ObjectiveTo investigate the mechanism of Naoxintong capsules on ischemia-reperfusion （I/R） injury in rats based on the changes of pericytes mediated by Ras homolog family member A （RHOA）/Rho-associated coiled-coil containing protein kinase 1 （ROCK1） pathway. MethodsNinety rats （15 rats for each group） were randomly divided into a sham operation group， a model group， a positive control group receiving Ginkgo biloba extract （21.6 mg·kg^-1）， and groups receiving Naoxintong capsules at low， medium， and high doses of 55， 110， and 220 mg·kg^-1 （NXT-L， NXT-M， and NXT-H groups）， respectively. Except for those in the sham operation group， all rats were subjected to transient middle cerebral artery occlusion （tMCAO） to establish the experiment model. Nerve function was assessed using a neurological function score. Cerebral blood flow was detected using a laser speckle contrast imager， and the cerebral infarction rate was calculated using 2，3，5-Triphenyl tetrazolium chloride （TTC） staining. Pathological changes were observed by hematoxylin-eosin （HE） staining and Nissl staining， while pericyte morphology was observed via transmission electron microscopy. Blood-brain barrier destruction was observed by Evans blue staining. Albumin and ischemia-modified albumin levels were measured using assay kits. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were used to detect the mRNA and protein expression levels of RHOA， ROCK1， platelet-derived growth factor receptor β （PDGFRB）， α-smooth muscle actin （α-SMA）， tight junction protein （ZO-1）， matrix metalloproteinase-2 （MMP-2）， and matrix metalloproteinase-9 （MMP-9）. ResultsCompared with the sham operation group， the model group exhibited decreased neurological function scores， higher percentage reduction in blood flow， and increased cerebral infarction rates （P<0.01）. Additionally， cortical neuronal nucleus shrinkage， edema， a decreased number of Nissl bodies， reduced pericyte area， elevated albumin content in the cortex （P<0.05）， and increased ischemic modified albumin levels （P<0.01） were observed. The mRNA and protein expression levels of RHOA， ROCK1， PDGFRB， α-SMA， MMP-2， and MMP-9 were increased （P<0.01）， while those of ZO-1 were decreased. Compared with the model group， all treatment groups showed improved neurological function scores， lower percentage reduction in blood flow， reduced cerebral infarction rates （P<0.01）， alleviated cortical histological changes， increased number of Nissl bodies， expanded pericyte area， decreased albumin content in the cortex， and reduced ischemia-modified albumin levels （P<0.01）. The mRNA and protein expression levels of RHOA， ROCK1， PDGFRB， α-SMA， MMP-2， and MMP-9 were decreased （P<0.01）， while those of ZO-1 were increased. Among the treatment groups， the NXT-M group showed the most pronounced improvement in cerebral I/R injury. ConclusionNaoxintong capsules can restore cerebral blood supply， reduce microcirculation disturbance， and protect blood-brain barrier in rats with I/R injury. Its mechanism of action may be related to the inhibition of the RHOA/ROCK1 signaling pathway and reduced pericyte contraction.

ObjectiveTo investigate the mechanism of Naoxintong capsules on ischemia-reperfusion （I/R） injury in rats based on the changes of pericytes mediated by Ras homolog family member A （RHOA）/Rho-associated coiled-coil containing protein kinase 1 （ROCK1） pathway. MethodsNinety rats （15 rats for each group） were randomly divided into a sham operation group， a model group， a positive control group receiving Ginkgo biloba extract （21.6 mg·kg^-1）， and groups receiving Naoxintong capsules at low， medium， and high doses of 55， 110， and 220 mg·kg^-1 （NXT-L， NXT-M， and NXT-H groups）， respectively. Except for those in the sham operation group， all rats were subjected to transient middle cerebral artery occlusion （tMCAO） to establish the experiment model. Nerve function was assessed using a neurological function score. Cerebral blood flow was detected using a laser speckle contrast imager， and the cerebral infarction rate was calculated using 2，3，5-Triphenyl tetrazolium chloride （TTC） staining. Pathological changes were observed by hematoxylin-eosin （HE） staining and Nissl staining， while pericyte morphology was observed via transmission electron microscopy. Blood-brain barrier destruction was observed by Evans blue staining. Albumin and ischemia-modified albumin levels were measured using assay kits. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were used to detect the mRNA and protein expression levels of RHOA， ROCK1， platelet-derived growth factor receptor β （PDGFRB）， α-smooth muscle actin （α-SMA）， tight junction protein （ZO-1）， matrix metalloproteinase-2 （MMP-2）， and matrix metalloproteinase-9 （MMP-9）. ResultsCompared with the sham operation group， the model group exhibited decreased neurological function scores， higher percentage reduction in blood flow， and increased cerebral infarction rates （P<0.01）. Additionally， cortical neuronal nucleus shrinkage， edema， a decreased number of Nissl bodies， reduced pericyte area， elevated albumin content in the cortex （P<0.05）， and increased ischemic modified albumin levels （P<0.01） were observed. The mRNA and protein expression levels of RHOA， ROCK1， PDGFRB， α-SMA， MMP-2， and MMP-9 were increased （P<0.01）， while those of ZO-1 were decreased. Compared with the model group， all treatment groups showed improved neurological function scores， lower percentage reduction in blood flow， reduced cerebral infarction rates （P<0.01）， alleviated cortical histological changes， increased number of Nissl bodies， expanded pericyte area， decreased albumin content in the cortex， and reduced ischemia-modified albumin levels （P<0.01）. The mRNA and protein expression levels of RHOA， ROCK1， PDGFRB， α-SMA， MMP-2， and MMP-9 were decreased （P<0.01）， while those of ZO-1 were increased. Among the treatment groups， the NXT-M group showed the most pronounced improvement in cerebral I/R injury. ConclusionNaoxintong capsules can restore cerebral blood supply， reduce microcirculation disturbance， and protect blood-brain barrier in rats with I/R injury. Its mechanism of action may be related to the inhibition of the RHOA/ROCK1 signaling pathway and reduced pericyte contraction.

Objective:To develop and evaluate a nomogram prediction model for poor outcome in patients with minor acute ischemic stroke (MIS) at 90 days after onset.Methods:Patients with MIS admitted to the Second People's Hospital of Hefei from January 2022 to June 2023 were retrospectively enrolled. At 90 days after onset, the modified Rankin Scale was used for outcome evaluation. <2 points were defined as good outcome and ≥2 points were defined as poor outcome. Multivariate logistic regression analysis was used to identify independent risk factors for poor outcome, and a nomogram prediction model was developed based on these factors. Results:A total of 177 patients with MIS were included, of which 61 (34.46%) had poor outcome. Multivariate logistic regression analysis showed that hypertension (odds ratio [ OR] 3.484, 95% confidence interval [ CI] 1.378-8.810; P=0.008), diabetes ( OR 2.936, 95% CI 1.301-6.625; P=0.009), National Institutes of Health Stroke Scale (NIHSS) score at admission ( OR 2.936, 95% CI 1.027-1.709; P=0.031) and systolic blood pressure at admission ( OR 1.083, 95% CI 1.053-1.115; P<0.001) were the independent risk factors for poor outcome. The established nomogram prediction model had a C-index of 0.828 and the area under the curve was 0.841 (95% CI 0.778-0.891). The calibration curve fitted well with the ideal curve. The clinical decision curve showed that the model had stronger clinical applicability. Conclusions:Hypertension, diabetes, NIHSS score and systolic blood pressure at admission are independent risk factors for poor outcome of patients with MIS. The nomogram based on the above factors has higher discriminative power and clinical value for predicting poor outcome in patients with MIS.

Post-stroke depression (PSD) is an important mental complication of stroke, affecting nearly 1/3 of stroke patients, seriously affecting patients' functional recovery and quality of life, and is associated with increased mortality of stroke patients. Traditional antidepressant treatments include medication and psychotherapy, but there may be problems with adverse reactions, tolerance, or limited effectiveness. Repetitive transcranial magnetic stimulation (rTMS), as a non-invasive neuroregulatory technique, offers a new treatment option for patients with PSD. This article reviews the application of rTMS in the treatment of PSD and its possible mechanism.

Objectives:To analyze and compare the disease burden of ischemic stroke due to tobacco exposure (including active and passive smoking) and its changing trends in China from 1990 to 2019,and to provide a reference for precise prevention and control of ischemic stroke. Methods:Based on the Global Burden of Disease Study 2019 database,we analyzed the burden of ischemic stroke disease attributable to tobacco exposure and its trends in different age and sex populations in China from 1990 to 2019,and compared the epidemiological differences in the burden of ischemic stroke disease attributable to active versus passive smoking. Results:Between 1990 and 2019,the disease burden of ischemic stroke attributable to tobacco exposure showed a decreasing trend in China and globally,but the decrease was relatively small in China.In 2019,the age-standardized mortality rate (ASMR) and age-standardized disability-adjusted life-year rate (ASDR) of ischemic stroke attributable to tobacco exposure in China were 10.64/100000 and 239.39/100000,both higher than the global average levels (5.85/100000 and 140.23/100000 respectively).The actual mortality and disability-adjusted life year (DALY) rates for ischemic stroke due to tobacco exposure in 2019 increased by 103.79％ and 90.48％,respectively,compared with 1990.There was a sex difference in the disease burden of ischemic stroke due to active and passive smoking,with the number of deaths,mortality,DALY,and DALY rates for ischemic stroke due to active smoking being significantly higher in men than in women.Conversely,the burden of ischemic stroke due to passive smoking was higher in women.At the age level,ischemic stroke attributable to both active and passive smoking presented the highest number of deaths,mortality,and DALY rates among those ≥70 years of age.Whereas DALY for ischemic stroke attributable to active smoking was mainly concentrated in those aged 50-69 years,DALY for ischemic stroke attributable to passive smoking was mainly concentrated in those aged ≥70 years. Conclusions:The disease burden of ischemic stroke attributable to tobacco exposure is higher in China than the global average level.The burden of ischemic stroke disease attributable to active and passive smoking varies significantly by sex and age,and more targeted tobacco control policies should be developed in China.

Objective The development of the expert consensus on self-management of skin adverse reactions in patients undergoing targeted cancer therapy(hereinafter referred to as"the consensus")aims to enhance the effectiveness of self-management for skin-related adverse reactions in cancer patients receiving targeted therapy.It seeks to reduce the incidence of these reactions and alleviate their severity.Methods Utilizing evidence-based approaches,a systematic search was conducted across both domestic and international databases and relevant websites.This process included the evaluation and summarization of pertinent evidence to create a preliminary draft of the consensus.Through 2 rounds of Delphi expert inquiries and a round of expert panel discussion,the content was refined,leading to the final draft of the consensus.Results The consensus comprises 11 sections:gathering information before medication,identifying risk factors prior to medication,self-assessment and proactive reporting,skin cleansing,skin moisturizing,sun protection,makeup application,appropriate clothing,engaging in household activities,prophylactic medication,and common management techniques.Conclusion This consensus provides a valuable reference for clinical nurses to guide cancer patients in the self-management of skin adverse reactions associated with targeted drug therapy.

Objective:To explore the clinical efficacy of 125I seeds implantation in treating cancer-induced pain and motor dysfunction caused by brachial plexus compression through neurophysiological monitoring. Methods:A retrospective study was conducted on 8 patients (4 males, 4 females; age 58-63 years) who underwent 125I seeds therapy for cancer-induced brachial plexus injury at Hebei Provincial People′s Hospital from January 2021 to August 2023. Pain severity was assessed by using the numerical rating scale (NRS) and motor function was evaluated by using the Fugl-Meyer (F-M) assessment. Electrophysiological monitoring was used to assess changes in sensory and motor branch conduction velocity (CV) of the musculocutaneous nerve, axillary nerve, median nerve, ulnar nerve, and radial nerve before and 3 months after treatment. Paired t-test was used for data analysis. Results:All 8 patients had moderate to severe pain (6 had motor dysfunction). The preoperative and postoperative NRS scores was 5.9±1.0 and 3.3±1.7, respectively ( t=4.93, P=0.002), while F-M scores was 44.8±7.6 and 54.8±5.7, respectively ( t=-3.52, P=0.017). Electrophysiological results showed that 7 patients had lesion involvement in the lower trunk of the brachial plexus, and 1 patient had involvement in the upper trunk. The preoperative and postoperative motor branch CV of the ulnar nerve was (47.2±2.6) and (59.7±8.2) m/s, respectively ( t=-3.17, P=0.034), while the sensory branch CV was (41.8±1.2) and (56.0±5.7) m/s, respectively ( t=-5.82, P=0.001). The nerve CV increased compared to the preoperative ones. Conclusions:125I seeds implantation has good clinical efficacy in treating cancer-related pain and motor dysfunction caused by brachial plexus compression. Changes in electrophysiology can quantitatively monitor the recovery of sensory and motor functions of the brachial plexus.

This study aims to establish a rat model of renal ischemia reperfusion injury (RIRI) to observe the alterations in the expression of phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway following various exosome treatments. Additionally, differential miRNA expression analysis will be conducted to elucidate the molecular mechanisms underlying the effects of exosomes derived from ischemic preconditioned (IPC) renal tubular cells in mitigating RIRI in rats. Initially, ten SD rats were subjected to bilateral nephrectomy under general anesthesia to prepare primary renal tubular cells. The second-generation renal tubular cells were then subjected to the following treatments for 12 hours: normoxia (38% O 2, 5% CO 2), hypoxia (1% O 2, 5% CO 2), and hypoxia plus inactivation (heated at 65 ℃ for 30 minutes). Following these treatments, exosomes were extracted, yielding normoxic exosomes, IPC exosomes, and inactivated exosomes, respectively. A subsequent cohort of 50 SD rats was randomly divided into five groups: Sham group, RIRI group, RIRI + normoxic exosome group (NC group), RIRI + IPC exosome group (IPC group), and RIRI + inactivated exosome group (INA group). RIRI model was established in the latter four groups. Twenty-four hours after RIRI modeling, the NC, IPC, and INA groups received intravenous injections of 200 μg of normoxic exosomes, IPC exosomes, and inactivated exosomes via the tail vein, respectively. Six days later, venous blood samples were collected, and both kidneys were excised to observe renal function, histopathological changes in kidney tissue, and alterations in the PI3K/AKT/mTOR signaling pathway among the five groups. Furthermore, differential miRNA expression analysis [ P<0.05, |log 2(Fold Change)|≥1] was conducted between the NC and IPC groups to investigate the changes in the miRNA expression profile. Subsequently, GO analysis and KEGG pathway enrichment analysis were performed. The results revealed that: (1) Compared with the Sham group, the RIRI and INA groups exhibited elevated levels of serum creatinine and urea nitrogen (all P<0.01). Histopathological examination of kidney tissues showed substantial inflammatory cell infiltration in the interstitium accompanied by varying degrees of edema, degenerative swelling of tubular structures, necrosis, and detachment of tubular epithelial cells. Notably, the number of TUNEL-positive cells was significantly increased, while the number of Ki67-stained positive cells was markedly decreased. Additionally, the mRNA and protein expression of PI3K/AKT/mTOR signaling pathway in RIRI group and INA group were down-regulated. (2) Compared to the NC group, the IPC group demonstrated lower levels of serum creatinine and urea nitrogen (both P<0.01). Notably, there was a significant decrease in the accumulation of inflammatory cells in the renal interstitium, and tissue edema was markedly improved. Moreover, the number of TUNEL-positive cells was reduced, while the number of Ki67-stained positive cells was significantly increased. Additionally, the mRNA and protein expressions of PI3K, PDK1, AKT, and mTOR were all up-regulated (all P<0.05). (3) Compared to the NC group, 56 miRNAs were up-regulated and 42 miRNAs were down-regulated in the IPC group. The target genes of GO enrichment analysis were PIK3C2A, PIK3CA, PIK3CB, PIK3CD, PIK3C2G, AKT1, mTOR, Rheb, and KEGG enrichment analysis revealed significant enrichment in PI3K/AKT signal pathway and mTOR signal pathway. In conclusion, this study reveals that during the course of RIRI, exosomes derived from IPC renal tubular cells induce differential miRNA expression in kidney tissues, resulting in enhanced expression of the PI3K/AKT/mTOR signaling pathway, which plays a pivotal role in mitigating RIRI in rats.

Objective To analyze the management and countermeasures of adverse nursing events in a municipal tertiary hospital in Guangxi Zhuang Autonomous Region.Methods The adverse nursing events in 2023 in a municipal tertiary hospital in Guangxi were retrospectively analyzed.Logistic regression analysis was utilized to identify the causes of these adverse events and propose suitable countermeasures.Results In 2023,a total of 121 adverse nursing events were recorded,with falls being the most prominent(42 cases,accounting for 34.71％),followed by drug extravasation,drug safety incidents and unplanned ex-tubation,accounting for 13.22％,9.92％,and 7.44％respectively.Logistic regression analysis revealed that factors such as age ≥70 years,coexisting diseases,Basel Index score ≤40,pain score ≥4,tube slip risk assessment ≥10,RASS sedation score ≥3,NGASR score ≥9,lost risk assessment score ≥ 7,GCS Coma Scale score ≤8,Stress Injury Assessment Scale score ≤10,and Morse score ≥45 were associated with the risk of adverse nursing events.In addition,inadequate awareness of nursing risks among nursing staff,ineffective patient health education methods,and non-compliance to nursing protocols were identified as primary causes of adverse nursing events.Conclusion Advanced age,combined with other diseases,and hospitali-zation scale assessment results are critical factors for adverse nursing events.Lack of nursing responsibility and risk awareness among nursing staff,inadequate system implementation,and irregular operations can increase the risk.Hospitals should optimize management systems and work processes,enhance nursing staff training,and develop targeted preventive measures for adverse nursing events to improve the quality of nursing management and reduce the risk of adverse nursing events.

From January 1, 2013, to March 1, 2024, nine patients with hematological malignancies complicated by Gilbert’s syndrome in Peking University People’s Hospital underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT). The patients comprised seven male and two female cases, with a median age of 38 (13-60) years old. Among them, three cases were acute myeloid leukemia, three cases were acute lymphocytic leukemia, two cases were myelodysplastic syndrome, and one case was chronic myelomonocytic leukemia. None of the patients had viral hepatitis. Of the nine cases, seven cases received the Bu-Cy+ATG regimen, while the other two cases received the TBI-Cy+ATG regimen (Bu, busulfan; Cy, cyclophosphamide; ATG, antithymocyte immunoglobulin; and TBI, total body irradiation). All patients achieved neutrophil engraftment, and eight received platelet engraftment. The median total bilirubin level was 45.4 (22.5-71.2) μmol/L before transplantation and 22.0 (18.0-37.2) μmol/L on -1d of preconditioning. The total bilirubin level on +20d after the transplantation of eight patients decreased compared with the baseline level before transplantation. Moreover, one patient had a transient increase in the total bilirubin level on +5d after transplantation, which was considered to be attributed to the toxicity of Bu. No patients were complicated by hepatic veno-occlusive disease. The median follow-up time was 739 (42-2 491) days. During the follow-up period, one patient died of recurrence, and the remaining eight patients had disease-free survival events.