Purpose: Human epidermal growth factor receptor 2 (HER2)-low breast cancer has the potential to emerge as a distinct subtype. Several studies have compared the differences between HER2-low and HER2-0 breast cancers, but no consensus has been reached.Additionally, a biomarker to predict pathological complete response (pCR) rates in patients with HER2-low breast cancer remains to be identified. Methods: We collected data from 777 patients across three centers, stratifying them into HER2-low and HER2-0 groups. We compared differences in survival and pCR rates between the two groups and investigated potential biomarkers that could reliably predict pCR. Results: The study found that patients with HER2-0 breast cancer had higher pCR rates compared to patients with HER2-low tumors (289 patients [30.1%] vs. 475 patients [18.1%], p < 0.0001). Survival analysis showed no significant advantage for HER2-low tumors over HER2-0 breast cancers. Binary logistic analysis revealed that androgen receptor (AR) expression predicts poorer pCR rates in both the overall patient group and the HER2-0 breast cancer group (overall patients: odds ratio [OR], 0.479; 95% confidence interval [CI], 0.250–0.917; p = 0.026 and HER2-0 patients: OR, 0.267; 95% CI, 0.080–0.892; p = 0.032). In contrast, programmed death ligand 1 (PD-L1) expression was associated with more favorable pCR rates in the overall patient group (OR, 3.199; 95% CI, 1.020–10.037; p = 0.046). Conclusion There is currently insufficient evidence to classify HER2-low breast cancer as a distinct subtype. Our study revealed that AR expression, along with negative PD-L1 expression, contributes to lower pCR rates.

Purpose: Human epidermal growth factor receptor 2 (HER2)-low breast cancer has the potential to emerge as a distinct subtype. Several studies have compared the differences between HER2-low and HER2-0 breast cancers, but no consensus has been reached.Additionally, a biomarker to predict pathological complete response (pCR) rates in patients with HER2-low breast cancer remains to be identified. Methods: We collected data from 777 patients across three centers, stratifying them into HER2-low and HER2-0 groups. We compared differences in survival and pCR rates between the two groups and investigated potential biomarkers that could reliably predict pCR. Results: The study found that patients with HER2-0 breast cancer had higher pCR rates compared to patients with HER2-low tumors (289 patients [30.1%] vs. 475 patients [18.1%], p < 0.0001). Survival analysis showed no significant advantage for HER2-low tumors over HER2-0 breast cancers. Binary logistic analysis revealed that androgen receptor (AR) expression predicts poorer pCR rates in both the overall patient group and the HER2-0 breast cancer group (overall patients: odds ratio [OR], 0.479; 95% confidence interval [CI], 0.250–0.917; p = 0.026 and HER2-0 patients: OR, 0.267; 95% CI, 0.080–0.892; p = 0.032). In contrast, programmed death ligand 1 (PD-L1) expression was associated with more favorable pCR rates in the overall patient group (OR, 3.199; 95% CI, 1.020–10.037; p = 0.046). Conclusion There is currently insufficient evidence to classify HER2-low breast cancer as a distinct subtype. Our study revealed that AR expression, along with negative PD-L1 expression, contributes to lower pCR rates.

Purpose: Human epidermal growth factor receptor 2 (HER2)-low breast cancer has the potential to emerge as a distinct subtype. Several studies have compared the differences between HER2-low and HER2-0 breast cancers, but no consensus has been reached.Additionally, a biomarker to predict pathological complete response (pCR) rates in patients with HER2-low breast cancer remains to be identified. Methods: We collected data from 777 patients across three centers, stratifying them into HER2-low and HER2-0 groups. We compared differences in survival and pCR rates between the two groups and investigated potential biomarkers that could reliably predict pCR. Results: The study found that patients with HER2-0 breast cancer had higher pCR rates compared to patients with HER2-low tumors (289 patients [30.1%] vs. 475 patients [18.1%], p < 0.0001). Survival analysis showed no significant advantage for HER2-low tumors over HER2-0 breast cancers. Binary logistic analysis revealed that androgen receptor (AR) expression predicts poorer pCR rates in both the overall patient group and the HER2-0 breast cancer group (overall patients: odds ratio [OR], 0.479; 95% confidence interval [CI], 0.250–0.917; p = 0.026 and HER2-0 patients: OR, 0.267; 95% CI, 0.080–0.892; p = 0.032). In contrast, programmed death ligand 1 (PD-L1) expression was associated with more favorable pCR rates in the overall patient group (OR, 3.199; 95% CI, 1.020–10.037; p = 0.046). Conclusion There is currently insufficient evidence to classify HER2-low breast cancer as a distinct subtype. Our study revealed that AR expression, along with negative PD-L1 expression, contributes to lower pCR rates.

Objective:To adapt the English version of exteroceptive body awareness questionnaire (EBA-q) into Chinese, and evaluate its reliability and validity in college students.Methods:English version EBA-q was translated and culturally adapted into Chinese, and the tests were administered from October to December 2024, with valid data collected from 1 071 college students. Item analysis, exploratory factor analysis, confirmatory factor analysis, criterion-related validity analysis, and reliability analysis were conducted by SPSS 23.0 and Mplus 8.3 softwares.Results:(1) The Chinese version of EBA-q contained seventeen items across five factors: visual awareness, tactile awareness, body coordination, awareness of body changes and awareness of clothing fit. The five-factor measurement model fitted the data well ( χ2/ df=2.24, CFI=0.95, TLI=0.94, RMSEA=0.05, SRMR=0.06). (2) The EBA-q scores were positively correlated with the scores of noticing, body listening, public self-consciousness, and private self-consciousness ( r=0.46, 0.36, 0.09, 0.25, all P<0.01). (3)The Cronbach's α coefficient, split-half reliability and test-retest reliability of the Chinese version of EBA-q were 0.79, 0.85 and 0.77, respectively(all P<0.01). Conclusion:The Chinese version of the EBA-q has demonstrated good reliability in assessing external body awareness among college students, but its validity requires further verification.

Objective·To construct truncations of CYLD,and to preliminarily analyze their effects on the proliferation of gastric cancer cells.Methods·TCGA,GTEx,and Kaplan-Meier Plotter databases were used to analyze the differences in the expression levels of CYLD between gastric cancer tissues and normal tissues,and their relationship with the prognosis of gastric cancer patients.Immunohistochemistry and Western blotting were used to detect the expression of CYLD in cancer tissues and adjacent noncancerous tissues.Western blotting and qRT-PCR were used to analyze the protein and mRNA expression levels of CYLD in gastric mucosal epithelial cells and gastric cancer cells.According to the sequence and structural characteristics of CYLD gene,primers were designed to construct its truncations.Their expression was detected and identified by agarose gel electrophoresis and Western blotting,and localization was observed by immunofluorescence.In the human gastric adenocarcinoma cells(AGS)with CYLD knockdown,blank NC was added to the control group,and the full-length CYLD,enzyme-inactivated mutant,and three truncated plasmids were added to the experimental group.The proliferation changes of cells in each group were detected by CCK-8 and plate cloning assays.Co-immunoprecipitation,deubiquitination,and Western blotting assays were performed to examine the binding ability of full-length CYLD,the enzyme-inactivated mutant,and the truncated variants to CAMK2A,the level of CAMK2A deubiquitination,and the expression of STAT3 and p-STAT3 proteins.Results·CYLD expression in normal gastric tissues and cells was significantly higher than in gastric cancer tissues and cells,and the prognosis of patients with high expression of CYLD was better.The truncations of human CYLD were successfully constructed,and full length CYLD,enzyme-inactivated mutant,and truncations were mainly localized in the cytoplasm.Knockdown of CYLD in gastric cancer cells significantly enhanced the proliferative ability of gastric cancer cells.Reconstitution of CYLD-knockdown cells with CYLD-WT,or truncated variants containing the CAP3 or USP domains significantly inhibited the proliferation of gastric cancer cells.In addition,CYLD bound to CAMK2A mediated K63 deubiquitination modification,and inhibited CAMK2A-induced phosphorylation of STAT3.Conclusion·The human CYLD truncation plasmids are successfully constructed,and the full length CYLD and its CAP3 and USP segments significantly inhibit the proliferation of gastric cancer cells.

Objective:To adapt the English version of exteroceptive body awareness questionnaire (EBA-q) into Chinese, and evaluate its reliability and validity in college students.Methods:English version EBA-q was translated and culturally adapted into Chinese, and the tests were administered from October to December 2024, with valid data collected from 1 071 college students. Item analysis, exploratory factor analysis, confirmatory factor analysis, criterion-related validity analysis, and reliability analysis were conducted by SPSS 23.0 and Mplus 8.3 softwares.Results:(1) The Chinese version of EBA-q contained seventeen items across five factors: visual awareness, tactile awareness, body coordination, awareness of body changes and awareness of clothing fit. The five-factor measurement model fitted the data well ( χ2/ df=2.24, CFI=0.95, TLI=0.94, RMSEA=0.05, SRMR=0.06). (2) The EBA-q scores were positively correlated with the scores of noticing, body listening, public self-consciousness, and private self-consciousness ( r=0.46, 0.36, 0.09, 0.25, all P<0.01). (3)The Cronbach's α coefficient, split-half reliability and test-retest reliability of the Chinese version of EBA-q were 0.79, 0.85 and 0.77, respectively(all P<0.01). Conclusion:The Chinese version of the EBA-q has demonstrated good reliability in assessing external body awareness among college students, but its validity requires further verification.

Objective·To construct truncations of CYLD,and to preliminarily analyze their effects on the proliferation of gastric cancer cells.Methods·TCGA,GTEx,and Kaplan-Meier Plotter databases were used to analyze the differences in the expression levels of CYLD between gastric cancer tissues and normal tissues,and their relationship with the prognosis of gastric cancer patients.Immunohistochemistry and Western blotting were used to detect the expression of CYLD in cancer tissues and adjacent noncancerous tissues.Western blotting and qRT-PCR were used to analyze the protein and mRNA expression levels of CYLD in gastric mucosal epithelial cells and gastric cancer cells.According to the sequence and structural characteristics of CYLD gene,primers were designed to construct its truncations.Their expression was detected and identified by agarose gel electrophoresis and Western blotting,and localization was observed by immunofluorescence.In the human gastric adenocarcinoma cells(AGS)with CYLD knockdown,blank NC was added to the control group,and the full-length CYLD,enzyme-inactivated mutant,and three truncated plasmids were added to the experimental group.The proliferation changes of cells in each group were detected by CCK-8 and plate cloning assays.Co-immunoprecipitation,deubiquitination,and Western blotting assays were performed to examine the binding ability of full-length CYLD,the enzyme-inactivated mutant,and the truncated variants to CAMK2A,the level of CAMK2A deubiquitination,and the expression of STAT3 and p-STAT3 proteins.Results·CYLD expression in normal gastric tissues and cells was significantly higher than in gastric cancer tissues and cells,and the prognosis of patients with high expression of CYLD was better.The truncations of human CYLD were successfully constructed,and full length CYLD,enzyme-inactivated mutant,and truncations were mainly localized in the cytoplasm.Knockdown of CYLD in gastric cancer cells significantly enhanced the proliferative ability of gastric cancer cells.Reconstitution of CYLD-knockdown cells with CYLD-WT,or truncated variants containing the CAP3 or USP domains significantly inhibited the proliferation of gastric cancer cells.In addition,CYLD bound to CAMK2A mediated K63 deubiquitination modification,and inhibited CAMK2A-induced phosphorylation of STAT3.Conclusion·The human CYLD truncation plasmids are successfully constructed,and the full length CYLD and its CAP3 and USP segments significantly inhibit the proliferation of gastric cancer cells.

Objective:To evaluate the clinical efficacy and safety of DC-CIK cell immunotherapy as an adjuvant to cetuximab combined with CAPEOX(oxaliplatin+capecitabine)chemotherapy regimen in the treatment of advanced colorectal cancer(CRC)with all RAS gene wild-type and BRAF gene wild-type.Methods:A retrospective analysis was conducted on the clinical data of 52 cases of advanced CRC treated in the Oncology Department of in the General Hospital of the Eastern Theatre Command between December 2020 and October 2023,with 26 cases in the control group and the observation group respectively.The observation group received DC-CIK cell therapy in addition to chemotherapy given to the control group.The clinical efficacy and adverse reactions of patients were recorded,and the recent efficacy,quality of life score,incidence of chemotherapy adverse reactions,the changes in tumour markers,and immune indicators before and after treatment were analysed.Results:Compared with those in the control group,the disease control rate(DCR)and quality of life of advanced CRC patients in the observation group were significantly improved(both P<0.05).The incidence of diarrheal/constipation and tumour marker CA72-4 were significantly reduced(all P<0.05),and the NK cell count increased significantly(P<0.05).Conclusion:DC-CIK cell immunotherapy,when used as an adjuvant to cetuximab in combination with the CAPEOX chemotherapy regimen in patients with advanced CRC,is safe and feasible.It can significantly improve the DCR and bring significant clinical benefits to patients.

Objective To investigate the effect of Yu's Qingre Huoxue prescription enema on colonic mucosa in rats with ulcerative colitis(UC).Methods A total of 30 Wistar rats were randomly divided into blank control group,model group,mesalazine group,Chinese medicine high-dose,medium-dose and low-dose groups(5 rats in each group).After successful modeling with trinitrobenzene sulfonic acid,the rats were given 14 days enema with distilled water,mesalazine suspension,and high,medium and low concentration Yu's Qingre Huoxue prescription.The general condition and weight changes of rats were recorded daily,and colon macroscopic damage index(CMDI)and mucosal injury score under microscope of rats in each group were compared.Results Compared with blank control group,the weight of rats in model group decreased significantly(P<0.05).The blank control group had normal water and food intake and activity,glossy fur and normal stool.The rats in model group and each administration group were found to have anal fouling,residual blood in stool,decreased appetite,messy fur,dim luster and other conditions,and the above conditions were gradually improved after enema treatment.Compared with blank control group,the CMDI and mucosal injury scores of model group were significantly increased(P<0.05).Compared with model group,CMDI and mucosal injury scores of mesalazine group and Chinese medicine high-dose,medium-dose and low-dose groups were significantly decreased(P<0.05).Conclusion Yu's Qingre Huoxue prescription can effectively improve the clinical symptoms of diarrhea,mucous,pus and blood stools in UC model rats,reduce the damage of colonic mucosa,promote mucosal repair,and have a good effect on the treatment of UC in rats.

Background and purpose:Esophageal carcinoma(ESCA)is one of the malignant tumors with high mortality rate,and the underlying mechanism of its development is largely unknown.CDC20 plays an important role in tumorigenesis,and its dysregulated expression is closely related to tumor occurrence and development.The expression of CDC20 is increased in a variety of tumors,and knocking down CDC20 can inhibit tumor cell proliferation.NLRP3 is the main component of the inflammasome,and inflammasome is also closely related to tumor occurrence and development.Here,our study aimed to investigate whether CDC20 promotes the proliferation of ESCA cells through NLRP3 and its regulatory mechanism.Methods:The expression levels of CDC20 and NLRP3 genes in ESCA patients were analyzed using The Cancer Genome Atlas(TCGA)detabase and GTEx public database.We collected clinical and pathological data and tissues from 80 ESCA patients at the First Affiliated Hospital of Xinxiang Medical College,and detected the protein expression of NLRP3 in ESCA patients through immunohistochemistry staining.This study was approved by the Ethics Committee of the First Affiliated Hospital of Xinxiang Medical College(Number:EC-021-137).We studied the effects of knocking down CDC20 and NLRP3 gene on the proliferation ability of esophageal squamous cell carcinoma cells EC9706 and KYSE150 using short hairpin RNA(shRNA)technology.Co-immunoprecipitation(Co-IP),proteasome inhibitors and ubiquitination experiments were used to detect whether CDC20 interacts with NLRP3,and to elucidate whether CDC20 regulates NLRP3 expression through the ubiquitination pathway.This study was approved by the Ethics Committee of the First Affiliated Hospital of Xinxiang Medical College(Number:EC-021-137).Results:The TCGA database analysis showed that the expression levels of CDC20 and NLRP3 mRNA were significantly higher in the cancer tissues of ESCA patients than in the adjacent tissues.The immunohistochemistry results further showed that compared with adjacent tissues,the protein expression levels of CDC20 and NLRP3 were increased in ESCA tissues.Knocking down CDC20 and NLRP3 genes inhibited the proliferation of ESCA cells.Co-IP,proteasome inhibitors and ubiquitination experiments confirmed that CDC20 interacted with NLRP3 through its leucine-rich repeat(LRR),and CDC20 stabilized its expression by promoting NLRP3 ubiquitination.Conclusion:CDC20 and NLRP3 are upregulated in ESCA tissues,and CDC20 stabilizes their expression through ubiquitination of NLRP3,promoting ESCA cell proliferation.This suggests that CDC20 and NLRP3 may be potential diagnostic targets for ESCA.