Background: High-mobility group box protein 1 (HMGB1) is a chromatin-binding protein involved in arthritis, ischemia, sepsis, atherosclerosis, neurodegenerative disorders, meningitis, and cancer. HMGB1 exhibits dual roles in cancer, acting as either a tumor suppressor or oncoprotein depending on context. Objective: This research aimed to elucidate HMGB1’s functional significance in cutaneous squamous cell carcinoma (cSCC). Methods: We overexpressed HMGB1 in cSCC cell lines using recombinant adenovirus and examined its effects on cell proliferation, colony formation, and cell migration. Results: Immunohistochemical analysis revealed elevated HMGB1 expression levels in cSCC tissue relative to normal epidermis. To assess the influence of HMGB1, we employed recombinant adenoviruses expressing HMGB1 to transduce SCC cell lines (SCC12 and SCC13). Enhanced HMGB1 expression significantly promoted cellular proliferation and colony formation capacity.Notably, HMGB1 overexpression elevated the levels of proliferation regulators, including P63, SOX2, CDK4 and CDK6. Furthermore, HMGB1 overexpression substantially enhanced tumor invasiveness, accompanied by upregulation of epithelial-mesenchymal transition (EMT) biomarkers. Mechanistically, overexpression of HMGB1 enhanced transforming growth factor-β signaling by increasing phosphorylation of SMAD2/3, the key mediators of EMT. Conclusion These data imply that HMGB1 acts as a tumor-promoting factor in cSCC.

Aim To investigate the effects of tran-scription factor FoxO1 on acute kidney injury(AKI)induced by ischemic reperfusion injury(IRI)and to explore the underlying mechanisms.Methods Male C57BL/6 mice were randomly divided into four groups:Sham,IRI,FoxO1 inducible cell-specific knockout(FoxO1 icKO),and IRI+FoxO1 icKO.Tamoxifen(25 mg·kg-1)was intraperitoneally injec-ted to specifically knock out FoxO1 in mouse macro-phages,and a unilateral renal IRI model was estab-lished.The levels of serum creatinine(Scr),blood u-rea nitrogen(BUN),Fe2+,malondialdehyde(MDA),reactive oxygen species(ROS),and reduced glutathi-one(GSH)in renal tissues were detected.Hematoxy-lin-eosin(HE)staining was used to observe the patho-logical changes in renal tissues.Quantitative polymer-ase chain reaction(qPCR)was used to detect the mR-NA levels of inflammatory factors such as IL-1β and MCP1 in renal tissues.Western blot was used to detect the expression levels of apoptosis and ferroptosis-relat-ed proteins.Results Compared with the control group,the levels of Scr and BUN in the IRI group were significantly upregulated,the infiltration of inflammato-ry factors IL-1β,TNF-α and MCP1 increased,the pro-tein expressions of Bax/Bc12,cleaved-caspase-3/caspase-3,cytochrome C,and FTH1 in renal tissues were significantly enhanced,while the expression of GPX4 decreased.In addition,the levels of Fe2+,MDA and ROS in the renal cortex of the IRI group signifi-cantly increased,and the level of GSH markedly de-creased(P＜0.05).Compared with the IRI group,the levels of Scr and BUN in the FoxO1 icKO group were significantly reduced,the infiltration of inflammatory factors was alleviated,the expression of apoptosis-relat-ed proteins in renal tissue decreased,the expression level of ferroptosis protein GPX4 increased,and the ex-pression of FTH1 decreased.The levels of Fe2+,MDA and ROS in the renal cortex decreased,and the level of GSH significantly increased(P＜0.05).Conclusion Inducing the specific knockout of FoxO1 in macro-phages can alleviate AKI induced by IRI,and its mech-anism may be related to the inhibition of ferroptosis caused by IRI by FoxO1.

The application of sensors to the monitoring of spinal morphology and motion was reviewed in terms of the research object and monitoring index.The present situation of the application of sensors was introduced,such as inertial sensor,stretchable strain sensor and electromagnetic sensor.The deficiencies of sensors applied to the monitoring of spinal morphology and motion were analyzed,and the future directions of the application were pointed out.[Chinese Medical Equipment Journal,2025,46(6):105-110]

Objective:To investigate mental health literacy and advance care planning(ACP)condition,their influencing fac-tors,and their correlation in elderly patients with coronary heart disease(CHD).Methods:General data of 500 elderly CHD patients admitted in the Second Affiliated Hospital of Chinese PLA Air Force Military Medical University between January 2020 and December 2021 were collected.Mental health literacy and ACP condition were assessed.Multivariate linear regres-sion was used to analyze their influencing factors,and Pearson method was used to analyze their association.Results:Total score of Multicomponent Mental Health Literacy(MHL)was(10.78±2.57)points,and total score of Advance Care Plan-ning Readiness Scale(ACPRS)was(71.41±4.84)points in the 500 elderly CHD patients.Multivariate linear regression a-nalysis indicated that level of disease uncertainty had negative impact on MHL score,presence of spouse and trust in medical care had positive impact on MHL score(P＜0.05 or＜0.01);number of complications had negative impact on ACPR score,while presence of spouse and family mean monthly income had positive impact on ACPRS score(P＜0.05 or＜0.01).Pearson correlation analysis indicated that MHL score was positively correlated with ACPRS score(r=0.476,P＜0.001).Conclusion:Both mental health literacy and ACP status need to be improved in elderly CHD patients.They are posi-tively correlated with each other.Presence of spouse,number of complications and trust in medical care are the important influencing factors.Therefore,medical staff can take targeted measures to improve ACP readiness and mental health quality.

Objective:This study aims to explore the rehabilitation effect of continuous rehabilitation management based on Internet thinking on patients with coronary heart disease(CHD)after percutaneous coronary intervention(PCI).Methods:This randomized controlled study enrolled 100 CHD patients admitted in Second Affiliated Hospi-tal of Chinese PLA Air Force Military Medical University between October 2020 and December 2021.They were di-vided into control group(n=50)and intervention group(n=50).Patients in control group received routine reha-bilitation nursing mode,compared to those in intervention group applying"Internet+"continuous rehabilitation nursing intervention program,both groups were intervened for 3 months.Cardiac function,cardiopulmonary exer-cise test indexes,depression,medication compliance,quality of life and incidence of adverse cardiovascular events within 1-year follow-up were compared between two groups.Results:Compared with patients in control group after 3 months,those in intervention group had significant higher oxygen uptake at anaerobic threshold(VO2@AT)[(11.75±0.39)ml·kg-1·min-1 vs.(10.17±0.76)ml·kg-1·min-1],peak oxygen uptake(Peak VO2)[(17.87±0.72)ml·kg-1·min-1 vs.(16.66±0.24)ml·kg-1·min-1],left ventricular ejection fraction(LVEF)[(51.15±2.42)％vs.(44.09±1.94)％],scores of Morisky Medication Adherence Scale(MMAS-8)[(5.29±0.30)points vs.(4.11±0.27)points]and Seattle Angina Questionnaire(SAQ)[(85.50±4.37)points vs.(73.27±2.53)points],and significant lower left ventricular end-diastolic diameter(LVEDd)[(40.51±0.41)mm vs.(46.64±0.99)mm],score of Patient Health Questionnaire-9(PHQ-9)[(7.67±0.85)points vs.(9.66±1.43)points]and total incidence of adverse cardiovascular events within 1-year follow-up(4.00％vs.16.00％)(P＜0.05 or＜0.01).Conclusion:Internet continuous rehabilitation intervention could improve car-diopulmonary exercise capacity and cardiac function,help to improve their quality of life and relieve depression,and reduce the risk of adverse cardiovascular events in CHD patients after PCI.

Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption. Methods: Renal tubule-specific Cckbr-knockout (CckbrCKO) mice and wild-type (WT) mice were utilized to investigate the effect of renal CCKBR on SGLT2 and systemic glucose homeostasis under normal diet, high-fat diet (HFD), and HFD with a subsequent injection of a low dose of streptozotocin. The regulation of SGLT2 expression by gastrin/CCKBR and the underlying mechanism was explored using human kidney (HK)-2 cells. Results: CCKBR was downregulated in kidneys of diabetic mice. Compared with WT mice, CckbrCKO mice exhibited a greater susceptibility to obesity and diabetes when subjected to HFD. In vitro experiments using HK-2 cells revealed an upregulation of glucose transporters after incubation with high glucose, a response that was significantly attenuated following gastrin intervention. The glucose uptake from the culture medium of cells was altered accordingly. Moreover, gastrin administration effectively mitigated hyperglycemia in WT diabetic mice by inhibition of SGLT2 mediated glucose reabsorption, but this effect was compromised in the absence of CCKBR, as seen in CckbrCKO mice. Mechanistically, gastrin/CCKBR substantially reduced SGLT2 expression in HK-2 cells exposed to high glucose, via modulating Erkuclear factor-kappa B (NF-κB) pathway. Conclusion Our study underscores the crucial role of renal gastrin/CCKBR in SGLT2 regulation and glucose reabsorption, and renal gastrin/CCKBR can be a promising therapeutic target for diabetes.

Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption. Methods: Renal tubule-specific Cckbr-knockout (CckbrCKO) mice and wild-type (WT) mice were utilized to investigate the effect of renal CCKBR on SGLT2 and systemic glucose homeostasis under normal diet, high-fat diet (HFD), and HFD with a subsequent injection of a low dose of streptozotocin. The regulation of SGLT2 expression by gastrin/CCKBR and the underlying mechanism was explored using human kidney (HK)-2 cells. Results: CCKBR was downregulated in kidneys of diabetic mice. Compared with WT mice, CckbrCKO mice exhibited a greater susceptibility to obesity and diabetes when subjected to HFD. In vitro experiments using HK-2 cells revealed an upregulation of glucose transporters after incubation with high glucose, a response that was significantly attenuated following gastrin intervention. The glucose uptake from the culture medium of cells was altered accordingly. Moreover, gastrin administration effectively mitigated hyperglycemia in WT diabetic mice by inhibition of SGLT2 mediated glucose reabsorption, but this effect was compromised in the absence of CCKBR, as seen in CckbrCKO mice. Mechanistically, gastrin/CCKBR substantially reduced SGLT2 expression in HK-2 cells exposed to high glucose, via modulating Erkuclear factor-kappa B (NF-κB) pathway. Conclusion Our study underscores the crucial role of renal gastrin/CCKBR in SGLT2 regulation and glucose reabsorption, and renal gastrin/CCKBR can be a promising therapeutic target for diabetes.

Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption. Methods: Renal tubule-specific Cckbr-knockout (CckbrCKO) mice and wild-type (WT) mice were utilized to investigate the effect of renal CCKBR on SGLT2 and systemic glucose homeostasis under normal diet, high-fat diet (HFD), and HFD with a subsequent injection of a low dose of streptozotocin. The regulation of SGLT2 expression by gastrin/CCKBR and the underlying mechanism was explored using human kidney (HK)-2 cells. Results: CCKBR was downregulated in kidneys of diabetic mice. Compared with WT mice, CckbrCKO mice exhibited a greater susceptibility to obesity and diabetes when subjected to HFD. In vitro experiments using HK-2 cells revealed an upregulation of glucose transporters after incubation with high glucose, a response that was significantly attenuated following gastrin intervention. The glucose uptake from the culture medium of cells was altered accordingly. Moreover, gastrin administration effectively mitigated hyperglycemia in WT diabetic mice by inhibition of SGLT2 mediated glucose reabsorption, but this effect was compromised in the absence of CCKBR, as seen in CckbrCKO mice. Mechanistically, gastrin/CCKBR substantially reduced SGLT2 expression in HK-2 cells exposed to high glucose, via modulating Erkuclear factor-kappa B (NF-κB) pathway. Conclusion Our study underscores the crucial role of renal gastrin/CCKBR in SGLT2 regulation and glucose reabsorption, and renal gastrin/CCKBR can be a promising therapeutic target for diabetes.

Aim To investigate the effects of tran-scription factor FoxO1 on acute kidney injury(AKI)induced by ischemic reperfusion injury(IRI)and to explore the underlying mechanisms.Methods Male C57BL/6 mice were randomly divided into four groups:Sham,IRI,FoxO1 inducible cell-specific knockout(FoxO1 icKO),and IRI+FoxO1 icKO.Tamoxifen(25 mg·kg-1)was intraperitoneally injec-ted to specifically knock out FoxO1 in mouse macro-phages,and a unilateral renal IRI model was estab-lished.The levels of serum creatinine(Scr),blood u-rea nitrogen(BUN),Fe2+,malondialdehyde(MDA),reactive oxygen species(ROS),and reduced glutathi-one(GSH)in renal tissues were detected.Hematoxy-lin-eosin(HE)staining was used to observe the patho-logical changes in renal tissues.Quantitative polymer-ase chain reaction(qPCR)was used to detect the mR-NA levels of inflammatory factors such as IL-1β and MCP1 in renal tissues.Western blot was used to detect the expression levels of apoptosis and ferroptosis-relat-ed proteins.Results Compared with the control group,the levels of Scr and BUN in the IRI group were significantly upregulated,the infiltration of inflammato-ry factors IL-1β,TNF-α and MCP1 increased,the pro-tein expressions of Bax/Bc12,cleaved-caspase-3/caspase-3,cytochrome C,and FTH1 in renal tissues were significantly enhanced,while the expression of GPX4 decreased.In addition,the levels of Fe2+,MDA and ROS in the renal cortex of the IRI group signifi-cantly increased,and the level of GSH markedly de-creased(P＜0.05).Compared with the IRI group,the levels of Scr and BUN in the FoxO1 icKO group were significantly reduced,the infiltration of inflammatory factors was alleviated,the expression of apoptosis-relat-ed proteins in renal tissue decreased,the expression level of ferroptosis protein GPX4 increased,and the ex-pression of FTH1 decreased.The levels of Fe2+,MDA and ROS in the renal cortex decreased,and the level of GSH significantly increased(P＜0.05).Conclusion Inducing the specific knockout of FoxO1 in macro-phages can alleviate AKI induced by IRI,and its mech-anism may be related to the inhibition of ferroptosis caused by IRI by FoxO1.

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.