This study aims to explore the pharmacodynamic material basis of Jinbei Oral Liquid(JBOL) against idiopathic pulmonary fibrosis(IPF) based on serum pharmacochemistry and network pharmacology. The ultra-high performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry(UHPLC-Q-TOF-MS/MS) technology was employed to analyze and identify the components absorbed into rat blood after oral administration of JBOL. Combined with network pharmacology, the study explored the pharmacodynamic material basis and potential mechanism of JBOL against IPF through protein-protein interaction(PPI) network construction, "component-target-pathway" analysis, Gene Ontology(GO) functional enrichment, and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis. First, a total of 114 compounds were rapidly identified in JBOL extract according to the exact relative molecular mass, fragment ions, and other information of the compounds with the use of reference substances and a self-built compound database. Second, on this basis, 70 prototype components in blood were recognized by comparing blank serum with drug-containing serum samples, including 28 flavonoids, 25 organic acids, 4 saponins, 4 alkaloids, and 9 others. Finally, using these components absorbed into blood as candidates, the study obtained 212 potential targets of JBOL against IPF. The anti-IPF mechanism might involve the action of active ingredients such as glycyrrhetinic acid, cryptotanshinone, salvianolic acid B, and forsythoside A on core targets like AKT1, TNF, and ALB and thereby the regulation of multiple signaling pathways including PI3K/AKT, HIF-1, and TNF. In conclusion, JBOL exerts the anti-IPF effect through multiple components, targets, and pathways. The results would provide a reference for further study on pharmacodynamic material basis and pharmacological mechanism of JBOL.
Drugs, Chinese Herbal/pharmacokinetics* ; Animals ; Tandem Mass Spectrometry ; Network Pharmacology ; Rats ; Chromatography, High Pressure Liquid ; Rats, Sprague-Dawley ; Male ; Idiopathic Pulmonary Fibrosis/metabolism* ; Humans ; Administration, Oral ; Protein Interaction Maps/drug effects* ; Signal Transduction/drug effects*

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Objective To analyze the risk factors for gait disorder in patients with developmental dysplasia of the hip(DDH)after total hip replacement.Methods Sixty DDH patients who underwent total hip replacement at The Second People's Hospital of Kunshan from August 2018 to August 2023 were selected as research objects.Of them,19 patients with gait disorders were assigned to observation group,and 41 without gait disorders were taken as control group.Univariate and multivariate logistic regression analyses were conducted to identify the risk factors for gait disorders in DDH patients after total hip replacement.Results There was no significant difference in the gender,age,disease duration,place of residence,educational level,American Society of Anesthesiologists(ASA)grade,surgical time,intraoperative blood loss,Tonnis classification,or symmetrical skin lines on lower limbs between the two groups(P>0.05).But there were significant differences in terms of equal length of lower limbs,anterior pelvic tilt,cerebral small vessel disease,Parkinson disease,and peripheral nerve injury in lower limbs between the two groups(P<0.05).Equal length of lower limbs,anterior pelvic tilt,cerebral small vessel disease,Parkinson disease,and peripheral nerve injury in lower limbs were risk factors for gait disorders in DDH patients after total hip replacement(P<0.05).Conclusion The occurrence of gait disorders is related to the equal length of lower limbs,anterior pelvic tilt,cerebral small vessel disease,Parkinson disease,and peripheral nerve injury in lower limbs in DDH patients after total hip replacement.Symptomatic treatment should be given timely so as to prevent gait disorders and improve the prognosis.

Objective To study the application of mesoporous silica nanoparticle(MSN)as drug carriers in the treatment of osteoarthritis(OA).Methods Core-cone structured MSN(MSN-CC)was synthesized by sol-gel method,modified by polyethyleneimine(PEI),and loaded with hyaluronic acid synthase 2(HAS2).Forty OA model rats were randomly assigned to OA group,MSN-CC-PEI group,hyaluronic acid(HA)group,or MSN-CC-PEI-HAS2 group.Ten healthy rats were assigned to control group.Normal saline 100 μL was injected into the knee joint in the control group and OA group.MSN-CC-PEI 100 μL,HA solution 100 μL,and MSN-CC-PEI-HAS2 100 μL were injected in MSN-CC-PEI group,HA group,and MSN-CC-PEI-HAS2 group,respectively.The levels of HA,interleukin-1β(IL-1β),and prostaglandin E2(PGE2)in the joint effusion and the foot swelling degree were measured at 1,2,and 3 weeks after injection.Results HA level in the MSN-CC-PEI-HAS2 group was significantly lower than that in the HA group at 1 week after intervention(P<0.05),while HA level in the MSN-CC-PEI-HAS2 group was significantly higher than that in the HA group at 2 and 3 weeks after intervention(P<0.05).With the time going on,HA level in the HA group was gradually decreased(P<0.05),but HA level in the MSN-CC-PEI-HAS2 group was gradually increased(P<0.05).At 1 and 2 weeks after intervention,compared with the HA group,IL-1β,PGE2 and foot swelling degree in the MSN-CC-PEI-HAS2 group were increased(P<0.05).At 3 weeks after intervention,compared with the HA group,IL-1β,PGE2 and foot swelling degree in the MSN-CC-PEI-HAS2 group were decreased(P<0.05).With the time going on,IL-1β,PGE2 and foot swelling degree in the HA group and MSN-CC-PEI-HAS2 group were gradually decreased(P<0.05).Conclusion MSN carrier can stably stimulate the secretion of endogenous HA,reduce the inflammatory response within joint cavity of OA rats,and improve the joint morphology and soft tissue pathological changes.

Objective To explore the molecular mechanism by which SOS Ras/Rac guanine nucleotide exchange factor 1-intronic transcript 1(SOS1-IT1)affects enhancer of zeste homolog 2(EZH2)protein expression in endometrial cancer cells Ishikawa and RL95-2.Methods Lentiviral transfection of short hairpin RNA(shRNA)and overexpression plasmid were used in Ishikawa and RL95-2 cell lines to knock down and overexpress SOS1-IT1.The mechanism of EZH2 expression regulation was studied using Real-time PCR,Western blotting,and chromatin immunoprecipitation.Results The expression of SOS1-IT1 and EZH2 genes was positively correlated in endometrial cancer tissues.Knocking down SOS1-IT1 significantly reduces the expression of EZH2,inhibited the proliferation and migration of Ishikawa and RL95-2 cells,and could reduced the acetylation of histone H3 at position 27(H3K27)and the enrichment of CREB binding protein(CBP)in the EZH2 gene promoter region.Overexpression of SOS1-IT1 could increased the expression of EZH2 and enhance the acetylation of H3K27 and the enrichment of CBP.CBP could bind to SOS1-IT1 RNA,and this binding ability was weakened when CBP was knocked down.Conclusion SOS1-IT1 can promote the expression level of EZH2 in endometrial cancer cells Ishikawa and RL95-2 by regulating the acetylation modification level of the EZH2 gene promoter region,thereby affecting the proliferation and migration ability of endometrial cancer cells.

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

Objective To explore the effects of different education and examination methods on the examination results during the screening/evaluation of patent foramen ovale by contrast-enhanced transcranial Doppler(cTCD).Methods Patients who underwent cTCD screening/evaluation for patent foramen ovale in our hospital from May 2023 to February 2024 were retrospectively selected as the research subjects.The patients were divided into the observation group and the control group according to different education and examination methods during the peri-examination period.Patients who received video education,modified Valsalva maneuver,and injection of contrast agent with 20 mL syringe were included into the observation group,and patients who received artificial education,Valsalva maneuver,and injection of contrast agent with 10 mL syringe were included into the control group.The positive detection rate of patent foramen ovale,right-to-left shunt microbubble grading during Valsalva/modified Valsalva maneuver,systolic blood flow velocity,pulsatility index(PI),resistive index(RI),examination duration,total physician-patient communication time,whether occlusion surgery was performed,and patient satisfaction were compared between the two groups.Results The positive detection rate of patent foramen ovale by cTCD(82.93%vs.95.92%),the detection rate of the maximum amout(grade Ⅲ)of microbubbles(39.02%vs.61.22%),the total physician-patient communication time during the peri-examination period[11.30(10.00,14.00)minutes vs.8.23(7.00,10.00)minutes],the rate of occlusion surgery(48.78%vs.73.47%),and the total patient satisfaction(80.49%vs.91.84%)showed statistically significant differences between the control group and the observation group(P<0.05).Additionally,the receiver operating characteristic(ROC)curve analysis showed that the area under the curve(AUC)for diagnosing patent foramen ovale were 0.718 in the control group and 0.855 in the observation group.Conclusion Peri-examination interventions such as video education,modified Valsalva maneuver,and injection of contrast agent with 20 mL syringe can improve the positive detection rate of patent foramen ovale,reduce ineffective physician-patient communication,and improve patient satisfaction.

Aim To reveal the mechanism of CIP4 homologs protein 1(RICH1)are involved in the regu-lation of myocardial fibrosis.Methods Mouse cardiac fibroblasts(MCFs)cells were treated with transforming growth factor-β(TGF-β1)to induce the formation of a myocardial fibrosis cell model;the level of the target protein was detected by Western blotting;and the RICH1 gene was detected by transfection of the cells with plasmid.The RICH1 gene was overexpressed(RICH 1 OE)using plasmid transfection;the RICH1 gene was silenced using siRNA fragment(siRICH1);and the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3 a1,and Acta2,were de-tected using RT-qPCR.Results RICH1 was signifi-cantly down-regulated in TGF-β1-treated MCFs;the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3a1,and Acta2,were down-regu-lated in the RICH1 OE+TGF-β1 group;and in the siRICH1+TGF-β1 group,myocardial fibrosis marker genes,such as Col1 a1,Col3a1 and Acta2 were up-regulated at the expression level;phosphorylated SMAD2(p-SMAD2)and phosphorylated SMAD3(p-SMAD3)levels were down-regulated in the siRICH1 OE+TGF-β1 group.p-SMAD2 and P-SMAD3 levels were upregulated in the siRICH1+TGF-β1 group.Conclusion RICH1 inhibits TGF-β1-induced myo-cardial fibrosis;RICH1 inhibits TGF-β1-induced myo-cardial fibrosis by negatively regulating the SMAD2/3 signaling pathway.

Objective:To explore the association between mouth breathing (MB) and functional speech sound disorders (FSSDs) in children, aiming to establish a novel theoretical basis for FSSD interventions.Methods:Eighty-nine children with an FSSD aged 4-12 years formed the FSSD group, while eighty-five age-matched healthy children served as controls. Their clinical data were processed using independent sample t-tests and chi-square tests to test for any significant differences between the two groups in terms of gender, age, mouth breathing status, post-frenotomy condition, Mandarin exposure before age 4, and delayed speech onset. Multivariate logistic regressions were evaluated to identify risk factors for FSSD in such children and to seek any association between mouth brea-thing and FSSD.Results:The regression analysis identified the following risk factors for childhood FSSD, ranked by odds ratio ( OR) magnitude: mouth breathing (adjusted OR=22.168, 95% CI=7.849-62.608, P≤0.01), delayed speech onset (adjusted OR=20.091, 95% CI=4.812-83.878, P≤0.01), age (a protective effect) (adjusted OR=0.979, 95% CI=0.962-0.997, P≤0.05). Univariate analysis of mouth breathing and associated factors revealed significant associations of FSSD with mouth breathing (χ 2=52.15, P≤0.01) and delayed speech onset (χ 2=25.873, P≤0.01). Conclusions:The significant risk factors for childhood functional speech sound disorders are mouth breathing (showing the highest adjusted OR), delayed speech onset and age. These findings suggest that early screening and therapeutic interventions for mouth breathing should be clinically prioritized to minimize FSSD risk.

Aim To reveal the mechanism of CIP4 homologs protein 1(RICH1)are involved in the regu-lation of myocardial fibrosis.Methods Mouse cardiac fibroblasts(MCFs)cells were treated with transforming growth factor-β(TGF-β1)to induce the formation of a myocardial fibrosis cell model;the level of the target protein was detected by Western blotting;and the RICH1 gene was detected by transfection of the cells with plasmid.The RICH1 gene was overexpressed(RICH 1 OE)using plasmid transfection;the RICH1 gene was silenced using siRNA fragment(siRICH1);and the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3 a1,and Acta2,were de-tected using RT-qPCR.Results RICH1 was signifi-cantly down-regulated in TGF-β1-treated MCFs;the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3a1,and Acta2,were down-regu-lated in the RICH1 OE+TGF-β1 group;and in the siRICH1+TGF-β1 group,myocardial fibrosis marker genes,such as Col1 a1,Col3a1 and Acta2 were up-regulated at the expression level;phosphorylated SMAD2(p-SMAD2)and phosphorylated SMAD3(p-SMAD3)levels were down-regulated in the siRICH1 OE+TGF-β1 group.p-SMAD2 and P-SMAD3 levels were upregulated in the siRICH1+TGF-β1 group.Conclusion RICH1 inhibits TGF-β1-induced myo-cardial fibrosis;RICH1 inhibits TGF-β1-induced myo-cardial fibrosis by negatively regulating the SMAD2/3 signaling pathway.