Objective To explore the clinical value of albumin-globulin ratio(AGR)combined with prostate-specific antigen(PSA)and Gleason score in predicting biochemical recurrence(BCR)after radical resection in patients with localized prostate cancer, and to provide reference for early identification of BCR high-risk patients and individualized treatment. Methods The clinical data of 114 patients with localized prostate cancer treated during Sep.2019 and Sep.2023 were retrospectively analyzed.According to postoperative BCR status, patients were divided into the BCR group(n=43)and non-BCR group(n=71).Preoperative clinical and pathological data were compared between the two groups.Univariate and multivariate Cox regression analyses were used to assess the correlation between these indicators and BCR.The predictive performance of the combined model was evaluated using receiver operating characteristic(ROC)curve.The Kaplan-Meier method was used to compare biochemical recurrence-free survival(BFS)among patients with different AGR, PSA levels and Gleason scores.Results Compared with the non-BCR group, the BCR group had significantly higher PSA level and ISUP grading, but significantly lower AGR level(P＜0.001).Multivariate Cox regression analyses showed that AGR was negatively correlated with BCR(HR=0.031, 95%CI:0.008-0.119, P＜0.001), PSA was positively correlated with BCR(HR=1.009, 95%CI:1.002-1.016, P=0.017), and Gleason score was positively correlated with BCR(HR=1.551, 95%CI:1.199-2.005, P＜0.001).The area under the ROC curve(AUC)for the combined prediction model(AGR + PSA + Gleason score)was 0.886, with a sensitivity of 90.7% and a specificity of 78.9%.Kaplan-Meier analyses showed that patients in the low AGR group, high PSA group, and high Gleason score group had significantly lower BFS than those in the high AGR group, low PSA group and low Gleason score group, respectively(all P＜0.0001).Conclusion The combination of AGR, PSA and Gleason score is closely associated with postoperative BCR in patients with localized prostate cancer.The combined prediction model demonstrates high predictive efficacy and can provide an important reference for the early identification of high-risk BCR patients and for guiding individualized postoperative treatment.

OBJECTIVE To explore the mechanism of Qiangxin decoction in the treatment of chronic heart failure （CHF） by regulating the inhibitor of nuclear factor-κB alpha/nuclear factor-κB p65 subunit （IκBα/NF-κB p65） signaling pathway-mediated M1 macrophage polarization. METHODS In animal experiments， mice were used as research subjects， and the CHF model was established via coronary artery ligation. Model mice were treated with Qiangxin decoction （21.69 g/kg） for 28 days. After intervention， pathological morphological changes of myocardial tissues and cardiomyocyte apoptosis were observed. Serum levels of inflammatory factors including tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6）， myocardial injury marker troponin I3 （TNNI3）， and macrophage-related markers F4/80 and cluster of differentiation 80 （CD80） were detected. In cell experiments， monocyte-macrophage leukemia RAW264.7 cells were induced to undergo M1 polarization by 10 ng/mL lipopolysaccharide combined with 10 ng/mL interferon-γ， followed by 48 h intervention with 10% drug-containing serum of Qiangxin decoction. After intervention， the nuclear translocation of NF-κB p65 and NF-κB p50 was observed. The positive rate of CD80 in cells was measured. The mRNA expression of inflammatory factors including IL-1β， IL-6， IL-8， IL-18， TNF-α， inducible nitric oxide synthase （iNOS）， cyclooxygenase-2 （COX2）， C-C motif chemokine receptor 7 isoform 2 （CCR7-2）， as well as the expression levels of proteins related to the IκBα/NF-κB p65 signaling pathway were detected. RESULTS Animal experimental results showed that Qiangxin decoction alleviated myocardial fibrosis in mice， and significantly reduced the cardiomyocyte apoptosis rate， serum levels of TNF-α and IL-6， as well as the protein expression of TNNI3， F4/80 and CD80 in myocardial tissues （P＜0.05）. Cell experimental results indicated that Qiangxin decoction significantly suppressed the nuclear translocation of NF-κB p65 and NF-κB p50 （P＜0.05）. It significantly decreased the CD80 positive rate， mRNA levels of IL-1β， IL-6， IL-8， IL-18， TNF-α， iNOS， COX2 and CCR7-2， total and nuclear expression of NF-κB p65， total， nuclear and cytoplasmic expression of phosphorylated NF-κB p65， total expression of phosphorylated IκBα （P＜0.05）. Meanwhile， it significantly elevated the total expression of IκBα and cytoplasmic expression of NF-κB p65 （P＜0.05）. CONCLUSIONS Qiangxin decoction can inhibit the activity of the IκBα/NF-κB p65 signaling pathway， reduce the release of pro-inflammatory factors， thereby restraining M1 macrophage polarization， mitigating myocardial fibrosis， and ultimately exerting therapeutic effects against CHF.

[Objective]To elucidate the role and molecular mechanisms of Liuwei Dihuang Decoction(LWDHD)in the treatment of experimental autoimmune encephalomyelitis(EAE).[Methods]Sixty male C57BL/6 mice were randomly divided into normal group,model group,positive control group[prednisone acetate(PA)],LWDHD low-dose group(7.7 g·kg-1),medium-dose group(15.4 g·kg-1)and high-dose group(30.8 g·kg-1).Mice EAE model was established by using myelin oligodendrocyte glycoprotein 35-55(MOG 35-55)combined with pertussis toxin(PTX)and tuberculin.The mice in LWDHD groups were given LWDHD by gavage for 20 consecutive days,and the mice in positive control group were given PA of 6 mg·kg-1 by gavage.Neurological damage was evaluated by neurological functional impairment scores,hematoxylin-eosin(HE)staining was used to detect pathological changes in brain tissue,interleukin-1β(IL-1β)and interleukin-6(IL-6)levels were detected by enzyme-linked immunosorbent assay(ELISA),and Western blot was utilized to examine the expression of proteins in the Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)pathway.T lymphocytes were extracted from the spleen of mice and treated with LWDHD containing serum.Flow cytometry was used to evaluate the proportion of CD4+and CD8+T lymphocytes and Western blot was used to detect the effect of LWDHD on the expression of proteins in the TLR4/NF-κB pathway.[Results]Different concentrations of LWDHD significantly improved the neurological function scores in EAE mice(P<0.01),reduced the abnormal proliferation of microglia in the cerebral cortex,and decreased neuronal cell death in the hippocampus.ELISA showed that LWDHD significantly inhibited the secretion of IL-1β and IL-6(P<0.01).Western blot analysis indicated that LWDHD markedly suppressed the expression and activation of proteins in the TLR4/NF-κB pathway(P<0.01).In cellular experiments,LWDHD containing serum significantly reduced the proportion of CD4+and CD8+T lymphocytes,and inhibited the expression and activation of proteins in the TLR4/NF-κB pathway(P<0.01).[Conclusion]LWDHD significantly inhibits brain inflammatory responses in EAE mice and reduces abnormal proliferation of microglia,which may be associated with the inhibition of protein activation in brain tissue and T lymphocytes via the TLR4/NF-κB pathway.

[Objective]To elucidate the role and molecular mechanisms of Liuwei Dihuang Decoction(LWDHD)in the treatment of experimental autoimmune encephalomyelitis(EAE).[Methods]Sixty male C57BL/6 mice were randomly divided into normal group,model group,positive control group[prednisone acetate(PA)],LWDHD low-dose group(7.7 g·kg-1),medium-dose group(15.4 g·kg-1)and high-dose group(30.8 g·kg-1).Mice EAE model was established by using myelin oligodendrocyte glycoprotein 35-55(MOG 35-55)combined with pertussis toxin(PTX)and tuberculin.The mice in LWDHD groups were given LWDHD by gavage for 20 consecutive days,and the mice in positive control group were given PA of 6 mg·kg-1 by gavage.Neurological damage was evaluated by neurological functional impairment scores,hematoxylin-eosin(HE)staining was used to detect pathological changes in brain tissue,interleukin-1β(IL-1β)and interleukin-6(IL-6)levels were detected by enzyme-linked immunosorbent assay(ELISA),and Western blot was utilized to examine the expression of proteins in the Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)pathway.T lymphocytes were extracted from the spleen of mice and treated with LWDHD containing serum.Flow cytometry was used to evaluate the proportion of CD4+and CD8+T lymphocytes and Western blot was used to detect the effect of LWDHD on the expression of proteins in the TLR4/NF-κB pathway.[Results]Different concentrations of LWDHD significantly improved the neurological function scores in EAE mice(P<0.01),reduced the abnormal proliferation of microglia in the cerebral cortex,and decreased neuronal cell death in the hippocampus.ELISA showed that LWDHD significantly inhibited the secretion of IL-1β and IL-6(P<0.01).Western blot analysis indicated that LWDHD markedly suppressed the expression and activation of proteins in the TLR4/NF-κB pathway(P<0.01).In cellular experiments,LWDHD containing serum significantly reduced the proportion of CD4+and CD8+T lymphocytes,and inhibited the expression and activation of proteins in the TLR4/NF-κB pathway(P<0.01).[Conclusion]LWDHD significantly inhibits brain inflammatory responses in EAE mice and reduces abnormal proliferation of microglia,which may be associated with the inhibition of protein activation in brain tissue and T lymphocytes via the TLR4/NF-κB pathway.

Pressure ulcer is a common complication of long-term bed rest in intensive care unit(ICU)patients,which can increase the risk of infection and prolong ICU hospitalization.They are an important indicator of patient safety and nursing quality in medical institutions.Early prevention of pressure ulcer is an important means of controlling their development.At present,the prevention of pressure ulcer mainly involves timed flipping and the use of pressure reducing devices.However,during the flipping process,it often requires two or more nursing staff to complete,which increases the workload and also exacerbates the occurrence of occupational lower back pain among nursing staff.In addition,existing pressure reducing devices still have certain limitations in use,and their functions are single,often requiring the combination of multiple tools to increase material and financial resources.Based on this,the research team from the department of critical care medicine of Hospital of Chengdu University of Traditional Chinese Medicine,has designed a nursing device for preventing pressure ulcer in critically ill patients,and has obtained a National Utility Model Patent of China(Patent Number:ZL 202320609787.6).It has several inflation components and connecting structures.The inflation components are equipped with a connected air inlet,a connected air outlet,and a discharge port on the side;the inflatable components are fitted together and can be detachably connected through a connecting structure.The connected air inlet of one inflatable component corresponds to the connected air outlet of adjacent inflatable components.This device is connected by multiple inflation components,which lower or raise the height of the airbag through inflation and deflation,adjust the pressure on various parts of the patient's body,and solve the problem of labor-intensive and heavy workload in nursing work;In addition,multiple inflatable components can be detachably connected to form an inflatable mattress.When in use,the number of inflatable component connections can be selected according to the specific needs of different patients or nursing areas.The device is easy to operate,flexible in combination,and suitable for timed flipping pressure reduction regulation in pressure ulcer high-risk areas under various postures.It has good clinical application value.

Objective To explore the mechanism of baicalin mediating inflammatory response in rats with inflammatory bowel disease through microRNA(miR-21)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Methods A total of 60 SD rats were selected to construct inflammatory bowel disease rat model by trinitro-benzene-sulfonic acid(TNBS)colon perfusion method,and randomly divided into 6 groups,with 10 rats in each group.They were divided into model group,low-dose group(gavage of 20 mg/kg baicalin),high-dose group(gavage of 80 mg/kg baicalin),high-dose+agomiR-NC group(gavage of 80 mg/kg baicalin+tail vein injection of 80 mg/kg miRNA negative control vector agomiR-NC),high-dose+agomiR-21 group(gavage of 80 mg/kg baicalin+tail vein injection of 80 mg/kg miR-21 agonist agomiR-21)and high-dose+agomiR-21+colivelin group(gavage of 80 mg/kg baicalin+tail vein injection of 80 mg/kg agomiR-21,along with intraperitoneal injection of 1 mg/kg STAT3 activator colivelin).Another 10 SD rats were selected as control group without any treatment.The body mass of rats in each group was measured every two days during administration,and the status of rats in each group was observed after administration.Hematoxylin and eosin(HE)staining was used to evaluate the pathological damage.The myeloperoxidase(MPO)activity,inflammatory factors and oxidative stress indexes were detected by the test kit.The mRNA levels of miR-21,STAT3 were detected by qRT-PCR.The expression of STAT3 and p-STAT3 protein was detected by Western blot.Results Compared with model group,the status of inflammatory bowel disease and pathological damage degree of colon tissue in low-dose group and high-dose group were significantly improved,the levels of interleukin-13(IL-13),superoxide dismutase(SOD)and glutathione peroxidase(GSH)were increased(P<0.05),while the levels of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),malondialdehyde(MDA),reactive oxygen species(ROS),and miR-21 mRNA,STAT3 mRNA,p-STAT3/STAT3 protein expression were decreased(P<0.05)in a dose-dependent manner.Compared with high-dose+agomiR-NC group,the status of inflammatory bowel disease and pathological damage degree of colon tissue were aggravated in high-dose+agomiR-21 group,the levels of IL-13,SOD and GSH were decreased(P<0.05),while the levels of TNF-α,IL-6,MDA,ROS,and miR-21 mRNA,STAT3 mRNA,P-STAT3/STAT3 protein expression were increased(P<0.05).Compared with high-dose+agomiR-NC group,the status of inflammatory bowel disease and pathological damage degree of colon tissue were aggravated in high-dose+agomiR-21+colivelin group,the levels of IL-13,SOD and GSH were decreased(P<0.05),while the levels of TNF-α,IL-6,MDA,ROS,and miR-21 mRNA,STAT3 mRNA and P-STAT3/STAT3 protein expression were increased(P<0.05).Conclusion Baicalin reduces inflammatory factors and oxidative stress levels through miR-21/STAT3 signaling pathway,and thereby ameliorates colonic injury in rats with inflammatory bowel disease.

Pulmonary alveolar proteinosis(PAP)is a rare progressive respiratory dysfunction disease of the lung characterized by insidious onset and non-specific clinical manifestations,often leading to misdiagnosed and mistreated.Herein,we reported a case of PAP patient admitted to Jiading District Central Hospital with an atypical appearance of alveolar lavage fluid and whose condition improved significantly after treatment with subcutaneous injection of recombinant human granulocyte-macrophage colony stimulating factor(GM-CSF).Additionally,we have reviewed and summarized the relevant literature to enhance the understanding of the diagnosis and treatment of this disease.

AIM:To observe the changes of Th17 related cytokines in tears of conjunctivochalasis(CCH)patients with liver-kidney yin deficiency treated with traditional Chinese medicine Qi Jing Mingmu decoction combined with artificial tears.METHODS:A total of 56 CCH patients(56 eyes)with liver-kidney yin deficiency of grade Ⅱ to Ⅲ were collected and randomly divided into treatment group(treated with Qi Jing Mingmu decoction combined with artificial tears)of 26 cases(26 eyes)and control group(treated with pure artificial tears)of 30 cases(30 eyes). The treatment course was 1 mo, and international ocular surface disease index(OSDI), tear film break-up time(BUT), tear meniscus height(TMH)and conjunctival congestion index of the patients were observed before and after treatment. The patients' tears were collected before and after treatment, and Th17 related cytokines in tears were detected using flow cytometry immunofluorescence luminescence method.RESULTS:After treatment, the OSDI, BUT and conjunctival congestion index of CCH patients in the treatment group and control group were significantly improved(all P<0.01). After treatment, the TMH of CCH patients in the treatment group was significantly reduced(P<0.01), while there was no statistically significant difference in TMH of the control group before and after treatment(P=0.41). After treatment, the levels of Th17 related cytokines IL-17A, IL-22, IFN-γ, IL-17F, and IL-1β in tears of CCH patients in the treatment group were significantly reduced after treatment(all P<0.01), and the changes in the treatment group were more significant(all P<0.05). There was no significant difference in the control group before and after treatment(all P>0.05). After treatment, the levels of IL-6 and TNF-α in the tears of both groups of CCH patients decreased compared to those before treatment(both P<0.05), but the changes in the treatment group were more significant(both P<0.01).CONCLUSION:Qi Jing Mingmu decoction combined with artificial tears can effectively improve the ocular surface microenvironment, enhance tear film stability, and inhibit ocular surface inflammation in CCH patients with liver-kidney yin deficiency. This may be related to its reduction in the secretion of Th17 related cytokines in tears.

Pressure ulcer is a common complication of long-term bed rest in intensive care unit(ICU)patients,which can increase the risk of infection and prolong ICU hospitalization.They are an important indicator of patient safety and nursing quality in medical institutions.Early prevention of pressure ulcer is an important means of controlling their development.At present,the prevention of pressure ulcer mainly involves timed flipping and the use of pressure reducing devices.However,during the flipping process,it often requires two or more nursing staff to complete,which increases the workload and also exacerbates the occurrence of occupational lower back pain among nursing staff.In addition,existing pressure reducing devices still have certain limitations in use,and their functions are single,often requiring the combination of multiple tools to increase material and financial resources.Based on this,the research team from the department of critical care medicine of Hospital of Chengdu University of Traditional Chinese Medicine,has designed a nursing device for preventing pressure ulcer in critically ill patients,and has obtained a National Utility Model Patent of China(Patent Number:ZL 202320609787.6).It has several inflation components and connecting structures.The inflation components are equipped with a connected air inlet,a connected air outlet,and a discharge port on the side;the inflatable components are fitted together and can be detachably connected through a connecting structure.The connected air inlet of one inflatable component corresponds to the connected air outlet of adjacent inflatable components.This device is connected by multiple inflation components,which lower or raise the height of the airbag through inflation and deflation,adjust the pressure on various parts of the patient's body,and solve the problem of labor-intensive and heavy workload in nursing work;In addition,multiple inflatable components can be detachably connected to form an inflatable mattress.When in use,the number of inflatable component connections can be selected according to the specific needs of different patients or nursing areas.The device is easy to operate,flexible in combination,and suitable for timed flipping pressure reduction regulation in pressure ulcer high-risk areas under various postures.It has good clinical application value.