ObjectiveTo systematically evaluate the rehabilitation effect of blood flow restriction training (BFRT) as an adjunctive rehabilitation intervention on lower-limb motor function, balance ability, walking endurance and activities of daily living in stroke patients. MethodsRandomized controlled trials (RCT) on BFRT combined with rehabilitation training for stroke patients published from database inception to January 31, 2026 were retrieved from CNKI, Wanfang data, PubMed, Embase, Cochrane Library and Web of Science. Two researchers independently conducted literature screening, data extraction and bias risk assessment based on the PICO principle. Meta-analysis, subgroup analysis and sensitivity analysis were performed using RevMan 5.4.1 and Stata 17.0. ResultsA total of 15 RCT were included, involving 712 stroke patients including 354 in the control group and 358 in the experimental group. Compared with rehabilitation training, combination of BFRT significantly improved Fugl-Meyer Assessment-Lower Extremities scores (MD = 1.77, 95%CI 0.02 to 3.52, P = 0.047), Berg Balance Scale scores (MD = 5.39, 95%CI 2.20 to 8.59, P < 0.001) and 6-Minute Walk Test distance (MD = 10.24, 95%CI 7.76 to 12.72, P < 0.001). There was no significant difference in modified Barthel Index scores and Timed Up and Go Test results between two groups (P > 0.05). Subgroup analysis indicated that the intervention protocol with a duration of more than four weeks and BFRT combined with resistance training achieved better rehabilitation effect. ConclusionAs an adjunctive rehabilitation method, BFRT can significantly improve lower-limb motor function, balance and walking endurance of stroke patients, while its effect on activities of daily living and functional mobility remains unclear. The protocol of BFRT combined with resistance training for more than four weeks is preferentially recommended, which is more suitable for chronic stroke patients with stable condition, basic walking ability and no cognitive impairment.

Abstract Ferroptosis , a novel , non-apoptotic form of cell death discovered in 2012 , has garnered significant at- tention. It is implicated in the pathogenesis and progression of various intestinal diseases , including colorectal canc- er, intestinal ischemia-reperfusion injury , functional gastrointestinal disorders , and inflammatory bowel disease. These processes involve multiple pathological mechanisms such as inflammation , immune dysregulation , and intesti- nal epithelial dysfunction. By reviewing and summarizing recent literature on ferroptosis-related mechanisms in in- testinal diseases , this article explores the roles and effects of ferroptosis in different intestinal pathologies.

PURPOSE: Postpancreatectomy hemorrhage (PPH) is a life-threatening complication after pancreatoduodenectomy. Stent-graft implantation is an emerging treatment option for PPH. This study reports the outcome of PPH treated with stent-graft implantation. METHODS: This was a single-center, retrospective study. Between April 2020 and December 2023, 1723 pancreatectomy cases were collected while we screened 12 cases of PPH after pancreatoduodenectomy treated with stent-graft implantation. Patients' medical and radiologic images were retrospectively reviewed. Technical and clinical success, complications, and stent-graft patency were evaluated. Continuous data are reported as means ± standard deviation when normally distributed or as median (Q₁, Q₃) when the data is non-normal distributed. Categorical data are reported as n (%). A p < 0.05 was considered statistically significant. Kaplan-Meier estimates were used for stent patency and patients' survival. RESULTS: Pancreatic fistula was identified in 6 cases (50.0%), and pseudoaneurysm was identified in 3 cases (25.0%), including pancreatic fistula together with pseudoaneurysm in 1 case (8.3%). All pseudoaneurysm or contrast extravasation sites were successfully excluded with patent distal perfusion, thus technical success was achieved in all cases. The overall survival rate at 6 months and 1 year was 91.7% and 78.6%, respectively. One patient had herniation of the small intestine into the thoracic cavity, which caused a broad thoracic and abdominal infection and died during hospitalization. Rebleeding occurred at the gastroduodenal artery stump in 1 case after stent-graft implantation for the splenic artery and was successfully treated with another stent-graft implantation. Two cases of asymptomatic stent-graft occlusion were observed at 24.6 and 26.3 after the operation, respectively. CONCLUSIONS With suitable anatomy, covered stent-graft implantation is an effective and safe treatment option for PPH with various bleeding sites and causes.
Humans ; Pancreaticoduodenectomy/adverse effects* ; Stents ; Male ; Retrospective Studies ; Female ; Middle Aged ; Postoperative Hemorrhage/surgery* ; Aged ; Adult

Objective To examine the anti-central-fatigue function of maca and its underlying mechanism.Methods Forty Sprague-Dawley rats were divided randomly into a negative control group,model control group,and low-,medium-,and high-dose maca groups(0.6,1.2,and 2.4 g/kg·body weight).Rats in all groups except the negative control group were subjected to multi-factor stimulation,including cold-water swimming,sleep deprivation,restraining,and tail-clamping,to establish central fatigue rat models.Rats in the low-,medium-,and high-dose maca groups received 0.6,1.2,or 2.4 g/kg maca,respectively,by gavage for 35 days.Behavioral testing was carried out using the Morris water-maze,sucrose-preference,and tail-suspension tests.Markers of oxidative stress in the hippocampus,including superoxide dismutase(SOD),malondialdehyde(MDA),and catalase(CAT),were detected using test kits.Proteins connected with the AMP-activated protein kinase(AMPK)/sirtuin 1(SIRT1)/peroxisome proliferator-activated receptor γ coactivator 1-α(PGC-1α)signaling pathway in the hippocampus were detected by Western blot.Results Rats in the low-,medium-,and high-dose maca groups spent significantly more time in the target quadrant compared with the model control group(P＜0.05 or P＜0.01),but there was no significant dose-effect relationship.Rats in the medium-and high-dose maca groups showed decreased escape latency(P＜0.05),increased time crossing the platform location(P＜0.05),increased sucrose preference(P＜0.05),decreased tail suspension time(P＜0.05),increased the activities of CAT(P＜0.01)and SOD(P＜0.05),and decreased MDA content(P＜0.01).Rats in the low-,medium-,and high-dose maca groups also showed significantly increased protein expression levels of AMPK and nuclear respiratory factor 1(P＜0.01 or P＜0.05),but no significant dose-effect relationship was observed.Rats in the medium-and high-dose maca groups showed increased protein expression of PGC-1α(P＜0.05 or P＜0.01),and rats in the high-dose maca group showed increased protein expression of SIRT1 and mitochondrial transcription factor A(P＜0.05 or P＜0.01).Conclusions Maca can improve the indicators of central fatigue in rats,determined by behavioral testing and oxidative stress-related factors.The underlying mechanism may be related to its regulatory effects on the AMPK/SIRT1/PGC-1α signaling pathway.

Objective To investigate the role of luteolin(Lut)in regulating reactive oxygen species(ROS)levels through nuclear factor erythroid 2-related factor 2(NFE2L2)/cystine glutamate antitransporter(x-CT)/glutathione peroxidase 4(GPX4)signaling axis to inhibit the viability of glioblastoma and promote apoptosis.Methods U87 MG and U251 cells were cultured in vitro.The CCK-8 assay was used to detect cell survival rates after 48 hours of treatment with different concentrations(0,6.25,12.5,25,50 and 100 μmol/L)of Lut.According to whether cells were treated with Lut,cells were divided into the U87 control group,the U87 Lut group,the U251 control group and the U251 Lut group.The half-maximal inhibitory concentration(IC50)at 48 hours was used as the unified treatment concentration for subsequent experiments.The apoptosis level of cells was detected by flow cytometry double staining method.Changes of reactive oxygen species(ROS)levels in cells were detected by the DCFH-DA method.Molecular docking was conducted using AutoDock software to verify the proteins related to the Lut and oxidative stress pathway.Real-time fluorescence quantitative reverse transcription(RT-qPCR)was used to detect the mRNA levels of NFE2L2 and GPX4.The expression levels of NFE2L2,x-CT and GPX4 proteins were detected by Western blot assay.Results After U87 MG and U251 cells were treated with Lut for 48 hours,the cell viability was significantly inhibited,and with the increase of Lut concentration,the cell viability decreased(P＜0.05).Compared with the U87 control group and the U251 control group respectively,the apoptosis rate of cells increased in the U87 Lut group and the U251 Lut group,the green fluorescence intensity was enhanced,and the intracellular ROS level was upregulated(P＜0.05).Results of molecular docking showed that Lut was tightly bound to NFE2L2,x-CT and GPX4.The results of RT-qPCR and Western blot assay showed that compared with the U87 control group and the U251 control group respectively,the protein and mRNA levels of NFE2L2 and GPX4 in cells of the U87 Lut group and the U251 Lut group,as well as the expression level of x-CT protein,decreased(P＜0.05).Conclusion Lut regulates ROS levels through the NFE2L2/x-CT/GPX4 signaling axis to inhibit the viability of glioblastoma and promote cell apoptosis.

Objective To investigate the therapeutic effect and potential mechanisms of allogeneic renal subcapsular transplantation of CD24+renal epithelial cells for the treatment of acute kidney injury(AKI)induced by ischemia-reperfusion(I/R).Methods CD24+renal epithelial cells were isolated from mouse kidneys using flow cytometric sorting and expanded by passaging.C57BL/6N mice were randomly divided into three groups:the normal control group(n=8,sham surgery only),the model control group(n=8,unilateral kidney I/R plus contralateral nephrectomy),and the CD24+cell treatment group(n=8,AKI model followed by renal subcapsular transplantation of CD24+cells).Mice were euthanized at 24 h after modeling and serum was collected to measure biochemical markers[serum creatinine(Scr),blood urea nitrogen(BUN),tumor necrosis factor-α(TNF-α),and interleukin-6(IL-6)].Renal tissues were subjected to pathological evaluation and macrophage staining.An M1-polarized macrophage model was established using mouse bone marrow-derived macrophages co-cultured with CD24+renal epithelial cells.The polarization state of macrophages was assessed by quantitative real-time polymerase chain reaction(qPCR)and flow cytometry.Results CD24+renal epithelial cells were successfully isolated and passaged stably.Compared with the normal control group,the model control group exhibited significantly elevated Scr and BUN levels and renal pathological damage.In contrast,the CD24+cell treatment group showed significant reduction in serum biochemical markers and pathological injury compared with the model control group,along with reduction in M1 macrophage infiltration in the kidneys(P<0.05,P<0.01).In vitro co-culture experiments demonstrated that in the CD24+co-culture group,the expression of M1 polarization-related markers in macrophages was significantly lower than that in the non-co-culture group,and the proportion of CD80+M1 macrophages in the co-culture group decreased(P<0.05,P<0.01).Conclusion Allogeneic renal subcapsular transplantation of CD24+renal epithelial cells can alleviate I/R-induced AKI by inhibiting M1 macrophage polarization through paracrine mechanisms.