Objective To analyze survival outcomes and influencing factors among patients with colorectal cancer in Yunnan Province. Methods Clinical data were retrospectively collected from 4 892 patients with colorectal cancer. Survival data were obtained through follow-up. Overall survival (OS) was calculated by using the Kaplan-Meier method. Univariate analysis was performed by applying the log-rank test. Meanwhile, multivariate analysis employed the Cox proportional hazards regression model. Results The 1-, 3-, 5-, and 10-year OS rates for the entire cohort were 91.90%, 74.40%, 64.40%, and 28.70%, respectively. Univariate analysis revealed that age, ethnicity, region, differentiation grade, TNM stage, clinical stage, metastatic status, histological type, and treatment modality (chemotherapy, radiotherapy, and surgery) were associated with patient prognosis (all P<0.05). Multivariate analysis identified age (HR=1.250), region (HR=1.262), differentiation grade (HR=0.761), clinical stage (HR=3.128), and treatment modality (chemotherapy, HR=0.644; radiotherapy, HR=1.605; surgery, HR=0.384) as independent factors affecting survival prognosis in patients with colorectal cancer (all P<0.001). Conclusion Age, region, clinical stage, and treatment modality are independent factors influencing survival among patients with colorectal cancer in Yunnan Province. In clinical practice, these factors should be integrated to develop individualized prevention and treatment strategies, thereby improving patient outcomes.

ObjectiveBased on the theory of "gut-prostate" axis， this study explored the effects and mechanisms of Zishen Tongguan formula and Cinnamomi Cortex in the formula in treating rats with chronic non-bacterial prostatitis（CNP） by detecting the levels of inflammatory factors， and the composition and structure of intestinal flora in CNP rats. MethodsEight out of 42 SD rats were randomly selected as the normal group， and the remaining rats were injected with carrageenan to prepare the CNP model. After successful modeling， 32 rats were randomly divided into the model group， Ningmitai capsule group（0.50 g·kg^-1）， Zishen Tongguan formula group（2.00 g·kg^-1）， and the Phellodendri Chinensis Cortex-Anemarrhenae Rhizoma pair group（PCC-AR group， 2.00 g·kg^-1）， with 8 rats in each group. The administered groups were given the corresponding medicinal solution by gavage， and the normal and model groups were intragastrically administered with an equal volume of normal saline， once a day for 14 consecutive days. The prostate tissues of rats were collected and subjected to hematoxylin-eosin（HE） staining and Masson staining to observe the pathological changes of the tissues in each group. Enzyme-linked immunosorbent assay（ELISA） was used to detect the levels of related inflammatory factors in rat serum， and 16S rDNA sequencing was used to analyze the abundance and diversity changes of gut microbiota before and after administration， and species difference analysis was performed. ResultsAll the administered groups could alleviate the inflammatory symptoms of CNP rats， increase the expression levels of anti-inflammatory factors and decrease the expression levels of pro-inflammatory factors， with the most sIgnificant effect observed in the Zishen Tongguan formula group. Compared with the normal group， the expression levels of interleukin（IL）-8， hypersensitive C-reactive protein（hs-CRP）， immunoglobulin（Ig）M， secretory IgA （sIgA）， and inducible nitric oxide synthase（iNOS） were sIgnificantly increased in the model group（P<0.01）. Compared with the model group， the expression levels of the above inflammatory factors in all administered groups were significantly reduced（P<0.01）. When compared with the PCC-AR group， the Zishen Tongguan formula group showed a significant decrease in transforming growth factor（TGF）-β₁ expression level（P<0.05） and a significant increase in IgM expression level（P<0.01）. The results of gut microbiota analysis showed that， compared with the PCC-AR group， at the order level， the Zishen Tongguan formula group significantly reduced the relative abundance of conditional pathogens such as Bacteroidales， Acidaminococcales， Rhodospirillales， Clostridiales， and Elusimicrobiales（P<0.01）. And at the genus level， the Zishen Tongguan formula group significantly decreased the relative abundance of pathogenic microbiota such as Lachnospira and Bacteroides（P<0.01） and significantly increased the relative abundances of beneficial microbiota such as Ruminococcus and Lactobacillus（P<0.01）. ConclusionZishen Tongguan formula can reduce the level of harmful intestinal bacteria， increase the level of beneficial intestinal bacteria， down-regulate the expression of serum inflammatory factors， and the small amount of Cinnamomi Cortex in the formula may play a key role in the treatment of CNP with this formula.

ObjectiveBased on the theory of "gut-prostate" axis， this study explored the effects and mechanisms of Zishen Tongguan formula and Cinnamomi Cortex in the formula in treating rats with chronic non-bacterial prostatitis（CNP） by detecting the levels of inflammatory factors， and the composition and structure of intestinal flora in CNP rats. MethodsEight out of 42 SD rats were randomly selected as the normal group， and the remaining rats were injected with carrageenan to prepare the CNP model. After successful modeling， 32 rats were randomly divided into the model group， Ningmitai capsule group（0.50 g·kg^-1）， Zishen Tongguan formula group（2.00 g·kg^-1）， and the Phellodendri Chinensis Cortex-Anemarrhenae Rhizoma pair group（PCC-AR group， 2.00 g·kg^-1）， with 8 rats in each group. The administered groups were given the corresponding medicinal solution by gavage， and the normal and model groups were intragastrically administered with an equal volume of normal saline， once a day for 14 consecutive days. The prostate tissues of rats were collected and subjected to hematoxylin-eosin（HE） staining and Masson staining to observe the pathological changes of the tissues in each group. Enzyme-linked immunosorbent assay（ELISA） was used to detect the levels of related inflammatory factors in rat serum， and 16S rDNA sequencing was used to analyze the abundance and diversity changes of gut microbiota before and after administration， and species difference analysis was performed. ResultsAll the administered groups could alleviate the inflammatory symptoms of CNP rats， increase the expression levels of anti-inflammatory factors and decrease the expression levels of pro-inflammatory factors， with the most sIgnificant effect observed in the Zishen Tongguan formula group. Compared with the normal group， the expression levels of interleukin（IL）-8， hypersensitive C-reactive protein（hs-CRP）， immunoglobulin（Ig）M， secretory IgA （sIgA）， and inducible nitric oxide synthase（iNOS） were sIgnificantly increased in the model group（P<0.01）. Compared with the model group， the expression levels of the above inflammatory factors in all administered groups were significantly reduced（P<0.01）. When compared with the PCC-AR group， the Zishen Tongguan formula group showed a significant decrease in transforming growth factor（TGF）-β₁ expression level（P<0.05） and a significant increase in IgM expression level（P<0.01）. The results of gut microbiota analysis showed that， compared with the PCC-AR group， at the order level， the Zishen Tongguan formula group significantly reduced the relative abundance of conditional pathogens such as Bacteroidales， Acidaminococcales， Rhodospirillales， Clostridiales， and Elusimicrobiales（P<0.01）. And at the genus level， the Zishen Tongguan formula group significantly decreased the relative abundance of pathogenic microbiota such as Lachnospira and Bacteroides（P<0.01） and significantly increased the relative abundances of beneficial microbiota such as Ruminococcus and Lactobacillus（P<0.01）. ConclusionZishen Tongguan formula can reduce the level of harmful intestinal bacteria， increase the level of beneficial intestinal bacteria， down-regulate the expression of serum inflammatory factors， and the small amount of Cinnamomi Cortex in the formula may play a key role in the treatment of CNP with this formula.

Aim To explore the effects of apolipoprotein A Ⅰ(ApoA Ⅰ)and apolipoprotein A Ⅰ binding protein(AIBP)on THP-1-derived macrophage pyroptosis.Methods The lactate dehydrogenase(LDH)detection kit was used to evaluate cell membrane integrity,Hoechst33342/PI staining was used to observe cell membrane permeability,ELISA was used to detect the levels of inflammatory factors such as interleukin-1 β(IL-1β)and interleukin-18(IL-18),Western blot was used to detect the expression of pyroptosis-related protein nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3(NLRP3),gasdermin D(GSDMD),cleaved Caspase-1,IL-1β and IL-18.Results Oxidized low density lipoprotein(ox-LDL)upregulated the expression of NLRP3,GSDMD-N,cleaved Caspase-1,IL-1β and IL-18 in THP-1-derived macrophages in a concentration-dependent manner,and promoted the release of IL-1β,IL-18 and LDH(P＜0.05 or P＜0.01),indicating that ox-LDL induced pyroptosis in THP-1-derived macrophages in a concentration-dependent manner.Co-treatment of macrophages with ApoA Ⅰ and AIBP significantly downregulated the ex-pression of NLRP3,GSDMD-N,cleaved Caspase-1,IL-1β and IL-18,reduced the release of IL-1 β,IL-18 and LDH,and inhibited ox-LDL induced pyroptosis(P＜0.05 or P＜0.01).After ATP-binding cassette transporter A1(ABCA1)siRNA transfection,co-treatment with ApoA Ⅰ and AIBP had no significant effect on the expression of pyroptosis-related proteins and secretion of inflammatory factors(P＞0.05).Co-treatment of macrophages with ApoA Ⅰ and AIBP significantly re-duced the expression of purinergic 2X7R receptor(P2X7R)on the cell membrane,inhibited P2X7R mediated protein ki-nase R(PKR)phosphorylation and NLRP3 inflammasome assembly(P＜0.05 or P＜0.01).After P2X7R siRNA trans-fection,co-treatment with ApoA Ⅰ and AIBP had no significant effect on the expression of pyroptosis-related proteins and secretion of inflammatory factors(P＞0.05).Conclusion ApoA Ⅰ and AIBP reduce the expression of P2X7R on the cell membrane through ABCA1,inhibiting P2X7R/PKR/NLRP3 mediated macrophage pyroptosis.

Objective:To establish and explore a novel model and its clinical application value based on abnormal des-gamma-carboxy prothrombin (DCP) for the early-stage diagnosis of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC).Methods:A total of 420 cases with chronic HBV infection with nodular liver lesions examined by imaging at the Third Hospital of Hebei Medical University from January 2021 to June 2024 were retrospectively selected. They were divided into the HBV-HCC group (182 cases) and the control group (238 cases) according to the current HCC diagnostic criteria. The basic information of patients, liver-related biochemical indicators, serum DCP, alpha-fetoprotein (AFP) levels, and the efficacy of combined detection in diagnosing early-stage HCC were collected and analyzed. A DSGAA model based on DCP (D) combined with gender (S), γ-glutamyl transferase (GGT, G), AFP (A) and age (A) as independent variables was constructed. The diagnostic performance of the novel model was compared with that of the traditional model through nomogram visualization output and calibration curve.Results:The age, sex, hemoglobin, albumin, alanine aminotransferase, alkaline phosphatase, and GGT levels were significantly higher in patients with HCC than those of the control group ( P<0.05). The positivity detection rate in patients with HBV-HCC was significantly higher in DCP than that of AFP (85.71% vs. 59.89%, P<0.05). The abnormal detection rate of DCP in patients with AFP-negative was 76.7%. The sensitivity for diagnosing HCC was significantly higher in DCP than AFP (73.63% vs. 64.29%, P<0.05), with specificity of 83.6% in all. The specificity for diagnosing early-stage HCC was 89.09%, surpassing that of AFP at 68.06% ( P<0.05). The area under the receiver operating characteristic curve (AUC) for the constructed DSGAA diagnostic model was 0.8841, with an optimal cutoff value of 0.377, a sensitivity of 80.22%, and a specificity of 86.13%. The AUC for diagnosing early-stage HCC was 0.8122, with a sensitivity of 66.18%, and a specificity of 86.13%, and the diagnostic efficacy was higher than other models ( P<0.05). Conclusion:DCP has superior diagnostic efficacy for HBV-related HCC, and the DSGAA model is expected to be used as a new method for screening and diagnosing early-stage HBV-related HCC.

Objective:To summarize the best evidence for nutrition management of sarcopenia in patients undergoing maintenance hemodialysis (MHD), to guide the development of nutrition management programs.Methods:Using the 6S evidence model, literature on nutrition management of sarcopenia in MHD patients was electronically retrieved from databases and websites including UpToDate, Guidelines International Network, Joanna Briggs Institute Evidence-Based Health Care Center Database, European Society for Clinical Nutrition and Metabolism, UK Kidney Association, PubMed, Web of Science, China Biology Medicine disc, China National Knowledge Infrastructure, and Wanfang Data. The search period was from database establishment to July 30, 2024. After screening and quality assessment of the literature, evidence was extracted and summarized.Results:A total of 19 articles were included, comprising one clinical decision, six guidelines, five systematic reviews, five expert consensus, and two randomized controlled trials. Twenty-six pieces of evidence were summarized from six aspects of nutrition team establishment and counseling, nutritional screening and assessment, nutritional support, nutrient intake, nutritional monitoring, and health education.Conclusions:The evidence summary on nutrition management of sarcopenia in MHD patients provides a basis for implementing nutritional interventions. Evidence transformation and application should be conducted in accordance with patient preferences and the actual clinical context.

Objective:To summarize the best evidence for nutrition management of sarcopenia in patients undergoing maintenance hemodialysis (MHD), to guide the development of nutrition management programs.Methods:Using the 6S evidence model, literature on nutrition management of sarcopenia in MHD patients was electronically retrieved from databases and websites including UpToDate, Guidelines International Network, Joanna Briggs Institute Evidence-Based Health Care Center Database, European Society for Clinical Nutrition and Metabolism, UK Kidney Association, PubMed, Web of Science, China Biology Medicine disc, China National Knowledge Infrastructure, and Wanfang Data. The search period was from database establishment to July 30, 2024. After screening and quality assessment of the literature, evidence was extracted and summarized.Results:A total of 19 articles were included, comprising one clinical decision, six guidelines, five systematic reviews, five expert consensus, and two randomized controlled trials. Twenty-six pieces of evidence were summarized from six aspects of nutrition team establishment and counseling, nutritional screening and assessment, nutritional support, nutrient intake, nutritional monitoring, and health education.Conclusions:The evidence summary on nutrition management of sarcopenia in MHD patients provides a basis for implementing nutritional interventions. Evidence transformation and application should be conducted in accordance with patient preferences and the actual clinical context.

Objective To analyze the effect of Midazolam(MID)on visceral pain in diarrheal irritable bowel syndrome(IBS-D)rats based on the forkhead box protein O1/forkhead box transcription factor O3a(FoxO1/FoxO3a)pathway.Methods An IBS-D rat model was constructed,and successfully modeled rats were randomly assigned into IBS-D group,low MID(MID-L)group,high MID(MID-H)group,and MID-H+AS1842856 group,with 12 rats in each group.Additionally,12 normal healthy rats were included as the Control group.The Control group and the IBS-D group were intraperitoneally injected with an equal volume of 0.9%sodium chloride.The MID-L and MID-H groups were intraperitoneally injected with 30 and 90 mg/kg MID respectively,while the MID-H+AS1842856 group was intraperitoneally injected with 90 mg/kg MID and given 50 mg/kg AS1842856 by gavage.Rats in each group were evaluated for abdominal wall withdrawal response(AWR)score.Enzyme-linked immunosorbent assay(ELISA)was applied to detect the levels of oxidative stress and pain factors in serum,and HE staining was applied to detect pathological changes in colonic tissue.Immunohistochemistry was applied to detect the expression of glial fbrillary acidic protein(GFAP)and nerve growth factor(NGF)in colon tissue,and Western Blot method was applied to detect the expression of proteins related to the FoxO1/FoxO3a pathway.Results The pathological damage in the colonic tissue in the IBS-D group was more severe than that in the Control group,and the AWR score,malondialdehyde(MDA),substance P(SP),5-hydroxytryptamine(5-HT),and GFAP and NGF expression elevated,while the superoxide dismutase(SOD)level and the expression of FoxO1 and FoxO3a decreased(P<0.05).The colonic tissue damage in the MID-L and MID-H groups was less severe compared with the IBS-D group,and the AWR score,MDA,SP,5-HT,and GFAP and NGF expression decreased,while SOD level and the expression of FoxO1,FoxO3a increased;the changes were more significant in the MID-H group(P<0.05).The colonic tissue damage in the MID-H+AS1842856 group was more severe than that in the MID-H group,and the AWR score,MDA,SP,5-HT,and GFAP and NGF expression increased,while SOD level level and the expression of FoxO1,FoxO3a decreased(P<0.05).Conclusion MID can improve visceral pain in IBS-D rats,and its mechanism of action is related to the activation of the FoxO1/FoxO3a pathway.

Objective To analyze the effect of Midazolam(MID)on visceral pain in diarrheal irritable bowel syndrome(IBS-D)rats based on the forkhead box protein O1/forkhead box transcription factor O3a(FoxO1/FoxO3a)pathway.Methods An IBS-D rat model was constructed,and successfully modeled rats were randomly assigned into IBS-D group,low MID(MID-L)group,high MID(MID-H)group,and MID-H+AS1842856 group,with 12 rats in each group.Additionally,12 normal healthy rats were included as the Control group.The Control group and the IBS-D group were intraperitoneally injected with an equal volume of 0.9%sodium chloride.The MID-L and MID-H groups were intraperitoneally injected with 30 and 90 mg/kg MID respectively,while the MID-H+AS1842856 group was intraperitoneally injected with 90 mg/kg MID and given 50 mg/kg AS1842856 by gavage.Rats in each group were evaluated for abdominal wall withdrawal response(AWR)score.Enzyme-linked immunosorbent assay(ELISA)was applied to detect the levels of oxidative stress and pain factors in serum,and HE staining was applied to detect pathological changes in colonic tissue.Immunohistochemistry was applied to detect the expression of glial fbrillary acidic protein(GFAP)and nerve growth factor(NGF)in colon tissue,and Western Blot method was applied to detect the expression of proteins related to the FoxO1/FoxO3a pathway.Results The pathological damage in the colonic tissue in the IBS-D group was more severe than that in the Control group,and the AWR score,malondialdehyde(MDA),substance P(SP),5-hydroxytryptamine(5-HT),and GFAP and NGF expression elevated,while the superoxide dismutase(SOD)level and the expression of FoxO1 and FoxO3a decreased(P<0.05).The colonic tissue damage in the MID-L and MID-H groups was less severe compared with the IBS-D group,and the AWR score,MDA,SP,5-HT,and GFAP and NGF expression decreased,while SOD level and the expression of FoxO1,FoxO3a increased;the changes were more significant in the MID-H group(P<0.05).The colonic tissue damage in the MID-H+AS1842856 group was more severe than that in the MID-H group,and the AWR score,MDA,SP,5-HT,and GFAP and NGF expression increased,while SOD level level and the expression of FoxO1,FoxO3a decreased(P<0.05).Conclusion MID can improve visceral pain in IBS-D rats,and its mechanism of action is related to the activation of the FoxO1/FoxO3a pathway.

Aim To explore the effects of apolipoprotein A Ⅰ(ApoA Ⅰ)and apolipoprotein A Ⅰ binding protein(AIBP)on THP-1-derived macrophage pyroptosis.Methods The lactate dehydrogenase(LDH)detection kit was used to evaluate cell membrane integrity,Hoechst33342/PI staining was used to observe cell membrane permeability,ELISA was used to detect the levels of inflammatory factors such as interleukin-1 β(IL-1β)and interleukin-18(IL-18),Western blot was used to detect the expression of pyroptosis-related protein nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3(NLRP3),gasdermin D(GSDMD),cleaved Caspase-1,IL-1β and IL-18.Results Oxidized low density lipoprotein(ox-LDL)upregulated the expression of NLRP3,GSDMD-N,cleaved Caspase-1,IL-1β and IL-18 in THP-1-derived macrophages in a concentration-dependent manner,and promoted the release of IL-1β,IL-18 and LDH(P＜0.05 or P＜0.01),indicating that ox-LDL induced pyroptosis in THP-1-derived macrophages in a concentration-dependent manner.Co-treatment of macrophages with ApoA Ⅰ and AIBP significantly downregulated the ex-pression of NLRP3,GSDMD-N,cleaved Caspase-1,IL-1β and IL-18,reduced the release of IL-1 β,IL-18 and LDH,and inhibited ox-LDL induced pyroptosis(P＜0.05 or P＜0.01).After ATP-binding cassette transporter A1(ABCA1)siRNA transfection,co-treatment with ApoA Ⅰ and AIBP had no significant effect on the expression of pyroptosis-related proteins and secretion of inflammatory factors(P＞0.05).Co-treatment of macrophages with ApoA Ⅰ and AIBP significantly re-duced the expression of purinergic 2X7R receptor(P2X7R)on the cell membrane,inhibited P2X7R mediated protein ki-nase R(PKR)phosphorylation and NLRP3 inflammasome assembly(P＜0.05 or P＜0.01).After P2X7R siRNA trans-fection,co-treatment with ApoA Ⅰ and AIBP had no significant effect on the expression of pyroptosis-related proteins and secretion of inflammatory factors(P＞0.05).Conclusion ApoA Ⅰ and AIBP reduce the expression of P2X7R on the cell membrane through ABCA1,inhibiting P2X7R/PKR/NLRP3 mediated macrophage pyroptosis.