OBJECTIVE To evaluate the efficacy， safety and economics of the centrally procured generic versus original esomeprazole in the treatment of acute non-variceal upper gastrointestinal bleeding （ANVUGIB）. METHODS A retrospective collection of real-world clinical data was conducted for ANVUGIB patients who received treatment at Shenzhen People’s Hospital and University of Hong Kong-Shenzhen Hospital from January 2018 to March 2024. Patients were divided into imported original drug group （original drug group， 221 cases） and centrally procured generic drug group （generic drug group， 75 cases） according to the types of drug used. Propensity score matching （PSM） was performed at a ratio of 3∶1 to compare the clinical efficacy， safety and economics between the two groups. RESULTS Totally 241 patients were included after PSM， with 170 in the original drug group and 71 in the generic drug group. There were no significant differences between the two groups in terms of rebleeding rate， rate of second endoscopic intervention， blood transfusion rate， length of hospital stay， mortality due to gastrointestinal bleeding， 30-day readmission due to rebleeding， and overall survival rate （P＞0.05）. The incidence of adverse events among all patients in both groups also showed no statistically significant difference （P＞0.05）； furthermore， the adverse events reported by the respective hospitals to the National Center for ADR Monitoring were comparable between the two groups. After PSM， the median total drug cost and high-dose esomeprazole cost in the generic drug group were significantly lower than those in the original drug group， while the median nursing fee and bed fee were significantly higher than those in the original drug group （P＜0.05）. There was no statistically significant difference between the two groups in terms of median total hospitalization expenses， total treatment costs， laboratory fees， examination fees， material costs， or consultation fees （P＞0.05）. CONCLUSIONS The clinical efficacy and safety of centrally procured generic esomeprazole in the treatment of ANVUGIB are comparable to those of the original drug， and it is more economical.

[Objective] To analyze the effects of different factors and red blood cell transfusion thresholds on the efficacy of neonatal red blood cell (RBC) transfusion, in order to provide more references for neonatal transfusions to better achieve rational and effective blood use. [Methods] A retrospective collection of data from 282 neonates who received RBC transfusions at our hospital from 2022 to 2023 was conducted, including birth weight, gestational age, number of blood transfusions, length of hospital stay, assisted ventilation during RBC transfusion, and laboratory test results before and after transfusion. SPSS software was used for statistical analysis to comprehensively analyze the impact of different factors on the efficacy of RBC transfusion in neonates. [Results] The results showed that the gestational age and weight of newborns at birth were negatively correlated with their length of hospital stay and the number of RBC transfusions during hospitalization. Newborns with younger gestational age and lower weight had longer hospital stays and more RBC transfusions during hospitalization. After administering RBCs according to the standard of 15 mL/kg, there was a statistically significant difference in the efficacy of RBC transfusion at different transfusion thresholds. In non-critical situations, RBC transfusions were ineffective when the pre-transfusion hemoglobin (Hb) level was >120 g/L. When the pre-transfusion Hb level was ≤70 g/L, RBC transfusions achieved higher efficacy in both critical and non-critical situations. [Conclusion] In critical situations, the group with pre-transfusion Hb values ≤ 70 g/L has the best RBC transfusion effect, while in non-critical situations, the group with pre-transfusion Hb levels between 81 and 90 g/L has the best RBC transfusion effect. Overall, the efficacy of RBC transfusion in non-critical situations is higher than that in critical situations.

Adipose tissue is a critical energy reservoir in animals and humans, with multifaceted roles in endocrine regulation, immune response, and providing mechanical protection. Based on anatomical location and functional characteristics, adipose tissue can be categorized into distinct types, including white adipose tissue (WAT), brown adipose tissue (BAT), beige adipose tissue, and pink adipose tissue. Traditionally, adipose tissue research has centered on its morphological and functional properties as a whole. However, with the advent of single-cell transcriptomics, a new level of complexity in adipose tissue has been unveiled, showing that even under identical conditions, cells of the same type may exhibit significant variation in morphology, structure, function, and gene expression——phenomena collectively referred to as cellular heterogeneity. Single-cell transcriptomics, including techniques like single-cell RNA sequencing (scRNA-seq) and single-nucleus RNA sequencing (snRNA-seq), enables in-depth analysis of the diversity and heterogeneity of adipocytes at the single-cell level. This high-resolution approach has not only deepened our understanding of adipocyte functionality but also facilitated the discovery of previously unidentified cell types and gene expression patterns that may play key roles in adipose tissue function. This review delves into the latest advances in the application of single-cell transcriptomics in elucidating the heterogeneity and diversity within adipose tissue, highlighting how these findings have redefined the understanding of cell subpopulations within different adipose depots. Moreover, the review explores how single-cell transcriptomic technologies have enabled the study of cellular communication pathways and differentiation trajectories among adipose cell subgroups. By mapping these interactions and differentiation processes, researchers gain insights into how distinct cellular subpopulations coordinate within adipose tissues, which is crucial for maintaining tissue homeostasis and function. Understanding these mechanisms is essential, as dysregulation in adipose cell interactions and differentiation underlies a range of metabolic disorders, including obesity and diabetes mellitus type 2. Furthermore, single-cell transcriptomics holds promising implications for identifying therapeutic targets; by pinpointing specific cell types and gene pathways involved in adipose tissue dysfunction, these technologies pave the way for developing targeted interventions aimed at modulating specific adipose subpopulations. In summary, this review provides a comprehensive analysis of the role of single-cell transcriptomic technologies in uncovering the heterogeneity and functional diversity of adipose tissues.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

Background and Objectives: Electronic cigarette (e-cigarette) is a device that generate vapor by heating e-cigarettes liquid. E-cigarette damages the respiratory immune system and renders the respiratory tract vulnerable to inflammations. However, there are no studies on how the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, and the effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigarette are unknown. This study aimed to compare the inflammatory reactions caused by e-cigarette and lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokine and mucin expression induced by e-cigarette in respiratory epithelial cells.Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects of KRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B (MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerase chain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results: Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNA expression and protein production were increased by e-cigarette, similar to LPS. KRG and saponin decreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced by e-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponin regulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratory epithelial cells. KRG and saponin may be an effective therapeutic option for inflammatory responses induced by e-cigarette in respiratory epithelial cells.

This study investigates the reproductive protective effect and potential mechanism of Cistanches Herba extract(CHE) on a rat model of kidney-Yang deficiency induced by adenine. Rats were randomly divided into five groups: normal, model, low-dose CHE(0.6 g·kg~(-1)·d~(-1)), high-dose CHE(1.2 g·kg~(-1)·d~(-1)), and L-carnitine(100 mg·kg~(-1)·d~(-1)). The rats were administered adenine(200 mg·kg~(-1)·d~(-1)) by gavage for the first 14 days to induce kidney-Yang deficiency, while simultaneously receiving drug treatment. After 14 days, the modeling was discontinued, but drug treatment continued to 49 days. The content of components in CHE was analyzed by high-performance liquid chromatography. The adenine-induced kidney-Yang deficiency model was assessed through symptom characterization and measurement of testosterone(T) levels using an enzyme-linked immunosorbent assay kit. Pathological damage to the testis and epididymis was evaluated based on the wet weight and performing hematoxylin-eosin staining. Sperm density and motility were measured using computer-aided sperm analysis, and sperm viability was assessed using live/dead sperm staining kits, and sperm morphology was evaluated using eosin staining, thereby determining rat sperm quality. Metabolomics was used to analyze changes in serum metabolites, enrich related metabolic pathways, and explore the mechanism of CHE in improving reproductive function damage in rats with kidney-Yang deficiency syndrome. Compared to the normal group, the model group exhibited significant kidney-Yang deficiency symptoms, reduced T levels, decreased testicular and epididymal wet weights, and significant pathological damage to the testis and epididymis. The sperm density, motility, and viability decreased, with an increased rate of sperm abnormalities. In contrast, rats treated with CHE showed marked improvements in kidney-Yang deficiency symptoms, restored T levels, alleviated pathological damage to the testis and epididymis, and improved various sperm parameters. Metabolomics results revealed 286 differential metabolites between the normal and model groups(191 upregulated and 95 downregulated). Seventy-five differential metabolites were identified between the model and low-dose CHE groups(21 upregulated and 54 downregulated). A total of 24 common differential metabolites were identified across the three groups, with 22 of these metabolites exhibiting opposite regulation trends between the two comparison groups. These metabolites were primarily involved in linoleic acid metabolism, ether lipid metabolism, and pantothenic acid and coenzyme A biosynthesis, as well as metabolites including 13-hydroperoxylinoleic acid, lysophosphatidylcholine, and pantethine. CHE can improve kidney-Yang deficiency symptoms in rats, alleviate reproductive organ damage, and enhance sperm quality. The regulation of lipid metabolism may be a potential mechanism through which CHE improves reproductive function in rats with kidney-Yang deficiency. The potential bioactive compounds of CHE include echinacoside, verbascoside, salidroside, betaine, and cistanoside A.
Animals ; Male ; Rats ; Yang Deficiency/physiopathology* ; Metabolomics ; Kidney/physiopathology* ; Rats, Sprague-Dawley ; Drugs, Chinese Herbal/administration & dosage* ; Cistanche/chemistry* ; Kidney Diseases/metabolism* ; Testis/metabolism* ; Humans ; Reproduction/drug effects* ; Testosterone/blood*

Based on the interleukin-17(IL-17) signaling pathway, this study explores the effect and mechanism of Bufei Decoction on Klebsiella pneumoniae pneumonia in rats. SD rats were randomly divided into the control group, model group, Bufei Decoction low-dose group(6.68 g·kg~(-1)·d~(-1)), Bufei Decoction high-dose group(13.36 g·kg~(-1)·d~(-1)), and dexamethasone group(1.04 mg·kg~(-1)·d~(-1)), with 10 rats in each group. A pneumonia model was established by tracheal drip injection of K. pneumoniae. After successful model establishment, the improvement in lung tissue damage was observed following drug administration. Core targets and signaling pathways were screened using transcriptomics techniques. Real-time fluorescence quantitative polymerase chain reaction was used to detect the mRNA expression of core targets interleukin-6(IL-6), interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α), and chemokine CXC ligand 6(CXCL6). Western blot was used to assess key proteins in the IL-17 signaling pathway, including interleukin-17A(IL-17A), nuclear transcription factor-κB activator 1(Act1), tumor necrosis factor receptor-associated factor 6(TRAF6), and downstream phosphorylated p38 mitogen-activated protein kinase(p-p38 MAPK), and phosphorylated nuclear factor-κB p65(p-NF-κB p65). Apoptosis of lung tissue cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling(TUNEL). The results showed that, compared with the control group, the model group exhibited significant pathological damage in lung tissue. The mRNA expression of IL-6, IL-1β, TNF-α, and CXCL6, as well as the protein levels of IL-17A, Act1, TRAF6, p-p38 MAPK/p38 MAPK, and p-NF-κB p65/NF-κB p65, were significantly increased, and the number of apoptotic cells was notably higher, indicating successful model establishment. Compared with the model group, both low-and high-dose groups of Bufei Decoction showed reduced pathological damage in lung tissue. The mRNA expression levels of IL-6, IL-1β, TNF-α, and CXCL6, and the protein levels of IL-17A, Act1, TRAF6, p-p38 MAPK/p38 MAPK, and p-NF-κB p65/NF-κB p65, were significantly decreased, with a significant reduction in apoptotic cells in the high-dose group. In conclusion, Bufei Decoction can effectively improve lung tissue damage and reduce inflammation in rats with K. pneumoniae. The mechanism may involve the regulation of the IL-17 signaling pathway and the reduction of apoptosis.
Animals ; Interleukin-17/metabolism* ; Drugs, Chinese Herbal/administration & dosage* ; Rats, Sprague-Dawley ; Signal Transduction/drug effects* ; Rats ; Male ; Klebsiella pneumoniae/physiology* ; Klebsiella Infections/immunology* ; Humans ; Lung/drug effects*