Background Depressive symptoms have become a significant factor affecting the physical and mental health of the occupational population, and workers in petroleum refining enterprises face multiple stressors in their work environment. Objective To explore the impact of occupational noise exposure on depressive symptoms among workers in a petroleum refining enterprise. Methods This cross-sectional study was conducted in July 2024 using a questionnaire survey among workers of a petroleum refining enterprise in Hainan Province. Basic information of the subjects was collected. The Center for Epidemiologic Studies Depression Scale (CES-D) was used to measure depressive symptoms, the Chinese version of the Pittsburgh Sleep Quality Index (PSQI) scale was used to assess sleep quality, and the Chinese version of the Effort-Reward Imbalance (ERI) scale was used to evaluate occupational stress. Chi-square test was employed to compare the differences in reporting depressive symptoms among populations with different characteristics. Binary logistic regression models were used to analyze the impact of occupational noise exposure and other factors on depressive symptoms. Results The overall positive rate of depressive symptoms in the study population was 42.7%. The results of the multifactor analysis indicated that compared with the control group, employees in both the low-exposure and high-exposure groups had elevated odds of depressive symptoms, with OR (95%CI) of 2.244 (1.131, 4.454) and 1.970 (1.009, 3.850), respectively. This association remained robust after adjusting for potential confounders, including gender, age, work tenure, and other occupational exposures. Additionally, female [OR (95%CI)=1.483 (1.039, 2.118)], exposure to benzene, toluene, or xylene [OR (95%CI)=1.621 (1.208, 2.174)], sleep disturbance [OR (95%CI)=3.772 (2.942, 4.838)], and occupational stress [OR (95%CI)=2.018 (1.575, 2.585)] were also significantly associated with higher odds of depressive symptoms. Conclusion The positive rate of depressive symptoms is relatively high among employees in this petrochemical enterprise, and occupational noise exposure may be a risk factor for depressive symptoms.

OBJECTIVE To systematically analyze the compatibility stability of commonly used intravenous antibiotics in the intensive care unit （ICU）， and to provide evidence-based support for rational clinical drug use. METHODS Medication data from the ICU of Hebei General Hospital between January and December 2024 were extracted from the Prescription Automatic Screening System. Commonly used intravenous antibiotics and other intravenous drugs in the ICU were selected through consultations with critical care and pharmacy experts in Hebei province， drug package inserts and compatibility information retrieved from Micromedex， Trissel’s Injectable Drug Handbook and PubMed. The physicochemical stability of drug combinations was analyzed. In addition， Cytoscape 3.10.2 software was used to construct a drug compatibility network for identifying high-risk drugs. RESULTS &CONCLUSIONS A total of 904 pairwise drug combinations involving 16 antibacterial agents and 65 intravenous drugs were collected. Among them， 549 combinations （60.7%） were compatible， 88 combinations （9.7%） were incompatible， 82 combinations （9.1%） had conflicting evidence， and 185 combinations （20.5%） lacked valid data support. High-risk combination drugs primarily involved Amphotericin B for injection， Ceftazidime for injection， Imipenem-cilastatin for injection， Ceftriaxone sodium for injection， Vancomycin hydrochloride for injection， etc. The main risk factors for drug-drug incompatibility included drug concentration， temperature， mixing rate， pH， and chemical structure. In clinical practice， drugs and diluents should be selected rationally based on specific compatibility data， and research and monitoring of drug compatibility should be further strengthened.

Hepatocellular carcinoma (HCC) is a lethal cancer with high morbidity rates worldwide. It is a major threat to public health in China, due to the combination of known and new risk factors, such as endemic hepatitis B virus (HBV), dietary aflatoxin exposure, and the occurrence of metabolic dysfunction-associated steatotic liver disease (MASLD). Although many methods for surveillance and multimodal therapies, such as surgery, local ablation, transarterial therapy, and new systemic agents, have been available, the survival rates of HCC remains poor. They have very limited durable responses, long post-treatment recurrence rates, and high resistance to treatment. This reflects an imperfect picture of the biological cause of the disease and a need for new mechanistic or targeted techniques. A significant characteristic of HCC, in common with other aggressive cancers, is the presence of reprogrammed, hyperactive cell metabolism. Tumor cells hijack metabolic pathways to promote their uncontrolled growth, stress survival, invasion and metastasis. While classical mechanisms such as the Warburg effect, lipid metabolism and glutamine utilization have been understood, the lysosome, which was once viewed as a static “waste disposal unit” to remove old organelles and proteins, is instead a dynamic signaling and metabolic core. The lysosomes incorporate nutrients, energy and stress signals by master regulators such as mTORC1 (activated on its surface) that balance anabolic growth and catabolic recycling to the cellular demands. In HCC, lysosomes are not passive, but are highly active and dysregulated. HCC cells upregulate lysosomes, which scavenge intracellular components via enhanced autophagy and engulf extracellular proteins via macropinocytosis, crucial for survival in the nutrient-poor, hypoxic tumor microenvironment. In addition to metabolism, lysosomes exhibit pro-invasive functions by secreting hydrolases to remodel the extracellular matrix, promote angiogenesis, and suppress stromal immune cells to foster a pro-tumor microenvironment. In a clinical context, lysosomes play an important role in therapeutic resistance: they sequester and inactivate chemotherapeutics via lysosomal sequestration, and enhanced autophagic flux protects the cell from therapy-induced damage, contributing to relapse, as lysosomal dysfunction is a key cause of treatment failure. This makes lysosomes promising yet challenging therapeutic targets in HCC. Recent preclinical and early clinical studies investigate multiple strategies to exploit the susceptibility of lysosomes: lysosome-specific agents, alkalinizing the lysosome lumen or inducing membrane permeabilization and lysosome-dependent cell death; pharmacological inhibition of key lysosomal enzymes or autophagy to impair nutrient recycling and stress adaptation; smart nanotherapeutic agents or antibody-drug conjugates, specifically activated in the acidic lysosomal environment or utilizing lysosomal pathways for efficient intracellular drug release; and combination strategies of lysosome-targeting agents with tyrosine kinase inhibitors or immunotherapy to overcome resistance and achieve synergistic antitumor effects. In summary, our review systematically presents the role of lysosomes in HCC, from metabolic reprogramming and microenvironmental adaptation to therapeutic resistance. By synthesizing the latest mechanistic insights and preclinical advances, this review highlights the indispensable role of lysosomes in the complex HCC biological network, emphasizing that an in-depth understanding of this dynamic organelle holds great promise for developing innovative, targeted therapies, offering new hope for improving the poor prognosis of global HCC patients.

arcopenia is a systemic skeletal muscle disorder characterized by a decrease in skeletal muscle mass and progressive decline in function， with multiple signaling pathways involved in its occurrence and development. Among them， the AMP-activated protein kinase （AMPK） signaling pathway， as a key pathway regulating cellular energy homeostasis， plays an important role in the regulation of skeletal muscle metabolism and functional maintenance by improving abnormalities in glucose and lipid metabolism， balancing skeletal muscle protein synthesis and degradation， improving mitochondrial function， promoting autophagy， and inhibiting inflammatory responses and oxidative stress. This article reviews the research progress on how various traditional Chinese medicine （TCM） monomers， including polyphenols， flavonoids， and terpenoids； various traditional Chinese medicine extracts， such as those from Lycium barbarum ， Asini Corii Colla， and Panax quinquefolium ， and TCM compounds， such as Guiqi zhuangjin decoction， Jianpi qiangji granules， and Qigu capsules， intervene in sarcopenia by regulating the AMPK signaling pathway to promote muscle protein synthesis， inhibit protein degradation， improve mitochondrial function， and alleviate inflammation and oxidative stress. Additionally， their molecular mechanisms are explored. The aim is to deeply elucidate the basis of TCM in the prevention and treatment of sarcopenia and to provide theoretical support for the development of related innovative drugs.

AIM: To investigate the effects of insulin-like growth factor 1(IGF-1)on the secretion of transforming growth factor β2(TGF-β2), matrix metalloproteinase 2(MMP-2)and hypoxia-inducible factor 1α(HIF-1α)in human scleral fibroblasts(HSF)and their mechanism.METHODS: The cells were cultured with IGF-1 and PI3K/AKT pathway inhibitor LY294002, respectively. CCK-8 method was used to detect cell viability and determine the optimal concentration and time of drug action. Cell migration activity was observed by cell scratch method. To determine the effects of IGF-1 on HSF cells and the regulatory role of PI3K/AKT pathway, HSF cells were divided into control group(without drugs), IGF-1(80 μg/L)group, IGF-1+LY294002(80 μg/L+5 mmol/L)group, and LY294002(5 mmol/L)group, and were cultured for 24 h; the protein expression levels of TGF-β2, MMP-2, HIF-1α, PI3K and AKT were detected by Western blot; the fluorescence expression of TGF-β2, MMP-2 and HIF-1α was detected by cellular immunofluorescence.RESULTS: The results of CCK-8 showed that the cell viability of the 80 μg/L IGF-1 group cultured with different concentrations of IGF-1 was the highest(all P<0.05), and the cell viability of the 80 μg/L IGF-1 group at 24 h was the highest under different culture times. Therefore, the concentration of IGF-1 was selected as 80 μg/L for 24 h. The viability of cells cultured with different concentrations of LY294002 gradually decreased from 6 h(all P<0.05). According to the IC50 value, therefore, the concentration of LY294002 was selected as 5 mmol/L for 24 h. The cell scratch results showed that compared with the control group, the cell mobility of 40 μg/L and 80 μg/L IGF-1 groups was increased(all P<0.05). Compared with the control group, cell mobility in the 2.5 and 5 mmol/L LY294002 groups was decreased(all P<0.05). Western blot results showed that compared with the control group, the protein expressions of TGF-β2, MMP-2, HIF-1α, PI3K and AKT in the IGF-1 group were increased, while those in the LY294002 group were decreased(all P<0.05). Compared with the IGF-1 group, the expression levels of TGF-β2, MMP-2, HIF-1α, PI3K and AKT in the IGF-1+LY294002 group were decreased(all P<0.05). The results of cell immunofluorescence showed that compared with the control group, the fluorescence expressions of TGF-β2, MMP-2 and HIF-1α in the IGF-1 group were increased, while those in the LY294002 group were decreased(all P<0.05). Compared with the IGF-1 group, the fluorescence expressions of TGF-β2, MMP-2 and HIF-1α in the IGF-1+LY294002 group were significantly decreased(all P<0.05).CONCLUSION: IGF-1 promoted the proliferation and migration of human HSF. IGF-1 may up-regulate the expression of TGF-β2, MMP-2 and HIF-1α in HSF through the PI3K/AKT signaling pathway, and participate in the occurrence and development of myopia.

Objective: To systematically analyze the revisions content and technological development trends of microbiological standards in the Chinese Pharmacopoeia (ChP) 2025 Edition, and explore its novel requirements in risk-based pharmaceutical product lifecycle management.
Methods: A comprehensive review was conducted on 26 microbiological-related standards to summarize the revision directions and scientific implications from perspectives including the revision overview, international harmonization of microbiological standards, risk-based quality management system, and novel tools and methods with Chinese characteristics.
Results: The ChP 2025 edition demonstrates three prominent features in microbiological-related standards: enhanced international harmonization, introduced emerging molecular biological technologies, and established a risk-based microbiological quality control system.
Conclusion: The new edition of the Pharmacopoeia has systematically constructed a microbiological standard system, which significantly improves the scientificity, standardization and applicability of the standards, providing a crucial support for advancing the microbiological quality control in pharmaceutical industries of China.

Objective:To explore the therapeutic strategy for laryngeal cysts in infants. Methods:A retrospective analysis of the clinical data of 19 children with laryngeal cysts treated in Kunming Children's Hospital from January 2020 to January 2023. All patients were diagnosed through electronic laryngoscopy examination. Twelve neonates were admitted to the neonatal intensive care unit. Five of them received mechanical ventilation with tracheal intubation before surgery due to severe respiratory distress, and seven received oxygen therapy with a head mask. The remaining seven children were admitted to Department of Otolaryngology Head and Neck Surgery, of which three cases were treated with oxygen therapy through a mask during sleep due to frequent shortness of breath during sleep. All patients underwent low-temperature plasma radiofrequency ablation under general anesthesia to remove the cysts. Results:Three newborns were unable to have their tracheal tubes removed due to complications with pneumonia after surgery, while the rest of the children were able to have their tubes successfully removed after complete anesthesia, and no gastric tubes were placed. All postoperative respiratory difficulties in the children disappeared, and there were no complications such as bleeding, hoarseness, or laryngeal stenosis. Five pediatric patients had incomplete relief of laryngeal ringing symptoms one month after surgery, and electronic laryngoscopy diagnosed laryngeal softening. Regular follow-up is recommended. One child relapsed 4 months after surgery and underwent a follow-up surgery six months later without recurrence. Conclusion:Endoscopic low-temperature plasma radiofrequency ablation is an effective surgical method for treating laryngeal cysts, with a low postoperative recurrence rate. Laryngeal cysts may be accompanied by laryngeal softening, which may be a possible reason for the postoperative symptoms not improving.
Humans ; Retrospective Studies ; Cysts/surgery* ; Laryngeal Diseases/surgery* ; Infant ; Laryngoscopy ; Infant, Newborn ; Male ; Female ; Radiofrequency Ablation

Environmental toxicants have been linked to aging and age-related diseases. The emerging evidence has shown that the enhancement of detoxification gene expression is a common transcriptome marker of long-lived mice, Drosophila melanogaster, and Caenorhabditis elegans. Meanwhile, the resistance to toxicants was increased in long-lived animals. Here, we show that farnesoid X receptor (FXR) agonist obeticholic acid (OCA), a marketed drug for the treatment of cholestasis, may extend the lifespan and healthspan both in C. elegans and chemical-induced early senescent mice. Furthermore, OCA increased the resistance of worms to toxicants and activated the expression of detoxification genes in both mice and C. elegans. The longevity effects of OCA were attenuated in Fxr ^-/- mice and Fxr homologous nhr-8 and daf-12 mutant C. elegans. In addition, metabolome analysis revealed that OCA increased the endogenous agonist levels of the pregnane X receptor (PXR), a major nuclear receptor for detoxification regulation, in the liver of mice. Together, our findings suggest that OCA has the potential to lengthen lifespan and healthspan by activating nuclear receptor-mediated detoxification functions, thus, targeting FXR may offer to promote longevity.

Alzheimer's disease (AD) is a common neurodegenerative disorder among the elderly, and BuChE has emerged as a potential therapeutic target. In this study, we reported the development of compound 8e, a selective reversible BuChE inhibitor (eqBuChE IC₅₀ = 0.049 μmol/L, huBuChE IC₅₀ = 0.066 μmol/L), identified through extensive virtual screening and lead optimization. Compound 8e demonstrated favorable blood-brain barrier permeability, good drug-likeness property and pronounced neuroprotective efficacy. Additionally, 8e exhibited significant therapeutic effects in zebrafish AD models and scopolamine-induced cognitive impairments in mice. Further, 8e significantly improved cognitive function in APP/PS1 transgenic mice. Proteomics analysis demonstrated that 8e markedly elevated the expression levels of very low-density lipoprotein receptor (VLDLR), offering valuable insights into its potential modulation of the Reelin-mediated signaling pathway. Thus, compound 8e emerges as a novel and potent BuChE inhibitor for the treatment of AD, with significant implications for further exploration into its mechanisms of action and therapeutic applications.

Background: s/Aims: Sarcomatoid hepatocellular carcinoma (HCC) is a rare histological subtype of HCC characterized by extremely poor prognosis; however, its molecular characterization has not been elucidated. Methods: In this study, we conducted an integrated multiomics study of whole-exome sequencing, RNA-seq, spatial transcriptome, and immunohistochemical analyses of 28 paired sarcomatoid tumor components and conventional HCC components from 10 patients with sarcomatoid HCC, in order to identify frequently altered genes, infer the tumor subclonal architectures, track the genomic evolution, and delineate the transcriptional characteristics of sarcomatoid HCCs. Results: Our results showed that the sarcomatoid HCCs had poor prognosis. The sarcomatoid tumor components and the conventional HCC components were derived from common ancestors, mostly accessing similar mutational processes. Clonal phylogenies demonstrated branched tumor evolution during sarcomatoid HCC development and progression. TP53 mutation commonly occurred at tumor initiation, whereas ARID2 mutation often occurred later. Transcriptome analyses revealed the epithelial–mesenchymal transition (EMT) and hypoxic phenotype in sarcomatoid tumor components, which were confirmed by immunohistochemical staining. Moreover, we identified ARID2 mutations in 70% (7/10) of patients with sarcomatoid HCC but only 1–5% of patients with non-sarcomatoid HCC. Biofunctional investigations revealed that inactivating mutation of ARID2 contributes to HCC growth and metastasis and induces EMT in a hypoxic microenvironment. Conclusions We offer a comprehensive description of the molecular basis for sarcomatoid HCC, and identify genomic alteration (ARID2 mutation) together with the tumor microenvironment (hypoxic microenvironment), that may contribute to the formation of the sarcomatoid tumor component through EMT, leading to sarcomatoid HCC development and progression.