Clinical death refers to the permanent cessation of life functions. This article reviews the definition of clinical death and the various scenarios in which it occurs, classifies the process of clinical death, and discusses the criteria for determining uncontrollable cardiac death, controllable cardiac death and the criteria and workflow for determining brain death. It elaborates on the relationship between brain death and death, and proposes the areas to note when standardizing the medical documentation of death cases. Based on this, it introduces the content of the management system and workflow construction for death determination in medical institutions, including management structure, personnel qualifications, document norms, quality control system and training mechanism. Paying attention to the construction of the management system and workflow for death determination in medical institutions is of great significance for ensuring medical quality and safety, promoting the healthy development of organ donation, and maintaining the seriousness of legal and ethical practices.

ObjectiveTo investigate the effects of Astragali Radix polysaccharides （APS） on the polarization of BV2 microglial cells in an oxygen-glucose deprivation/reoxygenation （OGD/R） model through regulation of the Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway. MethodsThe OGD/R injury model of BV2 microglia was established and divided into blank group， OGD/R group and APS group （0.4 g·L^-1 APS）. Neuroinflammatory injury was induced by lipopolysaccharide （LPS） and treated with APS. The cells were divided into blank group， LPS group （1 mg·L^-1 LPS） and APS group （0.4 g·L^-1 APS+1 mg·L^-1 LPS）. Cell viability was detected using the cell counting kit-8 （CCK-8） assay. Cell morphology was observed under an inverted microscope. Nitric oxide （NO） content in the cell supernatant was determined by the Griess assay. The secretion levels of tumor necrosis factor-α （TNF-α）， interleukin （IL）-6， IL-10， and IL-4 were measured by enzyme-linked immunosorbent assay （ELISA）. Immunofluorescence （IF） was used to detect the double-positive rates of ionized calcium-binding adapter molecule-1/inducible nitric oxide synthase （Iba-1⁺/iNOS⁺） and ionized calcium-binding adapter molecule-1/arginase 1 （Iba-1⁺/Arg1⁺）， as well as the nuclear translocation rate of nuclear factor-κB p65 （NF-κB p65）. Protein expression levels of Iba-1， iNOS， Arg1， TLR4， and NF-κB p65 were detected by Western blot. ResultsIn the OGD/R injury model， compared with the blank control group， BV2 microglial cells in the OGD/R group were activated and exhibited amoeboid morphological changes. The secretion levels of NO， TNF-α， and IL-6 were significantly increased （P<0.01）. The double-positive expression rate of Iba-1⁺/iNOS⁺ and the protein expression of Iba-1 and iNOS were significantly increased （P<0.01）. The nuclear translocation rate of NF-κB p65 and the protein expression levels of TLR4 and NF-κB p65 were significantly increased （P<0.01）. The levels of IL-10 and IL-4 were significantly decreased （P<0.01）， and the double-positive expression rate of Iba-1⁺/Arg1⁺ and Arg1 protein expression were significantly decreased （P<0.01）. Compared with the OGD/R group， the APS group （0.4 g·L^-1） showed reduced cell activation， significantly decreased secretion levels of NO， TNF-α， and IL-6 （P<0.01）， significantly decreased double-positive expression rate of Iba-1⁺/iNOS⁺ and relative protein expression of Iba-1 and iNOS （P<0.01）， significantly decreased nuclear translocation rate of NF-κB p65 and protein expression levels of TLR4 and NF-κB p65 （P<0.01）， significantly increased levels of IL-10 and IL-4 （P<0.01）， and significantly increased double-positive expression rate of Iba-1⁺/Arg1⁺ and Arg1 protein expression （P<0.01）. In the LPS-induced neuroinflammation model， compared with the blank control group， the LPS group showed increased cell activation， significantly increased levels of NO， TNF-α， and IL-6， significantly increased Iba-1⁺/iNOS⁺ double-positive expression rate， NF-κB p65 nuclear translocation rate， and protein expression levels of Iba-1， iNOS， TLR4， and NF-κB p65 （P<0.01）， while IL-10 and IL-4 levels， Iba-1⁺/Arg1⁺ double-positive expression rate， and Arg1 protein expression were significantly decreased （P<0.01）. Compared with the LPS group， the APS group showed reduced cell activation， significantly decreased levels of NO， TNF-α， and IL-6， Iba-1⁺/iNOS⁺ double-positive expression rate， NF-κB p65 nuclear translocation rate， and protein expression levels of Iba-1， iNOS， TLR4， and NF-κB p65 （P<0.01）， while IL-10 and IL-4 levels， Iba-1⁺/Arg1⁺ double-positive expression rate， and Arg1 protein expression were significantly increased （P<0.01）. ConclusionAPS may reduce microglial activation and promote their polarization toward the M2 phenotype by inhibiting activation of the TLR4/NF-κB signaling pathway， thereby alleviating the neuroinflammatory response induced by OGD/R.

ObjectiveTo investigate the effect of repetitive peripheral magnetic stimulation (rPMS) combined with upper limb intelligent robotic training on muscle tension, motor function and cortical excitability in children with unilateral spastic cerebral palsy (USCP). MethodsFrom March, 2023 to December, 2024, 90 children with USCP admitted to Children's Hospital of Soochow University were selected and randomly divided into control group (n = 30), rPMS group (n = 30) and combined group (n = 30). The control group received conventional occupational therapy. The rPMS group received rPMS intervention followed by conventional occupational therapy. The combined group received rPMS followed by upper limb intelligent robot training, for four weeks. Before and after treatment, muscle tension of biceps brachii was assessed using the modified Ashworth Scale (MAS); upper limb motor function was evaluated using the Fugl-Meyer Assessment-Upper Extremity (FMA-UE) and upper limb intelligent parameters; and cortical excitability was measured using transcranial magnetic stimulation (TMS), including resting motor threshold (RMT) and motor-evoked potential (MEP) amplitude of the affected hemisphere. ResultsAfter treatment, MAS grades improved in all groups (|Z| > 3.523, P < 0.001), and the improvement in the combined group was superior to that in the control group (P < 0.05). Significant intra-group (F > 65.21, P < 0.001), inter-group (F > 17.94, P < 0.001) and interaction effects (F > 5.36, P < 0.01) were observed in FMA-UE scores, upper limb intelligent parameters and TMS parameters. Post Hoc analysis showed that the combined group demonstrated significantly greater improvements in FMA-UE scores, upper limb intelligent parameters, and TMS parameters compared with both the control and rPMS groups (all P < 0.01). Except for FMA-UE scores, the rPMS group showed significantly greater improvements than the control group in upper limb intelligent parameters (mechanical feedback, trajectory, and range of motion) and TMS parameters (RMT and MEP amplitude) (P < 0.05). ConclusionrPMS combined with upper limb intelligent robotic training can reduce upper limb muscle tension, improve motor function, and enhance cortical excitability in children with USCP.

OBJECTIVE To explore the mechanism of the active ingredient compatibility（quercetin， quercitrin and kaempferol at a mass ratio of 2∶9∶3）of Dimocarpus longan Lour. leaves（abbreviated as CDL） on ameliorating glucose and lipid metabolism disorders in type 2 diabetes mellitus （T2DM） rats. METHODS SD rats were randomly divided into blank control group， model group， metformin hydrochloride group （100 mg/kg）， and CDL high-， medium- and low-dose groups （280， 140， 75 mg/kg）， with 10 rats in each group. Rats in the blank control group were fed with standard chow， while rats in the other groups were given high-sugar and high-fat diet combined with intraperitoneal injection of streptozotocin to establish the T2DM rat model. After successful modeling， rats in each administration group were given corresponding drug solution， and rats in the blank control group and model group were intragastrically administered with equal volume of pure water， once a day， for consecutive 4 weeks. Fasting blood glucose （FBG） was detected at fixed time every week. The curves of oral glucose tolerance test （OGTT） and intraperitoneal insulin tolerance test （IPITT） were plotted， and the area under curve （AUC） was calculated. The pancreatic islet function indexes [fasting insulin （FINS）， homeostasis model assessment of insulin resistance （HOMA-IR）， insulin sensitivity index （ISI）]，blood lipid indexes [total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）] and hepatic glycogen content were determined. The pathological morphological changes of liver and pancreatic tissues were observed. The protein and mRNA expression levels of molecules related to phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway in liver tissues were detected. RESULTS Compared with the blank control group， the FBG， AUC of IPITT curve， AUC of OGTT curve， HOMA-IR， the levels of FINS， TC， TG and LDL-C， as well as the protein and mRNA expression of phosphatase and tensin homolog， forkhead box protein O1 and glycogen synthase kinase-3β in liver tissues were significantly increased in the model group （ P ＜0.05）. ISI， the levels of HDL-C and hepatic glycogen content， along with the protein and mRNA expression of PI3K， insulin receptor substrate-1， Akt and protein expression of phosphorylated Akt in liver tissues were markedly decreased （ P ＜0.05）. In model group rats， the arrangement of hepatocytes was irregular， the overall structure of pancreatic lobules was disordered， and a large number of inflammatory cell infiltration was observed. Compared with the model group， most of the above quantitative indexes were significantly reversed in the CDL high-dose group （ P ＜0.05）， and the pathological lesions of liver and pancreas were obviously alleviated. CONCLUSIONS CDL can regulate glucose and lipid metabolism disorders， elevate insulin sensitivity and relieve insulin resistance in T2DM rats. Its mechanism may be related to the activation of the PI3K/Akt signaling pathway.

BackgroundBipolar disorder is a severe mental disorder characterized by alternating episodes of mania and depression. It has a high recurrence rate and a high rate of disability. Elderly patients often suffer from more severe cognitive impairment due to neurodegenerative changes. The clinical intervention for bipolar disorder mainly relies on drug treatment， but drugs have limited effects on improving cognitive function， and some drugs may even aggravate cognitive impairment. Aerobic exercise， as a non-drug intervention method， has shown positive effects in improving cognitive function in patients with mental disorders. However， there are still insufficient studies on elderly patients with bipolar disorder. ObjectiveTo explore the impact of aerobic exercise on the cognitive function of elderly patients with bipolar disorder， so as to provide references for the formulation of strategies to improve the cognitive function of this population. MethodsA randomized controlled trial was conducted. A total of 60 elderly patients who were hospitalized at the Third People's Hospital of Lanzhou from January 2024 to March 2025 and met the diagnostic criteria for bipolar disorder as defined in the International Classification of Diseases，tenth edition （ICD-10） were selected. They were divided into the study group and the control group， with 30 cases in each group， based on the random number table method. Both groups were given quetiapine fumarate tablets and magnesium valproate sustained-release tablets. The study group additionally received aerobic exercise （including slow walking， doing exercises， and running）， three times a week， for 30 minutes each time. At the baseline and at the end of the 3^rd， 6^th， 9^th， and 12^th week of the intervention， the Hamilton Depression Scale -24 item （HAMD-24）， the Young Manic Rating Scale （YMRS）， the Montreal Cognitive Assessment （MoCA）， and Wechsler Adult Intelligence Scale Revised in China （WMS-RC） were used for assessment. ResultsThe time effect of the HAMD-24 score was statistically significant （Wald χ²=124.564， P<0.01）. The time effect of the YMRS score was also statistically significant （Wald χ²=145.608， P<0.01）， and the interaction effect between time and group was statistically significant （Wald χ²=14.968， P<0.05）. At the 3^rd， 9^th， and 12^th week of the intervention， the YMRS score of the study group was lower than that of the control group in the same period， and the differences were statistically significant （P<0.05）. The time effect and group effect of the MoCA score were both statistically significant （F=99.347， 16.623， P<0.01）. The time effect， group effect， and interaction effect between time and group of the WMS-RC memory quotient were all statistically significant （F=64.678， 10.197， 12.472， P<0.01）. At the 6^th， 9^th， and 12^th weeks of the intervention， the MoCA score and WMS-RC memory quotient of the study group were higher than those of the control group， and the differences were statistically significant （P<0.05）. ConclusionAerobic exercise may help improve the manic symptoms and cognitive functions （especially memory ability） of elderly patients with bipolar disorder. ［Funded by Science and Technology Project of Gansu Province （number， 24JRRA775）； Science and Technology Project of Lanzhou City（number， 2022-5-155）］

OBJECTIVE To explore the mechanism of the active ingredient compatibility（quercetin， quercitrin and kaempferol at a mass ratio of 2∶9∶3）of Dimocarpus longan Lour. leaves（abbreviated as CDL） on ameliorating glucose and lipid metabolism disorders in type 2 diabetes mellitus （T2DM） rats. METHODS SD rats were randomly divided into blank control group， model group， metformin hydrochloride group （100 mg/kg）， and CDL high-， medium- and low-dose groups （280， 140， 75 mg/kg）， with 10 rats in each group. Rats in the blank control group were fed with standard chow， while rats in the other groups were given high-sugar and high-fat diet combined with intraperitoneal injection of streptozotocin to establish the T2DM rat model. After successful modeling， rats in each administration group were given corresponding drug solution， and rats in the blank control group and model group were intragastrically administered with equal volume of pure water， once a day， for consecutive 4 weeks. Fasting blood glucose （FBG） was detected at fixed time every week. The curves of oral glucose tolerance test （OGTT） and intraperitoneal insulin tolerance test （IPITT） were plotted， and the area under curve （AUC） was calculated. The pancreatic islet function indexes [fasting insulin （FINS）， homeostasis model assessment of insulin resistance （HOMA-IR）， insulin sensitivity index （ISI）]，blood lipid indexes [total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）] and hepatic glycogen content were determined. The pathological morphological changes of liver and pancreatic tissues were observed. The protein and mRNA expression levels of molecules related to phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway in liver tissues were detected. RESULTS Compared with the blank control group， the FBG， AUC of IPITT curve， AUC of OGTT curve， HOMA-IR， the levels of FINS， TC， TG and LDL-C， as well as the protein and mRNA expression of phosphatase and tensin homolog， forkhead box protein O1 and glycogen synthase kinase-3β in liver tissues were significantly increased in the model group （ P ＜0.05）. ISI， the levels of HDL-C and hepatic glycogen content， along with the protein and mRNA expression of PI3K， insulin receptor substrate-1， Akt and protein expression of phosphorylated Akt in liver tissues were markedly decreased （ P ＜0.05）. In model group rats， the arrangement of hepatocytes was irregular， the overall structure of pancreatic lobules was disordered， and a large number of inflammatory cell infiltration was observed. Compared with the model group， most of the above quantitative indexes were significantly reversed in the CDL high-dose group （ P ＜0.05）， and the pathological lesions of liver and pancreas were obviously alleviated. CONCLUSIONS CDL can regulate glucose and lipid metabolism disorders， elevate insulin sensitivity and relieve insulin resistance in T2DM rats. Its mechanism may be related to the activation of the PI3K/Akt signaling pathway.

ObjectiveTo investigate the neuroprotective effect of glycosides of cistanches （GCs） in 1-methyl-4-phenyl-1，2，3，6-tetrahydropyridine （MPTP）-induced Parkinson’s disease （PD） model mice and its potential mechanism. MethodsForty mice were randomly divided into control group， PD group， GCs group and levodopa （L-DOPA） group， with 10 mice in each group. The control group received intraperitoneal injection of normal saline， while the other groups were intraperitoneally injected with MPTP （30 mg/kg） once daily for 5 consecutive days. After model establishment， the control group and PD group were intragastrically administered normal saline， and the GCs group and L-DOPA group received intragastric administration once daily for 28 consecutive days， at doses of 100 mg/kg and 50 mg/kg， respectively. The open field test and rotarod test were used to evaluate motor function. Immunohistochemistry was performed to detect the number of tyrosine hydroxylase （TH）-positive neurons in the substantia nigra of the midbrain. Transmission electron microscopy was adopted to observe the ultrastructure of mitochondria in the substantia nigra. Biochemical assays were used to determine the levels of glutathione （GSH）， malondialdehyde （MDA）， total superoxide dismutase （T-SOD） and reactive oxygen species （ROS） in substantia nigra tissues. Western blot was applied to detect the protein expression of TH， nuclear factor erythroid 2-related factor 2 （Nrf2）， Kelch-like ECH-associated protein 1 （Keap-1） and heme oxygenase-1 （HO-1） in substantia nigra tissues. ResultsCompared with the control group， mice in the PD group exhibited markedly impaired motor function， significantly decreased T-SOD activity， obvious reductions in the number of TH-positive neurons and GSH content， as well as elevated MDA and ROS levels in the substantia nigra （P<0.01）. Compared with the PD group， mice in the GCs group showed improved motor function， increased T-SOD activity， higher number of TH-positive neurons and elevated GSH content， accompanied by decreased MDA and ROS levels （P<0.05）. In the control group， mitochondria in the substantia nigra displayed normal morphology without obvious blurred membrane structures or vacuolar degeneration. The PD group presented mitochondrial swelling， disordered cristae and vacuolar changes， whereas these mitochondrial pathological alterations were alleviated in the GCs group. Compared with the control group， the protein levels of TH， Nrf2 and HO-1 were significantly downregulated， while Keap-1 protein expression was markedly upregulated in the PD group （P<0.01）. Compared with the PD group， the GCs group showed significant upregulation of TH， Nrf2 and HO-1 protein levels and a notable reduction in Keap-1 protein level （P<0.05）. ConclusionGCs ameliorate motor dysfunction and attenuate dopaminergic neuronal and mitochondrial damage in MPTP-induced PD model mice. These effects may be associated with modulation of Nrf2/HO-1 pathway-related protein expression， enhancement of antioxidant capacity， and alleviation of oxidative stress.

The concept of "spirit" in traditional Chinese medicine （TCM） aligns closely with "the liver governs the designing of strategy". By exploring the relationship between the liver and executive function decline， it is proposed that prolonged liver constraint leads to indecisiveness in strategy designing， which is the initiating factor for executive function decline； liver blood deficiency causes difficulties in executing strategy， which forms an essential foundation for the progression of executive function decline； obstruction in the "liver-du mai-brain" pathway leads to unclear strategy designing， which accelerates executive function decline. This relationship is examined from the perspectives of TCM， modern medicine， and cognitive psychology， aiming to provide insights into addressing executive function decline through treatments focused on the liver.

This case report describes a 68-year-old male patient diagnosed with primary hepatocellular carcinoma (HCC). After receiving Yttrium-90 microsphere selective internal radiation therapy (⁹⁰Y-SIRT), the tumor significantly reduced in size, and tumor markers alpha fetoprotein (AFP) and abnormal prothrombin (PIVKA-Ⅱ) decreased. Postoperative pathological results showed minimal residual tumor cells, indicating that ⁹⁰Y-SIRT has good efficacy and safety in downstaging and conversion of HCC, thereby facilitating subsequent surgical resection.

Ferroptosis has received great attention as an iron-dependent programmed cell death for efficient cancer therapy. However, with the accumulation of iron in tumor cells, the antioxidant system is activated by reducing glutathione (GSH) with glutathione peroxidase 4 (GPX4), which critically limits the ferroptosis therapeutic effect. Herein, an iron and GPX4 silencing siRNA (siGPX4) co-encapsulated ferritin nanocage (HFn@Fe/siGPX4) was developed to enhance ferroptosis by disruption of redox homeostasis and inhibition of antioxidant enzyme synergistically. The siGPX4 were loaded into the nanocages by pre-incubated with iron, which could significantly improve the loading efficiency of the gene drugs when compared with the reported gene drug loading strategy by ferritin nanocages. And more iron was overloaded into the ferritin through the diffusion method. When HFn@Fe/siGPX4 was taken up by human breast cancer cell MCF-7 in a TfR1-mediated pathway, the excess iron ions in the drug delivery system could for one thing induce ferroptosis by the production of reactive oxygen species (ROS), for another promote siGPX4 escaping from the lysosome to exert gene silencing effect more effectively. Both the in vitro and in vivo results demonstrated that HFn@Fe/siGPX4 could significantly inhibit tumor growth by synergistical ferroptosis. Thus, the developed HFn@Fe/siGPX4 afforded a combined ferroptosis strategy for ferroptosis-based antitumor as well as a novel and efficient gene drug delivery system.