ObjectiveTo investigate the effect and underlying mechanism of the Wulao Qisun prescription on pathological new bone formation in ankylosing spondylitis （AS）. MethodsSynovial fibroblasts were isolated from the hip joints of AS patients and observed under a microscope to assess cell morphology. The cells were identified using immunofluorescence staining. The isolated AS fibroblasts were divided into blank group， low drug-containing serum group， medium drug-containing serum group， high drug-containing serum group， and positive drug group. After drug intervention， cell proliferation was measured using the cell counting kit-8 （CCK-8） assay to observe fibroblast growth and determine the optimal intervention time. Alkaline phosphatase （ALP） activity was measured using the alkaline phosphatase assay. Protein expression of osteocalcin （OCN）， osteopontin （OPN）， and runt-related transcription factor 2 （Runx2） was detected by Western blot. The mRNA expression levels of Wnt5a， β-catenin， and Dickkopf-1 （DKK-1） were measured by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the blank group， each drug-containing serum group of Wulao Qisun prescription and the positive drug group inhibited the proliferation of AS fibroblasts and reduced ALP expression （P<0.01）. Compared with the blank group， the low drug-containing serum group of Wulao Qisun prescription downregulated β-catenin mRNA expression （P<0.05）. The medium and high drug-containing serum groups and the positive drug group significantly downregulated Wnt5a and β-catenin mRNA expression （P<0.05， P<0.01）， with the positive drug group showing the most pronounced effect （P<0.01）. The high drug-containing serum group and the positive drug group significantly upregulated DKK-1 mRNA expression （P<0.01）. Compared with the blank group， the low drug-containing serum group of Wulao Qisun prescription inhibited the expression of OPN and Runx2 proteins （P<0.05， P<0.01）， while the medium and high drug-containing serum groups and the positive drug group inhibited the expression of OCN， OPN， and Runx2 proteins （P<0.05， P<0.01）. ConclusionThe Wulao Qisun prescription can inhibit the proliferation and osteogenic differentiation of AS fibroblasts， thereby delaying the formation of pathological new bone in AS. The possible mechanism involves the regulation of Wnt/β-catenin-related gene expression， further inhibiting the transcription of downstream target genes.

Abstract On September 26, 2024, a municipal hospital in Jiaxing City reported a maternal case of Listeria monocytogenes infection. In order to clarify the source of infection, the Jiaxing Center for Disease Control and Prevention immediately conducted the epidemiological investigation, laboratory testing and related disposal work. The case presented with fever (37.9 ℃), gradually intensifying paroxysmal abdominal pain without obvious cause, and went to hospital on the day of onset. Due to fetal intrauterine distress, a male infant was delivered by cesarean section on the same day. The epidemiological investigation identified that the case usually consumed fruits, often store fruits such as watermelon and grapes in the refrigerator alongside raw meat, and the refrigerator had never been cleaned or disinfected, posing a risk of cross contamination. Laboratory tests on amniotic fluid sample from the pregnant woman, infant blood sample showed positive results for Listeria monocytogenes infection. One strain of Listeria monocytogenes was detected in a smear sample from the inner wall of the refrigerator, and all the strains were ST2 type. Consuming fruits contaminated with Listeria monocytogenes may be the main source of infection. Food safety education for pregnant women and their family members should be strengthened to reduce the risk of infection.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Objective To explore the probability and associated factors of pulmonary fibrosis in 350 cases of elderly pneumonia. Methods Elderly patients who received diagnosis and treatment at Changzhi Medical College Affiliated Peace Hospital from January 2018 to December 2022 were selected, and 350 patients who met the criteria were included in the study. Analyze its clinical data, incidence of pulmonary fibrosis, and analyze the relationship between the two. Results The average age of 350 patients was (63.51 ± 5.74) years old; 219 cases were common type , 72 cases were severe type, and 59 cases were critically ill. At admission, the CT signs were: ground glass in 66 cases (18.86%) , paving stone in 37 cases (10.57%), consolidation in 73 cases (20.86%), nodules in 93 cases (26.57%) , fried egg sign in 20 cases (5.71%) , and mosaic sign in 61 cases (17.43%). At discharge, the lesion signs were as follows: 61 cases (17.43%) had no lesions, 207 cases (59.14%) maintained the original lesion signs, and 82 cases (23.43%) evolved into other signs. 76 cases of pulmonary fibrosis were discharged, with an incidence rate of 21.71%. There were significant differences in the incidence of pulmonary fibrosis among patients with different ages, lesion evolution during treatment, lesion signs at discharge, and clinical stages (all P<0.001). Pulmonary fibrosis is positively correlated with age (P=0.047), lesion signs at discharge (P=0.032), and clinical classification (P=0.010). The incidence of lesions presenting as paving stones (P=0.014) and fibrosis in critically ill patients (P=0.013) at discharge is higher. Age increase (P=0.047) , wide range of lesions at admission (P=0.042), evolution of lesions into other signs at discharge (P=0.016), and clinical classification as severe (P=0.008) or critically ill (P=0.021) are independent risk factors for the development of pulmonary fibrosis in elderly pneumonia patients. Conclusion The incidence of pulmonary fibrosis in elderly patients exceeds 20%. Increasing age, wide range of lesions upon admission, evolution of lesions into other signs upon discharge, and clinical classification as severe or critically ill are independent risk factors for the occurrence of pulmonary fibrosis in elderly pneumonia patients.

The ATP-binding cassette(ABC)transporter superfamily comprises membrane proteins that efflux various substrates across extra-and intracellular membranes.Among them,ABCB1,ABCG2,and ABCC1 are directly linked to tumor multidrug resistance(MDR).This review provides an overview of the current understanding on the novel mechanisms and functions of ABCB1,ABCG2,and ABCC1 transporters in tumor MDR,discusses the latest strategies to target these transporters,and explores further opportunities to overcome MDR.

Objective To investigate the correlations of computed tomography (CT), clinical, and pathological features in patients with invasive lung adenocarcinoma positive and negative for spread through air spaces (STAS). Methods A total of 236 patients with invasive lung adenocarcinoma confirmed by surgery and pathology were selected, including 118 patients in STAS-positive group and 118 patients in STAS-negative group. The clinical data, CT signs, and pathological features of the two groups were collected and analyzed. Results There was a correlation between age and the occurrence of STAS. The age of the positive group was higher than that of the negative group. Smoking history and family history of tumor had no correlation with the occurrence of STAS. CT features signs such as nodule type and shape, tumor-lung interface, lobulation sign, spiculation sign, vacuole/cavity, air-bronchogram, pleural indentation sign, vascular changes, mean diameter of tumor, mean diameter of solid component, and the percentage of tumor solid components were significantly different between patients with and without STAS. The incidence of STAS in patients with solid nodules and partial solid nodules was significantly higher than that in patients with ground glass nodules. Multivariate analysis showed that the percentage of tumor solid components, air-bronchogram sign, lobulation sign, and tumor-lung interface were independent risk factors for predicting the occurrence of STAS. Conclusion The clinical data and CT signs of patients with invasive lung adenocarcinoma are related to the occurrence of STAS. CT signs such as the percentage of tumor solid components, air-bronchogram, lobulation sign, and tumor-lung interface are of great significance to STAS prediction. Our findings provide an important basis for selection of personalized clinical treatment plans.

OBJECTIVE To study the correlation between SLCO1B1 （521T＞C and 388A＞G） gene polymorphisms and the efficacy and safety of rosuvastatin. METHODS Retrieved from PubMed， Embase， Cochrane Library， PharmGKB， CNKI database and Wanfang database， the studies about the effects of 521T＞C and 388A＞G gene polymorphisms on the efficacy and safety of rosuvastatin were collected during the inception to Dec. 2023. The included data were analyzed by using RevMan 5.3 software. RESULTS A total of 16 studies were included. The results of meta-analysis showed that 521T＞C gene polymorphism was significantly correlated with the efficacy of rosuvastatin. In the dominant gene model， compared with TT genotype， CC+TC genotype significantly improved the efficacy of rosuvastatin in raising high-density lipoprotein cholesterol （HDL-C） [MD＝2.38， 95%CI（0.61，4.16）， P＝0.009 0]. In the homozygous gene model， compared with TT genotype， CC genotype significantly improved the efficacy of rosuvastatin in reducing total cholesterol [MD＝－7.50，95%CI（－13.05， －1.95）， P＝0.008 0]. In heterozygous gene model， compared with TT genotype， TC genotype significantly improved rosuvastatin in reducing low-density lipoprotein cholesterol （LDL-C） [MD＝－5.14， 95%CI（－9.74， －0.53）， P＝0.03] and increasing HDL-C [MD＝5.67， 95%CI 232102311200） （2.61， 8.73）， P＝0.000 3]. 388A＞G gene polymorphism was also significantly correlated with the efficacy of rosuvastatin. In dominant or homozygous gene models， compared with AA E-mail：dushuzhang911@163.com genotype， GG+AG genotype [MD＝－6.88， 95%CI （－7.46，－6.30），P＜0.000 1] or GG genotype [MD＝－9.23， 95%CI（－9.41， 9.04）， P＜0.000 1] significantly improved the efficacy of rosuvastatin in lowering LDL-C. In the heterozygous gene model， compared with AA genotype， AG genotype significantly improved the efficacy of rosuvastatin in lowering LDL-C [MD＝－3.00， 95%CI（－3.19， －2.82）， P＜0.000 1]， total cholesterol [MD＝－5.80， 95%CI（－6.00， －5.59）， P＜0.000 1] and triglyceride [MD＝－11.79， 95%CI（－19.57， －4.02）， P＝0.003 0]. In the recessive gene model， compared with AA+AG genotype， GG genotype significantly improved the therapeutic efficacy of rosuvastatin in reducing LDL-C[MD＝－4.31， 95%CI（－8.47， －0.14）， P＝0.040 0] and elevating HDL-C [MD＝4.49， 95%CI （2.20， 6.77）， P＝0.000 1]. Under 4 gene models， there was a significant correlation between 521T＞C gene polymorphism and rosuvastatin-related ADR probability （P＜0.05）， but no significant correlation was found in 388A＞G gene polymorphism （P＞0.05）. CONCLUSIONS The polymorphism of 521T＞C gene is significantly related to the efficacy and safety of rosuvastatin in lowering lipid， and the C allele may be one of the factors leading to the increase of rosuvastatin in lipid-lowering efficacy and ADR. 388A＞ G gene polymorphism is significantly associated with the lipid-lowering efficacy of rosuvastatin， but not with its safety.

OBJECTIVE To construct an evaluation index system for the effectiveness of cough and wheeze pharmaceutical care clinic （CWPC） among asthma patients， and to provide assessment tools and a theoretical basis for improving the control level of asthma patients and standardizing pharmaceutical care. METHODS Literature analysis and semi-structured interviews were used to establish the evaluation index system for the effectiveness of CWPC among asthma patients. Delphi method was used to conduct two rounds of expert correspondence consultation， and the index weights were determined by the analytic hierarchy process. The reliability and validity of the constructed index system were analyzed by questionnaire. RESULTS Totally 29 experts from three disciplines of medicine， pharmacy and nursing were selected from the third-grade class A hospitals in Henan province. After two rounds of expert correspondence consultation， the effectiveness evaluation index system of CWPC asthma patients （including 9 sub- dimensions， such as lung function， symptoms； 35 measurement items， such as wheezing and respiratory rate） was finally determined from three core dimensions of structure level， function level and literacy management level， and the weight value of each dimension index was determined. The results of the reliability and validity analysis confirmed the scientific rationality of the index system. CONCLUSIONS The constructed CWPC effectiveness evaluation index system for asthma patients has a high degree of recognition， reliability and validity， and can be used as a measurement tool for the effectiveness evaluation of asthma patients.