ObjectiveTo establish three standardized rehabilitation unit models covering acute, critical and comprehensive recovery stages for traumatic brain injury (TBI) that fit the whole-course characteristics, clarify their multidisciplinary collaborative framework, standardized procedures, and information management system, and verify the clinical effectiveness of this staged rehabilitation unit on long-term functional prognosis and in-hospital complications of TBI patients. MethodsThis study was conducted at two stages: model construction and efficacy verification. At the first stage, TBI rehabilitation units for acute, critical and recovery stages were established in the Department of Neurosurgery, Intensive Care Unit and Department of Rehabilitation Medicine, respectively, with unified multidisciplinary team configuration, standardized assessment and treatment protocols, collaborative workflows, and a dedicated information management system. At the second stage, 324 TBI patients admitted to the newly built rehabilitation units from July, 2023 to July, 2025 were enrolled as the observation group, and 167 TBI patients receiving traditional management from January, 2018 to December, 2022 were retrospectively selected as the control group. The primary outcomes were 1-year post-injury Glasgow Outcome Scale (GOS) and Disability Rating Scale (DRS) scores. Secondary outcomes included the incidence of in-hospital complications and the mean indwelling time of tracheal intubation, gastric tube and urinary catheter. ResultsThe 1-year GOS score was significantly higher (t = -7.836, P < 0.001), and the DRS score was significantly lower (t = -6.742, P < 0.001) in the observation group than in the control group. The overall incidence of complications was significantly lower in the observation group than in the control group (χ² = 18.762, P < 0.001). The incidences of pulmonary infection, urinary tract infection, pressure ulcer, lower extremity venous thrombosis and joint contracture deformity were all significantly reduced (χ² > 4.328, P < 0.05). The indwelling time of tracheal intubation, gastric tube and urinary catheter was significantly shorter in the observation group than in the control group (t > 10.276, P < 0.001). ConclusionThe acute-critical-comprehensive three-stage standardized TBI rehabilitation unit could significantly improve the long-term functional outcomes of TBI patients, reduce the incidence of complications, and shorten the indwelling time of invasive tubes through multidisciplinary collaboration, whole-course standardized management and information-based quality control. This model conforms to the pathological and functional laws of TBI, realizes seamless whole-course connection from acute treatment to recovery rehabilitation, and has good clinical feasibility and promotion value. It can provide evidence-based evidence and practical reference for the homogenized and standardized development of TBI rehabilitation in China.

Nuclear factor E2-related factor 2 (Nrf2) is a major regulator of redox homeostasis in cells, and Nrf2 signaling pathway has anti-inflammatory, anti-oxidative stress, and anti-fibrosis effects while plays an important role in wound healing and pathological scar formation and progression. This article reviewed the related research regarding the effect of oxidative stress and Nrf2 signaling pathway on pathological scars, furthermore, it investigated the relationship between Nrf2 signaling pathway, oxidative stress and pathological scars, providing a new perspective for the study of mechanism and clinical prevention and treatments of pathological scars.

Nuclear factor E2-related factor 2 (Nrf2) is a major regulator of redox homeostasis in cells, and Nrf2 signaling pathway has anti-inflammatory, anti-oxidative stress, and anti-fibrosis effects while plays an important role in wound healing and pathological scar formation and progression. This article reviewed the related research regarding the effect of oxidative stress and Nrf2 signaling pathway on pathological scars, furthermore, it investigated the relationship between Nrf2 signaling pathway, oxidative stress and pathological scars, providing a new perspective for the study of mechanism and clinical prevention and treatments of pathological scars.

Objective:To test the expression of miR-146a-5p RNA, interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) as markers for predicting post-stroke cognitive impairment (PSCI).Methods:Forty cerebral infarction patients who had been followed up after 3 months formed a PSCI group, and another 40 who showed no post-stroke impairment formed the normal (PSCN) group. Forty healthy age-matched people were the AMC group. The executive functioning of each participant was quantified using the digital span test (DST), a Stroop color word test (SCWT), part B of the trail making test (TMT-B), and a semantic fluency test (SFT). Plasma expression levels of miR-146a-5p, IL-6 and TNF-α were also recorded. Receiver operating characteristics (ROC) curves were prepared to analyze the value of the miR-146a-5p, IL-6, TNF-α and Montreal cognitive assessment (MoCA) scores for predicting PSCI.Results:At baseline, the average expression of plasma miR-146a-5p in the PSCI group was significantly lower than in the other groups, with that of the PSCN group significantly higher than the AMC group′s average. Plasma IL-6 content in the PSCI group was significantly higher than in the other two groups on average, with that in the PSCN group significantly higher than in the AMC group. The average TNF-α levels in both the PSCI and PSCN groups were significantly higher than in the AMC group. Three months later, however, the average DST and SFT scores of the PSCI group were significantly lower than those of the other two groups, while TMT-B and stroop interference effects (SIE) times were significantly longer. TMT-B and SIE times in the PSCN group averaged significantly longer than in the AMC group. At baseline, the area under the curve predicting PSCI of plasma miR-146a-5P combined with MoCA scores was 0.90, with a sensitivity of 72.5% and specificity at the optimal critical point of 97.5%.Conclusions:A high level of plasma miR-146a-5p in the acute stage may protect an ACI patient′s cognitive functioning by inhibiting neuroinflammatory responses. Its expression level and the patient′s MoCA score can help to predict PSCI.

Objective This article aims to investigate the association between hypertension and the risk of GSD by conducting a national multicenter study,a systematic review,and a meta-analysis.Methods The study was conducted in three stages.In the first stage,subjects were recruited for health examination in four hospitals in Chengdu,Tianjin,Beijing,and Chongqing,China,from 2015 to 2020,and the multivariate logistic regression analysis was used to investigate the association between hypertension and the risk of GSD in each center.In the second stage,Embase,PubMed,Wanfang Data,VIP,and CNKI databases were searched for related studies published up to May 2021,and a meta-analysis was conducted to further verify such association.In the third stage,the random effects model was used for pooled analysis of the results of the multicenter cross-sectional study and the findings of previous literature.Results A total of 633 948 participants were enrolled in the cross-sectional study,and the prevalence rate of GSD was 7.844%.The multivariate logistic regression analysis showed that hypertension was positively associated with the risk of GSD(P＜0.05).Subgroup analysis showed that there was no significant difference in the association between hypertension and GSD between individuals with different sexes,ages,and subtypes of GSD.A total of 80 articles were included in the systematic review and the meta-analysis,and the results showed that the risk of GSD was increased by 1.022 times for every 10 mmHg increase in diastolic pressure and 1.014 times for every 10 mmHg increase in systolic pressure.Conclusion Hypertension significantly increases the risk of GSD,and the findings of this study will provide a basis for the etiology of GSD and the identification of high-risk groups.

Objective:To investigate the trajectories of intrinsic capacity in older adults and explore the impact of leisure activities on the decline of intrinsic capacity.Methods:This study is a prospective cohort study conducted in a community in Beijing, China.A convenience sampling method was used to select 284 cases of older adults from November to December 2020.The purpose of the study was to gather information on the general conditions, intrinsic abilities(including cognitive, vitality, motor, psychological, and sensory dimensions), and participation in leisure activities of older adults.A 2.5-year follow-up of the respondents was conducted.Results:A total of 243(85.6%, 243/284)respondents completed the 2.5-year follow-up.The follow-up intrinsic capacity score decreased from a baseline level of 4(3, 4)to 3(3, 4)( Z=-4.667, P<0.001).Among the respondents, 113(46.5%, 113/243)older adults showed a decrease in intrinsic capacity, with more significant decreases observed in the locomotor and psychometric dimensions( &chi;2=16.953, 23.510, both P<0.001).The number of declines in intrinsic ability was higher in the low group of leisure activities compared to the high group[62.2%(56/90) vs.37.3%(57/153), &chi;2=14.199, P<0.001].There was a positive correlation between leisure activity scores and the follow-up intrinsic capacity score( r=0.200, P=0.002), as well as with the value of change in the score of intrinsic capacity( r=0.146, P=0.023).The results of Logistic regression analysis indicated that leisure activities( OR=0.644, 95% CI: 0.507 to 0.818, P<0.001), physical leisure activities( OR=0.565, 95% CI: 0.395 to 0.809, P=0.002), and intellectual leisure activities( OR=0.742, 95% CI: 0.555 to 0.992, P=0.044)independently influenced the decline of intrinsic ability in the elderly, even after accounting for demographic information, number of diseases, and type of medicine taken. Conclusions:The decline in intrinsic abilities is a common occurrence among the elderly population.Engaging in leisure activities has been found to be effective in reducing this decline.It is important to emphasize the impact of leisure activities on the overall health of older individuals.

Objective:To investigate age-related characteristics of gait parameters in the elderly.Methods:From February 2023 to August 2023, a convenient sampling method was used to investigate the elderly over 60 years old in communities in Beijing.General characteristics and anthropometric data were collected.Gait parameters of the subjects during normal speed walking were measured using a wearable gait analyzer.Comparisons were made of the basic characteristics, physical status and gait parameters in different age groups.Linear regression analysis was used to evaluate the changes of physical status and gait parameters with age, with the 60-69-year-old group as the baseline standard.Results:A total of 670 elderly people were included, including 324(48.4%)aged 60-69 years, 285(42.5%)aged 70-79 years, and 61(9.1%)aged ≥80 years.Linear regression analysis showed that after adjusting for confounding factors, with increasing age, skeletal muscle mass index(SMI)( β=-0.018, 95% CI: -0.029--0.007), calf circumference( β=-0.096, 95% CI: -0.142--0.051), upper limb flexibility( β=-0.200, 95%, 95% CI: -0.355--0.046), lower limb flexibility( β=-0.244, 95% CI: -0.377--0.111), grip strength( β=-0.397, 95% CI: -0.491--0.303), the Short Physical Performance Battery(SPPB)( β=-0.080, 95% CI: -0.100--0.060)decreased( P<0.05), and the gait parameter such as speed( β=-0.010, 95% CI: -0.014--0.007), cadence( β=-0.398, 95% CI: -0.634--0.162), step length/height( β=-0.002, 95% CI: -0.003--0.002), stride length( β=-0.009, 95% CI: -0.011--0.007), swing power( β=-0.009, 95% CI: -0.012--0.006), ground impact( β=-0.020, 95% CI: -0.026--0.014), foot fall( β=-0.050, 95% CI: -0.064--0.036), pre-swing angle( β=-0.545, 95% CI: -0.714--0.377)all decreased( P<0.05), while stride time( β=0.005, 95% CI: 0.001-0.009), single limb support time( β=1.566, 95% CI: 0.499-2.633), terminal double limb support time( β=0.609, 95% CI: 0.084-1.134), swing duration( β=1.288, 95% CI: 0.024-2.552), single step time( β=2.417, 95% CI: 0.462-4.372)and support phase time( β=1.935, 95% CI: 0.421-3.449)all increased( P<0.05). Conclusions:The walking ability tends to decline with age in older people in the community who walk at a normal walking speed.

Objective:To understand the iron content and transferrin receptor 1 (TfR1) expression levels in keloid and normal skin tissues, an in vitro model of keloid fibroblasts (KFB) ferroptosis induced by Erastin was constructed, and the effects of Erastin and Ferrostatin-1(Fer-1) on cell viability, ferrous ion (Fe 2+) content and lipid peroxidation, ferroptosis and fibrosis-related regulatory factors were examined. Methods:Six keloid tissues and six normal skin tissues were collected from the First Affiliated Hospital of Xinjiang Medical University from March to June 2022, and the tissue iron content kit was used to determine the iron content in the dermis of the two tissues, and TfR1 protein expression was detected in the two tissues by Western blot. Primary KFB and normal skin fibroblasts (NFB) were obtained by tissue block culture method, and the effect of different concentrations of Erastin and Fer-1 on cell activity was detected by using Erastin-induced KFB ferroptosis model and CCK-8 method to screen the appropriate drug concentration. The follow-up experiments were divided into five groups: NFB group, control group, Erastin (0.6 μmol/L) group, Fer-1 (1 μmol/L) group, and Erastin (0.6 μmol/L) +Fer-1 (1 μmol/L) group, while KFB was used as the experimental object in the last 4 groups. Cell migration ability was detected by scratch assay, and malondialdehyde (MDA), reactive oxygen species (ROS) and Fe 2+ content in each group of cells were detected by fluorescent probe method and kits; the protein expression of TfR1, glutathione peroxidase 4 (GPx4), solute carrier family 7 member 11 (SLC7A11), α-smooth muscle actin (α-SMA) and type I collagen (COL-1) in each group of cells were detected by Western blot, and the protein expression and localization of TfR1, Gpx4 in KFB were detected by immunofluorescence. GraphPad Prism 9.0 statistical software was used, and the measurement data were expressed as Mean±SD. Independent sample t-test was used for comparison between 2 groups, and one-way ANOVA was used for comparison between multiple groups, then LSD-t test was used for pairwise comparison between groups. P< 0.05 indicated that the differences were statistically significant. Results:The iron content and TfR1 protein expression were significantly higher in keloid compared with normal skin tissue ( P<0.01). The proliferation rate of KFB with different Erastin concentrations decreased gradually, the IC 50 was 0.61 μmol/L, and Fer-1 had no obvious toxicity to KFB in the range of 0.1~20 μmol/L. Scratch test showed that the migration rate of control group was significantly higher than that of NFB group ( P< 0.01) ; compared with the control group, KFB migration rate decreased significantly after Erastin intervention ( P<0.01) ; compared with the Erastin group, KFB migration was significantly accelerated in the Erastin+Fer-1 group ( P<0.01). Compared with the NFB group, ROS, MDA levels were significantly increased in the control group ( P< 0.01) ; compared with the control group, ROS, MDA levels and Fe 2+ content were significantly higher in the Erastin group ( P<0.01), while ROS, MDA levels and Fe 2+ content were significantly lower in the Fer-1 group ( P<0.01) ; compared with the Erastin group, MDA, ROS levels and Fe 2+content in the Erastin+ Fer-1 group were significantly decreased ( P<0.01). Western Blot showed that, compared with the NFB group, iron death indexes of SLC7A11 and GPx4 protein expression were significantly reduced ( P<0.01 or P<0.05), TfR1 protein expression was increased ( P<0.01), and fibrosis indexes of α-SMA and COL-1 protein expression were significantly increased ( P<0.01) in the control group; compared with the control group, SLC7A11 expression was reduced ( P<0.01) and TfR1, COL-1 expression increased ( P<0.01), while SLC7A11, GPx4 expression increased ( P< 0.01) and TfR1, α-SMA, COL-1 expression significantly decreased ( P<0.01) in the Fer-1 group; compared with the Erastin group, the GPx4, SLC7A11 expression was increased ( P< 0.01) and TfR1, α-SMA, COL-1 expression was significantly decreased ( P< 0.01) in the Erastin+Fer-1 group, suggesting that Fer-1 was able to reverse Erastin-induced ferroptosis and pro-fibrotic effects in KFB. Immunofluorescence showed that GPx4 was expressed in both nucleus and cytoplasm. Compared with control group, Fer-1 increased the fluorescence intensity of GPx4 in KFB ( P<0.01). Compared with Erastin group, the fluorescence intensity of GPx4 in Erastin+ Fer-1 group was significantly increased ( P<0.01). TfR1 was mainly expressed in cytoplasm. Compared with control group, Erastin increased the fluorescence intensity of TfR1 in KFB ( P< 0.05), while Fer-1 group significantly decreased it ( P < 0.01). Compared with Erastin group, the fluorescence intensity of TfR1 in Erastin+Fer-1 group was significantly reduced ( P<0.01). Conclusions:Iron overload and free iron increase in keloids. Erastin induces ferroptosis in KFB and aggravates keloid fibrosis. Fer-1 reverses the oxidative damage and iron accumulation induced by Erastin and effectively inhibits ferroptosis and keloid fibrosis in KFB.

Nuclear factor E2-related factor 2 (Nrf2) is a major regulator of redox homeostasis in cells, and Nrf2 signaling pathway has anti-inflammatory, anti-oxidative stress, and anti-fibrosis effects and plays an important role in wound healing and pathological scar formation and progression. This article reviewed the related research on the effect of oxidative stress and Nrf2 signaling pathway on pathological scars, and expounded the relationship between Nrf2 signaling pathway, oxidative stress and pathological scars, providing a new perspective for the mechanism study and clinical prevention and treatment of pathological scars.

Objective:To investigate the iron content and transferrin receptor 1 (TfR1) expression levels in keloid and normal skin tissues. Erastin induced ferroptosis model of keloid fibroblasts (KFB) is constructed in vitro, and the effects of Erastin and Ferrostatin-1 (Fer-1) on cell viability, ferrous ion (Fe 2+ ) content and lipid peroxidation, ferroptosis and fibrosis-related regulatory factors are examined. Methods:Six keloid tissues and six prepuces were collected from the First Affiliated Hospital of Xinjiang Medical University from March to June 2022. The tissue iron content kit was used to determine the iron content in the dermis, and TfR1 protein expression level was detected by Western blotting. Primary KFB and normal skin fibroblasts (NFB) were obtained by tissue cultivation, Erastin-induced KFB ferroptosis model and CCK-8 assay were used to detect the effects of different concentrations of Erastin and Fer-1 on cell viability, and to screen the appropriate drug concentration. The subsequent experiments were divided into five groups: NFB group, control group, Erastin (0.6 μmol/L) group, Fer-1 (1 μmol/L) group, and Erastin (0.6 μmol/L) + Fer-1 (1 μmol/L) group. KFB was used in the last 4 groups. Cell migration ability was detected by scratch assay. The contents of malondialdehyde (MDA), reactive oxygen species (ROS) and Fe 2+ were detected by fluorescence probe and kits; the protein expression levels of TfR1, glutathione peroxidase 4 (GPx4), solute carrier family 7 member 11 (SLC7A11), α-smooth muscle actin (α-SMA) and type I collagen (COL-1) in each group of cells were detected by Western blotting; the protein expression and localization of TfR1 and Gpx4 in KFB were detected by immunofluorescence staining. GraphPad Prism 9.0 statistical software was used in the statistical analyses, and the measurement data were expressed as Mean±SD. Independent samples t-test was used for comparison between 2 groups, and one-way ANOVA was used for comparison between multiple groups, LSD- t test was used for pairwise comparison between groups. P<0.05 indicated statistical significance. Results:The iron content and TfR1 protein expression level were significantly higher in keloids compared with normal skin tissue ( P<0.01). The proliferation rate of KFB decreased as the Erastin concentration increased, the IC 50 was 0.61 μmol/L, and Fer-1 had no obvious toxicity to KFB in the range of 0.1-20 μmol/L. Scratch test showed that the migration rate of control group was significantly higher than that of NFB group ( P<0.01); compared with the control group, KFB migration rate decreased significantly after Erastin intervention ( P<0.01); compared with the Erastin group, KFB migration was significantly accelerated in the Erastin+ Fer-1 group ( P<0.01). Compared with the NFB group, ROS, MDA levels were significantly increased in the control group ( P<0.01); compared with the control group, ROS, MDA levels and Fe 2+ content were significantly higher in the Erastin group ( P<0.01), while ROS, MDA levels and Fe 2+ content were significantly lower in the Fer-1 group ( P<0.05); compared with the Erastin group, MDA, ROS levels and Fe 2+ content in the Erastin+ Fer-1 group were significantly decreased ( P<0.01). Western blotting results showed that, compared with the NFB group, ferroptosis indexes of SLC7A11 and GPx4 protein expression levels were significantly reduced ( P<0.01), TfR1 protein expression was increased ( P<0.01), and protein expression of fibrosis indexes, α-SMA and COL-1 were significantly increased ( P<0.01) in the control group; compared with the control group, Erastin group had reduced SLC7A11 expression ( P<0.01) and increased TfR1, COL-1 expression ( P<0.01), while SLC7A11, GPx4 expression increased ( P<0.01) and TfR1, α-SMA, COL-1 decreased ( P<0.01) in the Fer-1 group; compared with the Erastin group, the GPx4 and SLC7A11 expression levels were increased ( P<0.01) and TfR1, α-SMA, COL-1 expression levels were significantly decreased ( P<0.01) in the Erastin+ Fer-1 group, suggesting that Fer-1 was able to reverse the Erastin-induced ferroptosis and pro-fibrotic effects in KFB. Immunofluorescence staining showed that GPx4 was expressed in both the nucleus and the cytoplasm. Compared with the control group, Fer-1 increased the fluorescence intensity of GPx4 in KFB ( P<0.01). Compared with the Erastin group, the fluorescence intensity of GPx4 in Erastin+ Fer-1 group was significantly increased ( P<0.01). TfR1 was mainly expressed in the cytoplasm. Compared with the control group, Erastin increased the fluorescence intensity of TfR1 in KFB ( P<0.05), while Fer-1 group significantly decreased it ( P<0.01). Compared with Erastin group, the fluorescence intensity of TfR1 in Erastin+ Fer-1 group was significantly reduced ( P<0.01). Conclusion:Iron overload is present in keloids and the free iron level is increased. Erastin is able to induce ferroptosis in KFB and aggravate keloid fibrosis. Fer-1 can reverse the oxidative damage and iron accumulation induced by Erastin, and is able to effectively inhibit ferroptosis and keloid fibrosis in KFB.