Correlation of carotid contrast-enhanced ultrasonography parameters with nerve damage and plaque properties in patients with atherosclerosis cerebral infarction

Objective: To explore the correlation of carotid contrast-enhanced ultrasonography parameters with nerve damage and plaque properties in patients with atherosclerosis cerebral infarction. Methods: A total of 176 patients with atherosclerosis cerebral infarction who were sent to this hospital for medical treatment between August 2014 and February 2018 were enrolled in cerebral infarction group, and 100 healthy elderly subjects who received physical examination in this hospital during the same period were enrolled in normal control group. Carotid CEUS parameter levels as well as serum contents of indexes related to nerve injury and plaque property were compared between the two groups, and Pearson test was used to evaluate the correlation of CEUS parameters levels with nerve damage and plaque properties in patients with cerebral infarction. Results: CEUS parameter Tp level in cerebral infarction group was lower than that in normal control group whereas P and AUC levels were higher than those in normal control group;serum nerve damage-related indexes SAA, NT-proBNP, Hcy, NSE and copeptin contents were higher than those of normal control group;serum plaque property-related indexes Lp-PLA2, MMP-9, Cat S and CD62P contents were higher than those of normal control group while APN and Cys C contents were lower than those of normal control group. Correlation analysis confirmed that carotid CEUS parameter levels in patients with cerebral infarction were correlated with the contents of indexes related to nerve damage and plaque property. Conclusion: Carotid CEUS parameters are obviously abnormal in patients with atherosclerosis cerebral infarction, they are directly correlated with the specific nerve damage and plaque properties, and they can be used as the reliable indexes to forecast the risk of cerebral infarction and evaluate its severity.

Value of contrast-enhanced ultrasonography for evaluating the angiogenesis of carotid plaque in patients with cerebral infarction and its correlation with the changes of plaque properties

Objective: To study the value of contrast-enhanced ultrasonography for evaluating the angiogenesis of carotid plaque in patients with cerebral infarction and its correlation with the changes of plaque properties. Methods: The patients with carotid low-echo plaque detected by carotid artery ultrasound in Xinjiang Uygur Autonomous Region People's Hospital between January 2014 and January 2016 were selected as the research subjects, received at least 2 years of follow-up and divided into the cerebral infarction group who were with acute cerebral infarction during follow-up and the control group who were without cerebral infarction. CEUS was conducted on inclusion to measure the peak intensity (Peak) and time to peak (TP), and the serum was collected to determine the contents of angiogenesis molecules, inflammatory cytokines and collagen metabolism indexes. Results: The Peak level as well as serum VEGF, HGF, Ang-1, PDGF-BB, VE-cadherin, FKN, IL-17, ICTP, MMP10 and Caspase-3 contents of cerebral infarction group was higher than those of control group whereas TP level as well as serum IL-4, IL-10, TIMP1 and Vaspin contents was lower than those of control group;serum VEGF, HGF, Ang-1, PDGF-BB, VE-cadherin, FKN, IL-17, ICTP, MMP10 and Caspase-3 contents of cerebral infarction group were positively correlated with Peak level, and negatively correlated with TP level;serum IL-4, IL-10, TIMP1 and Vaspin contents were negatively correlated with Peak level, and positively correlated with TP level. Conclusion: CEUS parameters can be used to evaluate the angiogenesis in carotid plaque and the changes of plaque properties in patients with cerebral infarction.

Regional dynamic cerebral autoregulation across anterior and posterior circulatory territories:A detailed exploration and its clinical implications

Cerebral autoregulation(CA)is the mechanism that maintains stable cerebral blood flow(CBF)despite fluctuations in systemic blood pressure,crucial for brain homeostasis.Recent evidence highlights distinct regional variations in CA between the anterior(carotid)and posterior(vertebrobasilar)circulations.Noninvasive neuromonitoring techniques,such as transcranial Doppler,transfer function analysis,and near-infrared spectroscopy,facilitate the dynamic assessment of CBF and autoregulation.Studies indicate a robust autoregulatory capacity in the anterior circulation,characterized by rapid adjustments in vascular resistance.On the contrary,the posterior circulation,mainly supplied by the vertebral arteries,may have a lower autoregulatory capacity.in acute brain injuries such as intracerebral and subarachnoid hemorrhage,and traumatic brain injuries,dynamic CA can be significantly altered in the posterior circulation.Proposed physiological mechanisms of impaired CA in the posterior circulation include:(1)Decreased sympathetic innervation of the vasculature impairing compensatory vasoreactivity;(2)Endothelial dysfunction;(3)Increased cerebral metabolic rate of oxygen consumption within the visual cortex causing CBFmetabolism(i.e.,neurovascular)uncoupling;and(4)Impaired blood-brain barrier integrity leading to impaired astrocytic mediated release of vasoactive substances(e.g.nitric oxide,potassium,and calcium ions).Furthermore,more research is needed on the effects of collateral circulation,as well as the circle of Willis variants,such as the fetal-type posterior cerebral artery,on dynamic CA.Improving our understanding of these mechanisms is crucial to improving the diagnosis,prognosis,and management of various cerebrovascular disorders.

Intraoperative hemodynamic parameters of middle cerebral artery and other artery aneurysms utilizing transcranial Doppler ultrasonography

BACKGROUND： Hemodynamic changes accompany the initiation, development and rupture of middle cerebral artery （MCA） aneurysms. The complexity of the intraaneurysmal hemodynamic factors has not been completely clarified by the indirect measures and methods used in previous studies. OBJECTIVE： To evaluate correlations of intraoperative hemodynamic factors to initiation and rupture of MCA aneurysms. DESIGN, TIME AND SETTING： A case-control study was performed at the Department of Neurosurgery, Tiantan Hospital Affiliated to Capital Medical University, China between March and October 2008. PARTICIPANTS： A total of 12 consecutive patients diagnosed with MCA aneurysms （MCA aneurysms group） and five patients without middle cerebral artery aneurysms （with aneurysms located at other arteries, control group） were enrolled at the Department of Neurosurgery, Tiantan Hospital Affiliated to Capital Medical University, China. METHODS： The proximal and distal arteries of MCA aneurysms were exposed visibly in the MCA aneurysm group. The M1 segment of MCA without the aneurysm and the aneurysm on other arteries were also exposed visibly in the control group. Hemodynamic indices were then measured using an intraoperative 16 MHz probe installed in a Multi-Dop TCD8X4 device. MAIN OUTCOME MEASURES： Mean （time-averaged velocity） difference, maximum mean, pulsatility index difference, maximum pulsatility index, resistance index difference, maximum resistance index; correlation of development and rupture of MCA aneurysms to intraoperative hemodynamic factors of the parent artery. RESULTS： A total of 12 patients underwent microsurgery for treatment to occlude 15 MCA aneurysms. Of the 15 MCA aneurysms, 12 were located at the bifurcation, two at the M1 segment and one at the M3 segment; eight of the aneurysms were unruptured and seven were ruptured. The whole indices with combination mean difference, maximum mean, and maximum pulsatility index of the aneurysms were important factors influencing the rupture of MCA aneurysms （t = 2.92, P = 0.03, constant）. A higher velocity intraaneurismal flow at the bifurcation was identified （t = 3.48, P = 0.01, constant）. After the aneurysm was completely occluded, global high-velocity flow could not be detected in the parent arteries （t = 2.57, P=0.03, constant）. CONCLUSION： When short-term high-velocity blood flow is present, aneurysms can be easily initiated and ruptured at the bifurcation of MCA.

Blood-brain barrier pathology in cerebral small vessel disease

Cerebral small vessel disease is a neurological disease that affects the brain microvasculature and which is commonly observed among the elderly.Although at first it was considered innocuous,small vessel disease is nowadays regarded as one of the major vascular causes of dementia.Radiological signs of small vessel disease include small subcortical infarcts,white matter magnetic resonance imaging hyperintensities,lacunes,enlarged perivascular spaces,cerebral microbleeds,and brain atrophy;however,great heterogeneity in clinical symptoms is observed in small vessel disease patients.The pathophysiology of these lesions has been linked to multiple processes,such as hypoperfusion,defective cerebrovascular reactivity,and blood-brain barrier dysfunction.Notably,studies on small vessel disease suggest that blood-brain barrier dysfunction is among the earliest mechanisms in small vessel disease and might contribute to the development of the hallmarks of small vessel disease.Therefore,the purpose of this review is to provide a new foundation in the study of small vessel disease pathology.First,we discuss the main structural domains and functions of the blood-brain barrier.Secondly,we review the most recent evidence on blood-brain barrier dysfunction linked to small vessel disease.Finally,we conclude with a discussion on future perspectives and propose potential treatment targets and interventions.

Relationship between neonatal respiratory distress syndrome pulmonary ultrasonography and respiratory distress score,oxygenation index,and chest radiography grading

BACKGROUND Accurate condition assessment is critical for improving the prognosis of neonatal respiratory distress syndrome(RDS),but current assessment methods for RDS pose a cumulative risk of harm to neonates.Thus,a less harmful method for assessing the health of neonates with RDS is needed.AIM To analyze the relationships between pulmonary ultrasonography and respiratory distress scores,oxygenation index,and chest X-ray grade of neonatal RDS to identify predictors of neonatal RDS severity.METHODS This retrospective study analyzed the medical information of 73 neonates with RDS admitted to the neonatal intensive care unit of Liupanshui Maternal and Child Care Service Center between April and December 2022.The pulmonary ultrasonography score,respiratory distress score,oxygenation index,and chest Xray grade of each newborn before and after treatment were collected.Spearman correlation analysis was performed to determine the relationships among these values and neonatal RDS severity.RESULTS The pulmonary ultrasonography score,respiratory distress score,oxygenation index,and chest X-ray RDS grade of the neonates were significantly lower after treatment than before treatment(P<0.05).Spearman correlation analysis showed that before and after treatment,the pulmonary ultrasonography score of neonates with RDS was positively correlated with the respiratory distress score,oxygenation index,and chest X-ray grade(ρ=0.429–0.859,P<0.05).Receiver operating characteristic curve analysis indicated that pulmonary ultrasonography screening effectively predicted the severity of neonatal RDS(area under the curve=0.805–1.000,P<0.05).CONCLUSION The pulmonary ultrasonography score was significantly associated with the neonatal RDS score,oxygenation index,and chest X-ray grade.The pulmonary ultrasonography score was an effective predictor of neonatal RDS severity.

Cerebral arterial blood flow,attention,and executive and cognitive functions in depressed patients after acute hypertensive cerebral hemorrhage

BACKGROUND Intracerebral hemorrhage mainly occurs in middle-aged and elderly patients with hypertension,and surgery is currently the main treatment for hypertensive cerebral hemorrhage,but the bleeding caused by surgery will cause damage to the patient's nerve cells,resulting in cognitive and motor dysfunction,resulting in a decline in the patient's quality of life.AIM To investigate associations between cerebral arterial blood flow and executive and cognitive functions in depressed patients after acute hypertensive cerebral hemorrhage.METHODS Eighty-nine patients with depression after acute hypertensive cerebral hemorrhage who were admitted to our hospital between January 2019 and July 2021 were selected as the observation group,while 100 patients without depression who had acute hypertensive cerebral hemorrhage were selected as the control group.The attention span of the patients was assessed using the Paddle Pin Test while executive function was assessed using the Wisconsin Card Sorting Test(WCST)and cognitive function was assessed using the Montreal Cognitive Assessment Scale(MoCA).The Hamilton Depression Rating Scale(HAMD-24)was used to evaluate the severity of depression of involved patients.Cerebral arterial blood flow was measured in both groups.RESULTS The MoCA score,net scores I,II,III,IV,and the total net score of the scratch test in the observation group were significantly lower than those in the control group(P<0.05).Concurrently,the total number of responses,number of incorrect responses,number of persistent errors,and number of completed responses of the first classification in the WCST test were significantly higher in the observation group than those in the control group(P<0.05).Blood flow in the basilar artery,left middle cerebral artery,right middle cerebral artery,left anterior cerebral artery,and right anterior cerebral artery was significantly lower in the observation group than in the control group(P<0.05).The basilar artery,left middle cerebral artery,right middle cerebral artery,left anterior cerebral artery,and right anterior cerebral artery were positively correlated with the net and total net scores of each part of the Paddle Pin test and the MoCA score(P<0.05),and negatively correlated with each part of the WCST test(P<0.05).In the observation group,the post-treatment improvement was more prominent in the Paddle Pin test,WCST test,HAMD-24 score,and MoCA score compared with those in the pre-treatment period(P<0.05).Blood flow in the basilar artery,left middle cerebral artery,right middle cerebral artery,left anterior cerebral artery,and right anterior cerebral artery significantly improved in the observation group after treatment(P<0.05).CONCLUSION Impaired attention,and executive and cognitive functions are correlated with cerebral artery blood flow in patients with depression after acute hypertensive cerebral hemorrhage and warrant further study.

Investigation multi-target synergistic mechanism of Choerospondias axillaris in the treat of cerebral ischemia based on systems pharmacology and experimental verification

Background:Choerospondias axillaris(CA)is a traditional Mongolian medicine that has been proven to have a good therapeutic effect on cerebrovascular disease.Cerebral Ischemia(CI)is a severe and life-threatening cerebrovascular disease.However,the specific mechanism of action of CA in the treatment of CI is still unclear.Methods:In this study,the related targets and pathways of CA in the treatment of CI were first predicted by system pharmacology and then verified by relevant experiments.Results:The results showed that 12 active ingredients and 208 targets were selected.Further validation through protein-protein interaction(PPI)network analysis and active ingredients-target-pathway(A-T-P)network analysis has confirmed the pivotal roles of the main bioactive constituents,including quercetin,kaempferol,naringin,β-sitosterol,and gallic acid.These components exert their anti-ischemic effects by modulating key targets such as IL6,TNF,MAPK3,and CASP3,thereby regulating the PI3K-Akt,HIF-1,and MAPK signaling pathways,which are integral to processes like inflammation,apoptosis,and oxidative stress.More importantly,through experimental verification,this study confirmed our prediction that CAE significantly reduced neurological function scores,infarct volume,and the percentage of apoptosis neurons.Conclusion:This indicates that CA acts on CI through multi-target synergistic mechanism,and this study provides theoretical basis for the clinical application of CA.

Traditional craniotomy versus current minimally invasive surgery for spontaneous supratentorial intracerebral haemorrhage:A propensity-matched analysis

BACKGROUND Minimally invasive surgery(MIS)and craniotomy(CI)are the current treatments for spontaneous supratentorial cerebral haemorrhage(SSTICH).AIM To compare the efficacy and safety of MIS and CI for the treatment of SSTICH.METHODS Clinical and imaging data of 557 consecutive patients with SSTICH who underwent MIS or CI between January 2017 and December 2022 were retrospectively analysed.The patients were divided into two subgroups:The MIS group and CI group.Propensity score matching was performed to minimise case selection bias.The primary outcome was a dichotomous prognostic(favourable or unfavourable)outcome based on the modified Rankin Scale(mRS)score at 3 months;an mRS score of 0–2 was considered favourable.RESULTS In both conventional statistical and binary logistic regression analyses,the MIS group had a better outcome.The outcome of propensity score matching was unexpected(odds ratio:0.582;95%CI:0.281–1.204;P=0.144),which indicated that,after excluding the interference of each confounder,different surgical modalities were more effective,and there was no significant difference in their prognosis.CONCLUSION Deciding between MIS and CI should be made based on the individual patient,considering the hematoma size,degree of midline shift,cerebral swelling,and preoperative Glasgow Coma Scale score.

Human-induced pluripotent stem cell-derived neural stem cell exosomes improve blood-brain barrier function after intracerebral hemorrhage by activating astrocytes via PI3K/AKT/MCP-1 axis

Cerebral edema caused by blood-brain barrier injury after intracerebral hemorrhage is an important factor leading to poor prognosis.Human-induced pluripotent stem cell-derived neural stem cell exosomes(hiPSC-NSC-Exos)have shown potential for brain injury repair in central nervous system diseases.In this study,we explored the impact of hiPSC-NSC-Exos on blood-brain barrier preservation and the underlying mechanism.Our results indicated that intranasal delivery of hiPSC-NSC-Exos mitigated neurological deficits,enhanced blood-brain barrier integrity,and reduced leukocyte infiltration in a mouse model of intracerebral hemorrhage.Additionally,hiPSC-NSC-Exos decreased immune cell infiltration,activated astrocytes,and decreased the secretion of inflammatory cytokines like monocyte chemoattractant protein-1,macrophage inflammatory protein-1α,and tumor necrosis factor-αpost-intracerebral hemorrhage,thereby improving the inflammatory microenvironment.RNA sequencing indicated that hiPSC-NSC-Exo activated the PI3K/AKT signaling pathway in astrocytes and decreased monocyte chemoattractant protein-1 secretion,thereby improving blood-brain barrier integrity.Treatment with the PI3K/AKT inhibitor LY294002 or the monocyte chemoattractant protein-1 neutralizing agent C1142 abolished these effects.In summary,our findings suggest that hiPSC-NSC-Exos maintains blood-brain barrier integrity,in part by downregulating monocyte chemoattractant protein-1 secretion through activation of the PI3K/AKT signaling pathway in astrocytes.

Management of cerebral amyloid angiopathy and atrial fibrillation:We are still far from precision medicine

The use of anticoagulation therapy could prove to be controversial when trying to balance ischemic stroke and intracranial bleeding risks in patients with concurrent cerebral amyloid angiopathy(CAA)and atrial fibrillation(AF).In fact,CAA is an age-related cerebral vasculopathy that predisposes patients to intracerebral hemorrhage.Nevertheless,many AF patients require oral systemic dose-adjusted warfarin,direct oral anticoagulants(such as factor Xa inhibitors)or direct thrombin inhibitors to control often associated with cardioembolic stroke risk.The prevalence of both CAA and AF is expected to rise,due to the aging of the population.This clinical dilemma is becoming increasingly common.In patients with coexisting AF and CAA,the risks/benefits profile of anticoagulant therapy must be assessed for each patient individually due to the lack of a clear-cut consensus with regard to its risks in scientific literature.This review aims to provide an overview of the management of patients with concomitant AF and CAA and proposes the implementation of a risk-based decision-making algorithm.

Vagus nerve stimulation in cerebral stroke:biological mechanisms,therapeutic modalities,clinical applications,and future directions

Stroke is a major disorder of the central nervous system that poses a serious threat to human life and quality of life.Many stro ke victims are left with long-term neurological dysfunction,which adversely affects the well-being of the individual and the broader socioeconomic impact.Currently,poststroke brain dysfunction is a major and difficult area of treatment.Vagus nerve stimulation is a Food and Drug Administration-approved exploratory treatment option for autis m,refractory depression,epilepsy,and Alzheimer’s disease.It is expected to be a novel therapeutic technique for the treatment of stroke owing to its association with multiple mechanisms such as alte ring neurotransmitters and the plasticity of central neuro ns.In animal models of acute ischemic stroke,vagus nerve stimulation has been shown to reduce infarct size,reduce post-stroke neurological damage,and improve learning and memory capacity in rats with stroke by reducing the inflammatory response,regulating bloodbrain barrier permeability,and promoting angiogenesis and neurogenesis.At present,vagus nerve stimulation includes both invasive and non-invasive vagus nerve stimulation.Clinical studies have found that invasive vagus nerve stimulation combined with rehabilitation therapy is effective in im proving upper limb motor and cognitive abilities in stroke patients.Further clinical studies have shown that non-invasive vagus nerve stimulation,including ear/ce rvical vagus nerve stimulation,can stimulate vagal projections to the central nervous system similarly to invasive vagus nerve stimulation and can have the same effect.In this paper,we first describe the multiple effects of vagus nerve stimulation in stroke,and then discuss in depth its neuroprotective mechanisms in ischemic stroke.We go on to outline the res ults of the current major clinical applications of invasive and non-invasive vagus nerve stimulation.Finally,we provide a more comprehensive evaluation of the advantages and disadvantages of different types of vagus nerve stimulation in the treatment of cerebral ischemia and provide an outlook on the developmental trends.We believe that vagus nerve stimulation,as an effective treatment for stroke,will be widely used in clinical practice to promote the recovery of stroke patients and reduce the incidence of disability.

Endoscopic ultrasonography-related diagnostic accuracy and clinical significance on small rectal neuroendocrine neoplasms

This research aimed to examine the diagnostic accuracy and clinical significance of endoscopic ultrasonography(EUS)in the context of small rectal neuroendocrine neoplasms(NENs).A total of 108 patients with rectal subepithelial lesions(SELs)with a diameter of<20 mm were included in the analysis.The diagnosis and depth assessment of EUS was compared to the histology findings.The prevalence of NENs in rectal SELs was 78.7%(85/108).The sensitivity of EUS in detecting rectal NENs was 98.9%(84/85),while the specificity was 52.2%(12/23).Overall,the diagnostic accuracy of EUS in identifying rectal NENs was 88.9%(96/108).The overall accuracy rate for EUS in assessing the depth of invasion in rectal NENs was 92.9%(78/84).Therefore,EUS demonstrates reasonable diagnostic accuracy in detecting small rectal NENs,with good sensitivity but inferior specificity.EUS may also assist physicians in assessing the depth of invasion in small rectal NENs before endoscopic excision.

Double contrast-enhanced ultrasonography improves diagnostic accuracy of T staging compared with multi-detector computed tomography in gastric cancer patients

BACKGROUND Gastric cancer(GC)is the most common malignant tumor and ranks third for cancer-related deaths among the worldwide.The disease poses a serious public health problem in China,ranking fifth for incidence and third for mortality.Knowledge of the invasive depth of the tumor is vital to treatment decisions.AIM To evaluate the diagnostic performance of double contrast-enhanced ultrasonography(DCEUS)for preoperative T staging in patients with GC by comparing with multi-detector computed tomography(MDCT).METHODS This single prospective study enrolled patients with GC confirmed by preoperative gastroscopy from July 2021 to March 2023.Patients underwent DCEUS,including ultrasonography(US)and intravenous contrast-enhanced ultrasonography(CEUS),and MDCT examinations for the assessment of preoperative T staging.Features of GC were identified on DCEUS and criteria developed to evaluate T staging according to the 8th edition of AJCC cancer staging manual.The diagnostic performance of DCEUS was evaluated by comparing it with that of MDCT and surgical-pathological findings were considered as the gold standard.RESULTS A total of 229 patients with GC(80 T1,33 T2,59 T3 and 57 T4)were included.Overall accuracies were 86.9%for DCEUS and 61.1%for MDCT(P<0.001).DCEUS was superior to MDCT for T1(92.5%vs 70.0%,P<0.001),T2(72.7%vs 51.5%,P=0.041),T3(86.4%vs 45.8%,P<0.001)and T4(87.7%vs 70.2%,P=0.022)staging of GC.CONCLUSION DCEUS improved the diagnostic accuracy of preoperative T staging in patients with GC compared with MDCT,and constitutes a promising imaging modality for preoperative evaluation of GC to aid individualized treatment decision-making.

Genetic pathways in cerebral palsy:a review of the implications for precision diagnosis and understanding disease mechanisms

Ce rebral palsy is a diagnostic term utilized to describe a group of permanent disorders affecting movement and posture.Patients with cerebral palsy are often only capable of limited activity,resulting from non-progressive disturbances in the fetal or neonatal brain.These disturbances severely impact the child’s daily life and impose a substantial economic burden on the family.Although cerebral palsy encompasses various brain injuries leading to similar clinical outcomes,the unde rstanding of its etiological pathways remains incomplete owing to its complexity and heterogeneity.This review aims to summarize the current knowledge on the genetic factors influencing cerebral palsy development.It is now widely acknowledged that genetic mutations and alterations play a pivotal role in cerebral palsy development,which can be further influenced by environmental fa ctors.Des pite continuous research endeavors,the underlying fa ctors contributing to cerebral palsy remain are still elusive.However,significant progress has been made in genetic research that has markedly enhanced our comprehension of the genetic factors underlying cerebral palsy development.Moreove r,these genetic factors have been categorized based on the identified gene mutations in patients through clinical genotyping,including thrombosis,angiogenesis,mitochondrial and oxidative phosphorylation function,neuronal migration,and cellular autophagy.Furthermore,exploring targeted genotypes holds potential for precision treatment.In conclusion,advancements in genetic research have substantially improved our understanding of the genetic causes underlying cerebral palsy.These breakthroughs have the potential to pave the way for new treatments and therapies,consequently shaping the future of cerebral palsy research and its clinical management.The investigation of cerebral palsy genetics holds the potential to significantly advance treatments and management strategies.By elucidating the underlying cellular mechanisms,we can develop to rgeted interventions to optimize outcomes.A continued collaboration between researchers and clinicians is imperative to comprehensively unravel the intricate genetic etiology of cerebral palsy.

Treatment with β-sitosterol ameliorates the effects of cerebral ischemia/reperfusion injury by suppressing cholesterol overload, endoplasmic reticulum stress, and apoptosis

β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unknown whetherβ-sitosterol treatment reduces the effects of ischemic stroke.Here we found that,in a mouse model of ischemic stroke induced by middle cerebral artery occlusion,β-sitosterol reduced the volume of cerebral infarction and brain edema,reduced neuronal apoptosis in brain tissue,and alleviated neurological dysfunction;moreover,β-sitosterol increased the activity of oxygen-and glucose-deprived cerebral cortex neurons and reduced apoptosis.Further investigation showed that the neuroprotective effects ofβ-sitosterol may be related to inhibition of endoplasmic reticulum stress caused by intracellular cholesterol accumulation after ischemic stroke.In addition,β-sitosterol showed high affinity for NPC1L1,a key transporter of cholesterol,and antagonized its activity.In conclusion,β-sitosterol may help treat ischemic stroke by inhibiting neuronal intracellular cholesterol overload/endoplasmic reticulum stress/apoptosis signaling pathways.

Activation of cerebral Ras-related C3 botulinum toxin substrate(Rac) 1 promotes post-ischemic stroke functional recovery in aged mice

Brain functional impairment after stroke is common;however,the molecular mechanisms of post-stroke recovery remain unclear.It is well-recognized that age is the most important independent predictor of poor outcomes after stroke as older patients show poorer functional outcomes following stroke.Mounting evidence suggests that axonal regeneration and angiogenesis,the major forms of brain plasticity responsible for post-stroke recovery,diminished with advanced age.Previous studies suggest that Ras-related C3 botulinum toxin substrate(Rac)1 enhances stroke recovery as activation of Rac1 improved behavior recovery in a young mice stroke model.Here,we investigated the role of Rac1 signaling in long-term functional recovery and brain plasticity in an aged(male,18 to 22 months old C57BL/6J)brain after ischemic stroke.We found that as mice aged,Rac1 expression declined in the brain.Delayed overexpression of Rac1,using lentivirus encoding Rac1 injected day 1 after ischemic stroke,promoted cognitive(assessed using novel object recognition test)and sensorimotor(assessed using adhesive removal tests)recovery on days 14–28.This was accompanied by the increase of neurite and proliferative endothelial cells in the periinfarct zone assessed by immunostaining.In a reverse approach,pharmacological inhibition of Rac1 by intraperitoneal injection of Rac1 inhibitor NSC23766 for 14 successive days after ischemic stroke worsened the outcome with the reduction of neurite and proliferative endothelial cells.Furthermore,Rac1 inhibition reduced the activation of p21-activated kinase 1,the protein level of brain-derived neurotrophic factor,and increased the protein level of glial fibrillary acidic protein in the ischemic brain on day 28 after stroke.Our work provided insight into the mechanisms behind the diminished plasticity after cerebral ischemia in aged brains and identified Rac1 as a potential therapeutic target for improving functional recovery in the older adults after stroke.

Optimization of nursing interventions for postoperative mental status recovery in patients with cerebral hemorrhage

BACKGROUND Hypertensive cerebral hemorrhage(HCH),the most common chronic diseases,has become a topic of global public health discussions.AIM To investigate the role of rehabilitative nursing interventions in optimizing the postoperative mental status recovery phase and to provide clinical value for future rehabilitation of patients with HCH.METHODS This randomized controlled study included 120 patients with cerebral HCH who were contained to our neurosurgery department between May 2021–May 2023 as the participants.The participants have randomly sampled and grouped into the observation and control groups.The observation group received the rehabilitation nursing model,whereas the control group have given conventional nursing.The conscious state of the patients was assessed at 7,14,21,and 30 d postoperatively.After one month of care,sleep quality,anxiety,and depression were compared between the two groups.Patient and family satisfaction were assessed using a nursing care model.RESULTS The results showed that the state of consciousness scores of the patients in both groups significantly increased(P<0.05)after surgical treatment.From the 14th day onwards,differences in the state of consciousness scores between the two groups of patients began to appear(P<0.05).After one month of care,the sleep quality,anxiety state,and depression state of patients were significantly better in the observation group than in the control group(P<0.05).Satisfaction with nursing care was higher in the observation group than in the control group(P<0.05).CONCLUSION The rehabilitation nursing model has a more complete system compared to conventional nursing,which can effectively improve the postoperative quality of life of patients with cerebral hemorrhage and improve the efficiency of mental state recovery;however,further analysis and research are needed to provide more scientific evidence.

The action mechanism by which C1q/tumor necrosis factor-related protein-6 alleviates cerebral ischemia/reperfusion injury in diabetic mice

Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.

Cognitive impairment in cerebral small vessel disease induced by hypertension

Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease,the most common cerebrovascular disease.Howeve r,the causal relationship between hypertension and cerebral small vessel disease remains unclear.Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease.Chronic hypertension and lifestyle factors are associated with risks for stro ke and dementia,and cerebral small vessel disease can cause dementia and stroke.Hypertension is the main driver of cerebral small vessel disease,which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction,leukoaraiosis,white matter lesions,and intracerebral hemorrhage,ultimately res ulting in cognitive decline and demonstrating that the brain is the to rget organ of hypertension.This review updates our understanding of the pathogenesis of hypertensioninduced cerebral small vessel disease and the res ulting changes in brain structure and function and declines in cognitive ability.We also discuss drugs to treat cerebral small vessel disease and cognitive impairment.