aims to systematically compare the volatile and non-volatile components of AMR and its processed products， investigate the key differential components， evaluate their anti-inflammatory activities， and elucidate the synergistic mechanism of processing. MethodsThe chemical compositions of volatile and non-volatile components in AMR and AFI-processed AMR were systematically characterized using gas chromatography-mass spectrometry（GC-MS） and ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry（UPLC-Q-TOF-MS）， with relative mass fractions and response values determined separately. Volatile components were identified through searches in the National Institute of Standards and Technology（NIST）17 database， comparison with retention index（RI） and fragmentation pattern matching. Non-volatile components were identified by searching Waters Traditional Chinese Medicine （TCM） spectral library， in conjunction with PubChem and MassBank， characteristic fragmentation patterns and response values were also used to support identification. Differential components were screened using principal component analysis（PCA）， orthogonal partial least squares-discriminant analysis（OPLS-DA）， with variable importance in the projection（VIP） value >1. Components with high log₂fold change（FC） among major differential groups were selected as those exhibiting significant changes before and after processing. The anti-inflammatory activity of the differential compounds was evaluated by assessing their effects on nitric oxide（NO） production in a lipopolysaccharide（LPS）-induced RAW264.7 macrophage model. Enzyme-linked immunosorbent assay（ELISA） was used to detect the effects of the differential components on tumor necrosis factor（TNF）-α， interleukin（IL）-1β， IL-6， and monocyte chemotactic protein（MCP）-1 levels， and immunofluorescence（IF） was employed to assess their effects on nuclear transcription factor（NF）-κB p65 translocation， thereby elucidating the underlying molecular mechanisms. ResultsA total of 36 compounds were identified in the volatile components of AMR and AFI-processed AMR， among which， sesquiterpenes and monoterpenes were significantly increased after processing. In the non-volatile components， 36 compounds were identified， and the main differential components were flavonoids， sesquiterpenoids， and triterpenoids. Flavonoids were the primary differential components distinguishing AMR from its processed products， representing compounds directly introduced during processing. Five compounds， including atractylenolide Ⅲ， tangeritin， nobiletin， hesperidin and narirutin， were selected as representatives of three classes based on their most prominent differential expression among different compound types for subsequent anti-inflammatory activity studies. The results showed that 100 μmol·L^-1 tangerine and narirutin could significantly inhibit LPS-induced NO production（P<0.01） in a concentration-dependent manner. Tangeritin was able to significantly inhibit the levels of TNF-α and MCP-1 secreted by RAW264.7（P<0.05）， while narirutin significantly inhibited the levels of TNF-α， IL-1β， MCP-1 and IL-6（P<0.01）. IF revealed that both tangeritin and narirutin significantly blocked the translocation of NF-κB p65 from the cytoplasm to the nucleus. ConclusionAFI-processed AMR significantly alters the chemical composition profile of AMR， and the newly introduced flavonoid components during processing may be key to its enhanced anti-inflammatory effects.

[摘 要] 目的：探究环状RNA（circRNA）调控舌鳞状细胞癌（TSCC）顺铂（CDDP）耐药的机制。方法：本研究以TSCC化疗敏感CAL27细胞与耐药CAL27-res细胞为研究对象，RT-qPCR检测两种细胞内hsa_circ_0034762的表达量差异，流式细胞术检测细胞凋亡率，Western blotting检测自噬相关蛋白p62及LC3-Ⅱ/LC3-Ⅰ比值，透射电镜观察自噬小体的数量，双萤光素酶报告实验检测hsa_circ_0034762与miR-17-3p的结合关系，荧光原位杂交实验检测二者在细胞中的共定位，敲低hsa_circ_0034762联合抑制miR-17-3p进行功能回复实验。结果：相比亲本化疗敏感细胞，TSCC耐药细胞CAL27-res自噬水平显著提升，表现为自噬小体数量增加、LC3-Ⅱ/LC3-Ⅰ比值升高及p62蛋白表达降低。hsa_circ_0034762在TSCC耐药组织及CAL27-res细胞中高表达。敲低hsa_circ_0034762后，CAL27-res细胞凋亡率升高，自噬小体数量减少，p62蛋白表达增加，LC3-Ⅱ/LC3-Ⅰ比值降低（均P < 0.05）。双萤光素酶报告实验与荧光原位杂交实验发现hsa_circ_0034762与miR-17-3p存在靶向结合作用。抑制miR-17-3p可部分逆转hsa_circ_0034762敲低所致的促凋亡及抑制自噬效应。结论：hsa_circ_0034762在TSCC耐药细胞及组织中高表达。敲低hsa_circ_0034762可能通过miR-17-3p抑制细胞自噬并促进细胞凋亡，从而降低TSCC细胞的化疗耐药性。

In March 2024, three male and two female specimens of the genus Lispe were intercepted on cargo ships inbound for Wan Zai Port under Gongbei Customs. Based on morphological characteristics and molecular analysis, the specimens were identified as Lispe pumila. In this study, we describe the morphological features, diagnostic characteristics, and geographical distribution of L. pumila, with the aim of providing a reference for the identification of this species when intercepted at ports.

Objective To summarize the clinical features and treatment strategies of acute mercury poisoning caused by intramuscular injection of metallic mercury. Methods The clinical data of a patient with acute mercury poisoning following intramuscular injection of metallic mercury were collected, and a retrospective analysis of the diagnosis and treatment process was conducted. Results The patient was a 14-year-old boy who self-injected 20 g of metallic mercury into the left upper arm muscle. Clinical manifestations included fever, chest tightness, cough, and a painful mass at the injection site. Laboratory tests of the patient indicated that blood mercury level was 4.160 μmol/L, urinary mercury level was 6 545.50 μg/g creatinine, urinary retinol-binding protein was 6 556 μg/L, urinary β₂-microglobulin was 8 726.48 μg/g creatinine, and urinary α1-microglobulin was 41.60 mg/L at day 11 after injection. Thoracoabdominal imaging revealed mercury deposition in the lungs, heart, liver, kidneys, and other organs. The patient's clinical symptoms were markedly relieved after one course of treatment with sodium dimercaptopropanesulfonate for mercury chelation. Subsequent treatment included continued mercury chelation therapy, debridement of muscle tissue at the injection site, removal of retained foreign bodies, and other supportive measures. Reexamination showed a blood mercury level of 2.810 μmol/L and urinary mercury level of 5 280 μg/L at day 127 after injection. Conclusion The clinical manifestations of intramuscular injection of metallic mercury poisoning differ from those of occupational mercury poisoning. Debridement of the injection site combined with sodium dimercaptopropanesulfonate chelation therapy can alleviate systemic symptoms and reduce mercury levels in such patients.

ObjectiveTo investigate the expression of family with sequence similarity 162 member A （Fam162a）， a mitochondrial inner membrane protein， in the fibrosis of cardiac fibroblasts and its regulatory role in modulating the fibrotic phenotype of cardiac fibroblasts. MethodsFam162a protein expression was detected in myocardial samples from patients with heart failure （HF） and mice with transverse aortic constriction （TAC）-induced myocardial remodeling. Primary neonatal mouse cardiac fibroblasts （mCFs） were isolated and cultured， and a cell model of angiotensin Ⅱ （Ang Ⅱ）-induced myocardial fibrosis was established to determine Fam162a protein expression. Recombinant adenovirus was used to mediate Fam162a overexpression， while small interfering RNA （si-RNA） was employed for Fam162a knockdown. Western blot was performed to detect the expression of fibrosis-related proteins， including COL1A1， COL3A1， and α-SMA. EdU staining assay was used to evaluate cell proliferation capacity， and scratch assay combined with Transwell assay was conducted to assess cell migration ability. Immunofluorescence assay was applied to measure mitochondrial membrane potential for reflecting mitochondrial dysfunction； reactive oxygen species （ROS） detection was performed to evaluate cellular oxidative stress status； MitoSox assay was used to reflect the degree of mitochondrial oxidative damage； and ATP detection was conducted to assess the overall cellular energy metabolism. ResultsFam162a expression was significantly downregulated in the myocardium of HF patients and TAC mice， and Ang Ⅱ-treated mCFs， accompanied by increased expression of COL1A1， COL3A1， and α-SMA （all P＜0.05）. Adenovirus-mediated overexpression of Fam162a significantly inhibited Ang Ⅱ-induced upregulation of fibrosis-related genes， as well as cell proliferation and migration. Accordingly， silencing Fam162a aggravated the fibrotic phenotypes of mCFs treated with Ang II. Further studies revealed that the inhibitory effect of Fam162a overexpression on Ang Ⅱ-induced fibrotic phenotype was suppressed following the addition of rotenone （a mitochondrial oxidative respiratory chain inhibitor）， which was accompanied by mitochondrial membrane potential depolarization， excessive ROS production， and insufficient ATP generation. ConclusionFam162a exerts its inhibitory effect on the fibrotic phenotype of cardiac fibroblasts by maintaining mitochondrial membrane potential， promoting ATP production， reducing reactive oxygen species （ROS） generation， and suppressing Smad3 signaling activation.

Objective To propose a framework for risk assessment and stepwise management of pulmonary nodules based on existing guidelines and key studies, and to clarify the boundaries for triage, workup escalation, and referral in different detection scenarios. Methods A problem-oriented evidence synthesis approach was used, prioritizing Chinese expert consensus, Fleischner Society Guidelines, British Thoracic Society (BTS) Guidelines, and Lung-RADS. This was supplemented by studies on risk models, imaging measurements, liquid biopsy, tissue sampling, and surgical treatments. This paper is not presented as a formal consensus or a validated clinical pathway. Results A three-tiered framework consisting of basic non-invasive assessment, advanced assessment, and invasive diagnosis was established. It specified the applicable populations, boundaries for the use of risk models, imaging review, management of conflicting results, evaluation of histopathological consistency, and post-intervention follow-up. Liquid biopsy, genetic testing, and artificial intelligence were defined as investigational or adjunctive tools. Conclusion This framework can serve as a preliminary reference for multidisciplinary teams in developing local protocols. It cannot replace applicable guidelines, pathological diagnosis, shared decision-making with patients, or real-world validation.

ObjectiveMethylthioadenosine phosphorylase (MTAP) is found to be frequently deleted in malignant cancers, but the role of MTAP underlying metastasis and stemness of liver cancer remains far from clear. 5-fluorouracil (5-Fu) is clinically used in treating advanced liver cancer, however, chemoresistance is one of the major barriers impeding its efficacy. Liver cancer stem cells are considered to be the reservoir for tumor progression and chemoresistance. This study aims to explore the role of MTAP in regulating stemness and chemoresistance of 5-Fu in liver cancer. It is designed to elucidate the molecular mechanisms underlying MTAP-manipulated stemness. How MTAP influences metastasis and chemoresistance against 5-Fu in liver cancer is also elaborated. MethodsThe correlation of MTAP expression with stemness marker CD133 was evaluated by flow cytometry. Colony formation assays were conducted to analyze the tumorigenic ability. Western blot assays were applied to delineate the molecular mechanisms underlying MTAP-regulated stemness. Trans-well assays were conducted to analyze the metastatic potential of liver cancer cells.In vivo experiments were performed using subcutaneous xenograft and lung metastasis model on nude mice. Tumor size and weight were analyzed upon 5-Fu treatment. Metastatic nodules on lungs were evaluated. Immunohistochemical and TUNNEL assays were performed on slides obtained from tumor tissues. ResultsMTAP overexpression inhibited expression of CD133 and colony formation, which is further ablated by MTAP inhibitor. MTAP deprivation augmented stemness and colony formation, which is reversed by protein arginine methyltransferase 5 (PRMT5) overexpression but not its catalytically inactive counterparts. Critically, SRY-box transcription factor 2 (SOX2) was found to be a downstream regulator of MTAP/PRMT5, leading to stemness of liver cancer cells. MTAP overexpression suppressed SOX2 expression, while MTAP inhibition augmented expression of SOX2. Critically, MTAP overexpression inhibited migration and invasion of liver cancer cells. In vivo experiments in animal model found that MTAP deprivation promotes tumor growth and metastatic nodules of liver cancer. Additionally, MTAP overexpression inhibits tumor growth. Moreover, MTAP deprivation contributes to chemoresistance shown by increased tumor size and weight treated by 5-Fu. In contrast, MTAP overexpression led to further decline in tumor size and weight elicited by 5-Fu treatment. Accordingly, SOX2 was inhibited in tumor tissues after MTAP overexpression. Marker of proliferation Ki67 (Ki67) expression was dampened while apoptosis was found in MTAP-overexpressed tumor tissues. ConclusionIn this study, plethora of experimental studies collectively demonstrated that MTAP deprivation enhances stemness of liver cancer by regulating SOX2, exerting anti-cancer and chemoresistant role against 5-Fu in liver cancer. It is also worth noting that MTAP inhibition promoted metastasis of liver cancer. MTAP overexpression augmented tumor shrinking elicited by 5-Fu and SOX2 was involved in this process. These results concluded that MTAP/PRMT5/SOX2 signaling axis was involved in regulating stemness and chemoresistance of liver cancer. These findings help to exploit novel therapies by targeting stemness in MTAP-depleted liver cancer. It shed novel light on unveiling MTAP-regulated stemness in antagonizing 5-Fu treatment in liver cancer. It also adds mounting evidence to the theoretical basis for accomplishing personalized chemotherapy of liver cancer patients by targeting MTAP or its downstream PRMT5/SOX2.

The recombinant human thyroid-stimulating hormone (rhTSH) can be used for differentiated thyroid cancer (DTC) preparation before ¹³¹I therapy, and follow-up. Since its approval by the American Food and Drug Administration (FDA) in 1998, rhTSH has been clinically used in European countries, the United States, and other countries for nearly 30 years. In April 2024, China’s first independently developed rhTSH agent was approved. Based on clinical experience and evidence from domestic and international studies, an expert consensus on the application of rhTSH has been developed following thorough consultations among experts. The consensus offers evidence-based recommendations to guide the appropriate use of rhTSH in clinical practice.

Abstract: To explore the latent profiles of physical activity among junior and senior high school students and the association with short-video addiction, so as to provide evidence for the prevention of short-video addiction among adolescents. Methods: In November 2024, a stratified random sampling method was used to select 20 840 students from 120 junior and senior high schools in Guangdong Province. Physical activity and short-video addiction were assessed using International Physical Activity Questionnaire and Short-video Addiction Scale. Latent profile analysis was used to identify latent classes of physical activity. The robust three-step approach was used to examine the effects of demographic variables, including sex, school stage, age, and residence, on profile membership, and the Bolck-Croon-Hagenaars (BCH) method was used to compare short-video addiction levels across profiles after adjusting for demographic variables. Results: Four latent profiles of physical activity in junior and senior high school students were identified:low-frequency low-duration profile ( n =1 668, 8.00%), weekday high-frequency activity profile ( n = 12 408 , 59.54%), weekday low-frequency activity profile ( n =5 107, 24.51%), and high frequency high-duration profile ( n = 1 657 , 7.95%). With the high-frequency high-duration profile as the reference, girls were more likely to be assigned to the weekday high-frequency activity profile and less likely to be in the low-frequency low-duration profile compared with boys ( B =0.27, -0.33 ); senior high school students had higher odds of membership in the other three profiles than junior high school students ( B =0.63- 1.09 ); increasing age was associated with increased odds of the low-frequency low-duration profile ( B =0.11); rural students were less likely to belong to the other three profiles than urban students ( B =-0.97 to -0.79) (all P <0.01). After adjusting for demographic variables, short-video addiction scores differed significantly across physical activity profiles in junior and senior high school students ( χ 2=390.23, P <0.01), with scores decreasing in the following order:low-frequency low-duration profile, weekday low-frequency activity profile, weekday high-frequency activity profile, and high-frequency high-duration profile. Conclusions Short-video addiction levels vary across different physical activity patterns in junior and senior high school students. Overall, participants with high-frequency and high-duration participation score the lowest, whereas those with low-frequency and low-duration participation score the highest.