Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Traditional development of small protein scaffolds has relied on display technologies and mutation-based engineering, which limit sequence and functional diversity, thereby constraining their therapeutic and application potential. Protein design tools have significantly advanced the creation of novel protein sequences, structures, and functions. However, further improvements in design strategies are still needed to more efficiently optimize the functional performance of protein-based drugs and enhance their druggability. Here, we extended an evolution-based design protocol to create a novel minibinder, BindHer, against the human epidermal growth factor receptor 2 (HER2). It not only exhibits super stability and binding selectivity but also demonstrates remarkable properties in tissue specificity. Radiolabeling experiments with ^99mTc, ⁶⁸Ga, and ¹⁸F revealed that BindHer efficiently targets tumors in HER2-positive breast cancer mouse models, with minimal nonspecific liver absorption, outperforming scaffolds designed through traditional engineering. These findings highlight a new rational approach to automated protein design, offering significant potential for large-scale applications in therapeutic mini-protein development.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Background and Aims:Whether to close mesenteric fissures during laparoscopic radical resection of colorectal cancer remains controversial.Traditional suture closure is technically demanding and may injure mesenteric vessels.This study aimed to evaluate the safety and efficacy of using α-cyanoacrylate medical glue to close mesenteric fissures during laparoscopic colorectal cancer surgery.Methods:A retrospective analysis was conducted on patients who underwent laparoscopic radical resection of colorectal cancer in the Department of Colorectal Surgery,the Sixth Affiliated Hospital of Sun Yat-sen University,from January 2022 to December 2023.Seventy-eight patients who received intraoperative α-cyanoacrylate glue closure of mesenteric fissures were included as the observation group,and 74 patients without fissure closure were selected as the control group using the propensity score matching method.Perioperative parameters,postoperative recovery,and complications were compared between the two groups.Results:No significant differences were observed in baseline characteristics or main intraoperative variables between groups(all P>0.05).The observation group had significantly less ascitic drainage within 3 days after operation[(203.14±116.44)mL vs.(384.53±243.89)mL,P<0.01]and shorter postoperative gas passage,defecation,and drainage tube removal times(all P<0.01).The incidence of postoperative complications and intestinal obstruction was comparable between groups(all P>0.05).Multivariate analysis showed that intraoperative application of α-cyanoacrylate glue was an independent promoting factor for intestinal exhaust within 3 days after surgery(OR=5.739,P=0.000).Conclusion:The use of α-cyanoacrylate medical glue for closing mesenteric fissures during laparoscopic radical resection of colorectal cancer is safe and feasible.It effectively reduces postoperative ascitic drainage and accelerates bowel recovery,offering a simple and reliable alternative to traditional suture closure.

Background and Aims:Whether to close mesenteric fissures during laparoscopic radical resection of colorectal cancer remains controversial.Traditional suture closure is technically demanding and may injure mesenteric vessels.This study aimed to evaluate the safety and efficacy of using α-cyanoacrylate medical glue to close mesenteric fissures during laparoscopic colorectal cancer surgery.Methods:A retrospective analysis was conducted on patients who underwent laparoscopic radical resection of colorectal cancer in the Department of Colorectal Surgery,the Sixth Affiliated Hospital of Sun Yat-sen University,from January 2022 to December 2023.Seventy-eight patients who received intraoperative α-cyanoacrylate glue closure of mesenteric fissures were included as the observation group,and 74 patients without fissure closure were selected as the control group using the propensity score matching method.Perioperative parameters,postoperative recovery,and complications were compared between the two groups.Results:No significant differences were observed in baseline characteristics or main intraoperative variables between groups(all P>0.05).The observation group had significantly less ascitic drainage within 3 days after operation[(203.14±116.44)mL vs.(384.53±243.89)mL,P<0.01]and shorter postoperative gas passage,defecation,and drainage tube removal times(all P<0.01).The incidence of postoperative complications and intestinal obstruction was comparable between groups(all P>0.05).Multivariate analysis showed that intraoperative application of α-cyanoacrylate glue was an independent promoting factor for intestinal exhaust within 3 days after surgery(OR=5.739,P=0.000).Conclusion:The use of α-cyanoacrylate medical glue for closing mesenteric fissures during laparoscopic radical resection of colorectal cancer is safe and feasible.It effectively reduces postoperative ascitic drainage and accelerates bowel recovery,offering a simple and reliable alternative to traditional suture closure.

Objective To explore the work experiences and needs of nutrition specialist nurses,so as to provide a basis in career development and management practices among the nutrition specialist nurses.Methods A method of descriptive phenomenological research was adopted in this study.Purposive sampling was used to select 12 nutrition specialist nurses who came from different regions across the country with over one year of clinical working experiences as well as had completed the specialist training and been qualified by the Nutrition Committee of Guangdong Nursing Association between January and February 2024.Semi-structured on-line interviews were conducted among the participants and the data acquired from the interviews were analysed and summarised.Themes were extracted using NVivo12 and Colaizzi's seven-step analysis from the data from interview.Results Three main themes and eight sub-themes were identified regarding the work experience of nutrition specialist nurses:growth and gains(continuously learning in nutrition therapy-related knowledge to enhance professional skills;actively practice in nutrition therapy to achieve the self-worth);sense of responsibility and mission(increased awareness of responsibility and proactive services;sense of mission to cultivate talents and promotion of the development of nutrition nursing discipline);challenges(lack of an established role in nutrition nursing,conflict in responsibilities;insufficient communication in a medical team regarding nutrition therapy;limited resource to support the development of nutrition nursing;and the professional knowledge and skills unable to fully meet the job demands).Conclusion Hospitals managers should strengthen the support and training for nutrition specialist nurses,clarify their roles,leverage their professional value and promote the career development.

AIM:To explore the role and mechanism of natriuretic peptide A(NPPA)/natriuretic peptide re-ceptor 1(NPR1)signaling in luteinizing hormone(LH)-induced ovarian follicle expansion in mice.METHODS:Three-week-old female mice were injected with pregnant mare serum gonadotropin/equine chorionic gonadotrophin(eCG)48 h before use to stimulate follicle development,or injected with eCG followed by human chorionic gonadotropin(hCG)treat-ment for 4 or 8 h,with 6 mice in each group.Periodic acid-Schiff(PAS)staining in ovarian sections was used to observe the follicular diameter,and qPCR was used to detect the expression of Npr1 mRNA levels in granulosa cells.Wild-type(WT)and Npr1 knockout(Npr1-/-)mice were injected with eCG,or injected with eCG followed by hCG treatment for 4 h.PAS staining was used to observe the follicular diameter,with 6 mice in each group.Superovulation and fertility assays were performed to count the number of ovulated oocytes and pups,with 6 mice in each group subjected to superovulation and 7 mice in each group subjected to fertility assays.The isolated follicles were randomly divided into control,NPPA,LH,LH+NPPA,LH+NPPA+KT5823[protein kinase G(PKG)inhibitor],and LH+NPPA+PPQ-102[cystic fibrosis transmembrane conductance regulator(CFTR)inhibitor]groups,with 20 follicles in each group.In addition,WT and Npr1-/-mice were injected with eCG 48 h or eCG 48 h/hCG 4 h,with 3 mice in each group.In vitro follicle culture and qP-CR were used to explore the effects of PKG and CFTR signalling on NPPA/NPR1-induced follicular expansion.The prolif-eration of granulosa cells in WT and Npr1-/-mice was detected via immunofluorescence staining,with 5 mice in each group.RESULTS:The results revealed that hCG treatment significantly increased the follicle expansion and Npr1 mRNA expression in granulosa cells(P<0.01).The capacity for ovarian follicle expansion,the number of ovulations,and the number of pups per litter were significantly lower in Npr1-/-mice compared with WT mice(P<0.01).In in vitro follicular culture,the addition of PKG inhibitor KT5823 and CFTR inhibitor PPQ-102 significantly inhibited NPPA/NPR1-induced ovarian follicle expansion(P<0.01),and the expression of Pkg mRNA and Cftr mRNA in granulosa cells of Npr1-/-mice was significantly lower than that in WT mice(P<0.01).In addition,the proliferation ability of granulosa cells in Npr1-/-mice was significantly lower than that in WT mice(P<0.01).CONCLUSION:LH promotes mouse ovarian follicle ex-pansion by NPPA/NPR1 signalling-induced PKG and CFTR pathways and granulosa cell proliferation.