Objectives: To characterize urodynamic findings after lower-level spinal cord injury (LSCI) and to evaluate a new pressure-based classification framework-the bladder-sphincter dyscoordination syndrome (BSDS)-for describing voiding patterns. We also introduce a descriptive "neurogenic bladder outlet obstruction" (NBOO) phenotype for straining-dependent voiding difficulty. Methods: We retrospectively analyzed the first urodynamic studies (December 2020-August 2024) in 81 men with LSCI (injury at T10 or below). Key urodynamic measures included detrusor and intravesical pressures during filling and voiding, bladder volumes (first desire to void and capacity), compliance, maximum flow rate (Q_max), post-void residual (PVR), voiding efficiency, and the ratio of detrusor to abdominal pressure rise (ΔPdet/ΔPabd). We compared cases with detrusor overactivity (DO) versus those without DO. Among those with voiding discoordination, we distinguished classical detrusor-sphincter dyssynergia (DSD) from a proposed NBOO phenotype (characterized by abdominal straining pressure ≥ 40 cmH2O, detrusor pressure < 20 cmH2O, incomplete emptying, and no anatomic obstruction). We further classified discoordination cases using the BSDS framework into four subtypes-dual high-pressure (DHP), detrusor-muscle predominant (DMP), dual low-pressure (DLP), and abdominal-pressure predominant (APP)-based on reference pressure thresholds (detrusor 20 cmH2O; abdominal 40 cmH2O). Results: Patients with DO (43.2%) showed significantly higher detrusor pressures during filling (at first desire to void and at capacity) and a lower first desire volume than non-DO patients, while maximum capacity was similar (p = 0.105). During voiding, DO cases had lower PVR and higher emptying rates, although the detrusor-vs-abdominal pressure contribution (ΔPdet/ΔPabd) was comparable between groups. Among 63 patients with voiding discoordination, 32 (50.8%) met NBOO criteria; these NBOO cases exhibited lower detrusor and intravesical voiding pressures but worse emptying (higher PVR) compared to classical DSD cases. Overall, 76 of 81 patients (93.8%) fit within the BSDS classification-distributed as 22 DHP, 13 DMP, 15 DLP, and 26 APP patterns. Conclusions: The BSDS framework (and the NBOO descriptor when conventional indices cannot be applied) offers a novel way to describe voiding patterns after LSCI. It links urodynamic observations to potential management strategies (by identifying whether the bladder or outlet is the primary issue). Prospective studies are needed to validate this framework against outcomes such as upper tract integrity, continence, and dependence on catheterization.

BACKGROUND Chlorfenapyr poisoning is a highly lethal condition that damages high-energy-demand organs such as the central nervous system. Only a few surviving patients have been reported. Survivors may develop focal neurological symptoms, including motor and urinary dysfunction, and the prognosis for these deficits remains unclear. CASE REPORT A 55-year-old man developed chest tightness, profuse sweating, dyskinesia, and paresthesia in both lower limbs, as well as urinary dysfunction, after working for 2 months in a chlorfenapyr production facility. Laboratory toxicology tests confirmed chlorfenapyr and its metabolite in his blood. Magnetic resonance imaging showed diffuse leukoencephalopathy and thoracic cord edema. After repeated detoxification, the patient became clinically stable and was transferred to the Rehabilitation Department of our hospital. Magnetic resonance imaging on admission revealed resolution of central nervous system lesions. After 2 months of pharmacologic treatment, intensive physical therapy, and neuromodulation, the patient progressed from being unable to stand to walking independently, and from indwelling catheterization to voluntary urination. However, abnormal sensations in the lower limbs and excessive sweating showed no significant improvement. CONCLUSIONS This case demonstrates the reversibility of chlorfenapyr-induced leukoencephalopathy and spinal cord lesions. It indicates that chlorfenapyr poisoning-induced motor and urinary dysfunction can be substantially improved through early and multidisciplinary rehabilitation. The persistence of abnormal sensations and sweating suggests that further investigation is required to clarify the underlying mechanisms and optimize management of these symptoms.

BackgroundPathological upper-limb synergistic movement is a prevalent symptom of post-stroke motor dysfunction and pose a significant challenge in the rehabilitation of hemiplegia. However, the underlying mechanisms remain elusive, hindering the development of effective therapeutic strategies.ObjectiveThis study aims to explore the mechanisms underlying pathological synergic movements post-stroke by examining the interrelationship between motor modules associated with upper limb flexion synergy and the repetitive action of "taking food to the mouth."MethodsSurface electromyography (sEMG) was employed to capture the EMG signals of normal elbow flexion, the act of "taking food to the mouth," and post-stroke upper limb flexion synergy. Non-negative matrix factorization (NMF) was employed to compare and analyze the corresponding modular and coefficient matrices derived from these three motor tasks.ResultsThe modular matrix associated with flexion synergy exhibited the most significant correlation with the "taking food to the mouth" task, whereas the coefficient matrix shared the lowest correlation.ConclusionUpper limb flexion synergy after stroke may be related to the activation of the highly excitatory motor module formed by previously repeated movement of "taking food to mouth".

Objective: To investigate the effect of combined repetitive peripheral magnetic stimulation and transcranial magnetic stimulation on upper extremity function in subacute stroke patients. Design: Pilot study. Subjects: Subacute stroke patients. Methods: Included patients were randomized into 3 groups: a central-associated peripheral stimulation (CPS) group, a central-stimulation-only (CS) group, and a control (C) group. The CPS group underwent a new paired associative stimulation (combined repetitive peripheral magnetic stimulation and transcranial magnetic stimulation), the CS group underwent repetitive transcranial magnetic stimulation, and the C group underwent sham stimulation. All 3 groups received physiotherapy after the stimulation or sham stimulation. The treatment comprised 20 once-daily sessions. Primary outcome was the Fugl-Meyer Assessment Upper Extremity (FMA-UE) score, and secondary outcomes were the Barthel Index and Comprehensive Functional Assessment scores, and neurophysiological assessments were mainly short-interval intracortical inhibition. A 3-group (CPS, CS, C) × 2-time (before, after intervention) repeated measures analysis of variance was conducted to determine whether changes in scores were significantly different between the 3 groups. Results: A total of 45 patients were included in the analysis. Between-group comparisons on the FMA-UE demonstrated a significant improvement (group × time interaction, F2,42 = 4.86; p = 0.013; C vs CS, p = 0.020; C vs CPS, p = 0.016; CS vs CPS, p = 0.955). Correlation analysis did not find any substantial positive correlation between changes in FMA-UE and short-interval intracortical inhibition variables (C, r = –0.196, p = 0.483; CS, r = –0.169, p = 0.546; CPS, r = –0.424, p = 0.115). Conclusion: This study suggests that the real-stimulus (CS and CPS) groups had better outcomes than the control (C) group. In addition, the CPS group showed a better trend in clinical and neurophysiological assessments compared with the CS group.

Introduction: Respiratory dysfunction in patients with Parkinson’s disease (PD) could present in the early stage and worsen in the late stages. These changes could be a factor affecting the ability of daily living and quality of life of patients with PD. The primary objective of this study was to assess the respiratory function and its association with motor function in patients with different stages of PD. Methods: This was a cross-sectional study conducted at the Huashan Hospital of Fudan University in Shanghai, China. The study included 65 patients diagnosed with PD (the Hoehn and Yahr scale between 1 and 4) and 20 healthy individuals of similar age, gender, weight, and height. The ventilatory function was assessed using the spirometry. Motor function was evaluated using subscale III of the United Parkinson’s disease rating scale (UPDRS-III). After confirming the normality of data distribution, we performed one-way ANOVA with a Tukey’s post hoc test. Results: Compared with the healthy individuals, there was no statistical significance in forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC) in the H&Y 1 group and H&Y 2 group (p > 0.05) but reduced peak expiratory flow (PEF) in the H&Y 2 group (p = 0.002). Reduced FVC, FEV1, and PEF was seen in the H&Y 3 group (p = 0.002, p = 0.001, and p = 0.0001, respectively). Reduced FVC, FEV1, PEF, and FEF25–75% was seen in the H&Y 4 group (p = 0.001, p = 0.0001, p = 0.0001, and p = 0.025, respectively). The correlation analysis revealed that there was a significant negative correlation between FVC and UPDRS-III scores (r = −0.248, p = 0.046), disease duration (r = −0.276, p = 0.026), H&Y scale (r = −0.415, p = 0.001). FEV1 was negatively correlated with UPDRS-III scores (r = −0.277, p = 0.025), disease duration (r = −0.291, p = 0.019), H&Y scale (r = −0.434, p = 0.0001). FEF25–75% was negatively correlated with disease duration (r = −0.247, p = 0.047), H&Y scale (r = −0.278, p = 0.025). Conclusion: Our findings revealed that respiratory impairment is present in moderate and advanced PD patients, and directly related to the severity of the disease. It is important to conduct respiratory function test in the clinical practice.

Background:Exploring the brain reorganization patterns associated with language recovery would promote the treatment of global aphasia. While functional near-infrared spectroscopy (fNIRS) has been widely used in the study of speech and language impairment, its application in the field of global aphasia is still limited.Aims:We aimed to identify cortical activation patterns of patients with global aphasia during naming and repetition tasks.Methods and procedures:We recruited patients with post-stroke aphasia from the Department of Rehabilitation Medicine at Huashan Hospital. These individuals were diagnosed with global aphasia without cognitive impairments, as assessed by speech-language pathology evaluations. Age- and sex-matched healthy controls were recruited from the greater Shanghai area. During fNIRS measurement, patients and healthy controls completed the picture-naming and phrase repetition task. Cortical activation patterns on each of these language tasks were then compared between groups.Outcomes and results:A total of nine patients with global aphasia and 14 healthy controls were included in this study. Compared with the healthy subjects, patients with global aphasia showed increased activation in the left Broca's area, middle temporal gyrus (MTG), superior temporal gyrus (STG), and pre-motor and supplementary motor cortex (SMA) (p < 0.05) in the picture-naming task. Furthermore, the latency of the oxyhemoglobin (HbO) concentration in the left supramarginal gyrus (SMG) region had a strong negative correlation with their score of the naming task (p < 0.01). In the phrase repetition task, decreased activation was detected in the left SMA and SMG (p < 0.05) of patients relative to controls.Conclusion:The left SMG plays a critical role in the language function of patients with global aphasia, especially in their abilities to name and repeat. fNIRS is a promising approach to revealing the changes in brain activities in patients with aphasia, and we believe it will contribute to a deeper understanding of the neurological mechanisms and the establishment of a novel treatment approach for global aphasia.

Transcranial magnetic stimulation (TMS) modulation over the cerebellum, primary motor cortex, and supplementary motor cortex individually can improve the balance function of patients with stroke. However, whether their combination could have a better balance modulation effect is uncertain. Therefore, we hypothesized that performing TMS over a combination of these targets can regulate the balance function of patients with stroke. We compared the effects of one-session TMS on eye-open and eye-closed balance conditions in patients with stroke, using different target pairs of unilateral cerebellar (CB-single), cerebellar-primary motor cortex (CB-M1), and cerebellar-supplementary motor area (CB-SMA) targets. A total of 31 patients with stroke were enrolled and randomly divided into three groups to receive single sessions of intermittent theta burst stimulation each. Functional near-infrared spectrum data on resting and standing task states (eye-open and eye-closed) and center of pressure parameters (eye-open and eye-closed) were collected before and after the intervention. Compared with the results in the CB-single group, five intergroup differences in the changes in the center of pressure parameters in the CB-M1 group and two significant differences in the CB-SMA group were observed after one session of intermittent theta burst stimulation. In the CB-SMA group, 12 out of the 14 parameters improved significantly in the EC condition after the intervention. Meanwhile, the functional near-infrared spectrum results showed that the CB-SMA group exhibited a significant inhibitory pattern in the resting-state functional connectivity, which was not observed in the other two groups. In conclusion, we believe that paired targeting of the CB-SMA can reshape the brain network and improve the balance function of patients with stroke.

目的:观察对比外周磁刺激(peripheral magnetic stimulation,PMS)和中枢磁刺激对脑卒中后中重度上肢运动功能障碍的影响.方法:共42例符合纳入标准的脑卒中患者参加试验,将所有受试者随机分为对照组(14例)、PMS组(13例)和中枢组(15例).对照组接受常规康复治疗,PMS组在常规康复治疗的基础上接受患侧上肢Erb点的磁刺激干预,中枢组在常规康复治疗的基础上接受患侧初级运动皮层间歇性Theta节律性刺激(iTBS).每天1次干预,每周5天,共2周.在干预前、干预结束后对受试者进行上肢Fugl-Meyer评分(UL-FMA)、改良Barthel指数(BI)、改良Ashworth量表(MAS)、简易智力状态检查量表(MMSE)的评估和双侧皮质静息运动阈值(RMT)测定.结果:42例患者均完成了 10天的干预,未出现任何不良反应.磁刺激干预对脑卒中患者UL-FMA和BI的改善效果优于对照组,中枢组与对照组之间存在显著差异(P＜0.05).MAS和MMSE评分在干预前后的组间和组内比较均不存在显著性差异.多数患者患侧不能诱发MEP,能诱发MEP的患者其患侧RMT远高于健侧,组间RMT在干预前、干预后都不存在显著变化(P＞0.05).结论:与常规治疗相比,磁刺激能够促进脑卒中后中重度上肢运动功能障碍患者上肢功能的恢复和日常生活活动能力的提高,中枢磁刺激效果优于外周磁刺激.

Objective: This study examined the activation difference of muscles innervated by cervical cord 5-6 (C5-C6) and cervical cord 8- thoracic cord 1 (C8-T1) in upper limb flexion synergy after stroke.Methods: Surface electromyography (sEMG) signals were collected during elbow flexion in stroke patients and healthy controls. The study compared normalized activation of two pairs of muscles that could cause similar joint movement but which dominated different spinal cord segments (clavicular part of the pectoralis major, PC vs. Sternocostal part of the pectoralis major, PS; Flexor carpi radialis, FCR vs. Flexor carpi ulnaris, FCU). In each muscle pair, one muscle was innervated by the same spinal cord segment (C5-C6), dominating the elbow flexion and the other was not. The comparison of the activation of the same muscle between patients and healthy controls was undertaken after standardization based on the activation of the biceps brachii in elbow flexion.Results: There was no difference between the PC and PS's normalized activation in healthy controls while the PC's normalized activation was higher than PS in stroke patients during elbow flexion. Similarly, there was no significant difference in normalized activation between FCR and FCU in healthy controls, and the same is true for stroke patients. However, the standardized activation of both FCR and FCU in stroke patients was significantly lower than that in healthy controls.Conclusion: After stroke, the activation of the distal muscles of the upper limb decreased significantly regardless of the difference of spinal cord segments; while the activation of the proximal muscles innervated by the same spinal cord segment (C5-C6) dominating the elbow flexion showed higher activation during flexion synergy. The difference in muscle activation based on spinal cord segments may be the reason for the stereotyped joint movement of upper limb flexion synergy.

Background : The present study was designed to investigate the effects of neuromuscular electrical stimulation (NMES) and peripheral magnetic stimulation (PMS) applied to the wrist extensor muscle on the cortical activity of healthy adults by using fNIRS. Methods : Fifteen healthy adult subjects (7 males, mean age: 27.13 ± 4.52 years) all received two different conditions of peripheral muscle stimulation in random order: (1) NMES and (2) PMS. The sessions were separated by at least 48 h as a washout period. During muscle stimulation, the motor evoked potential (MEP) of the left primary motor cortex (M1) was measured by transcranial magnetic stimulation (TMS) and the concentration of oxygenated (HbO) and deoxygenated (HbR) hemoglobin detected by fNIRS were used to evaluate the excitability and the activity of the cortex. Results : After the stimulation of the wrist extensor, the MEP amplitude in the left M1 area did not change in both conditions, and there was no difference between NMES and PMS condition. NMES reduced HbO values of several channels in the Prefrontal cortex (PFC), Somatosensory motor cortex (SMC) and Occipital cortex (OC), and HbR valus of several channels in the PFC and SMC. During the PMS stimulation period, the HbO value of all brain areas did not change significantly, while the HbR value of the SMC area decreased. The HbO and HbR value of the channels in the SMC did not differ between NMES and PMS. Inter-region of interest and inter-channel analysis between NMES and PMS showed no difference in functional connectivity. Conclusions : In the case of wrist extensor muscle stimulation, both NMES and PMS can induce cortical activation. PMS targeted to increases the activity of the contralateral SMC, while NMES increased contralateral SMC activity and negatively activated the PFC and OC.

The effect of stem cell transplantation in the treatment of neural lesions is so far not satisfactory. Magnetic stimulation is a feasible exogenous interference to improve transplantation outcome. However, the effect of magnetic stimulation on the differentiation of induced pluripotent stem cells (iPSCs) into neuron has not been studied. In this experiment, an in vitro neuron differentiation system from human iPSCs were established and confirmed. Three magnetic stimuli (high frequency [HF], low frequency [LF], intermittent theta-burst stimulation [iTBS]) were applied twice a day during the differentiation process. Immunofluorescence and quantitative polymerase chain reaction (Q-PCR) were performed to analyze the effect of magnetic stimulation. Neural stem cells were obtained on day 12, manifested as floating neurospheres expressing neural precursor markers. All groups can differentiate into neurons while glial cell markers were not detected. Both Immunofluorescence and PCR results showed LF and iTBS increased the transcription and expression of neuronal nuclei (NeuN). HF significantly increased vesicular glutamate transporters2 transcription while iTBS promoted transcription of both synaptophysin and postsynaptic density protein 95. These results indicate that LF and iTBS can promote the generation of mature neurons from human iPSCs; HF may promote differentiate into glutamatergic neurons while iTBS may promote synapse formation during the differentiation.

An enriched environment (EE) has been demonstrated to improve functional recovery in animal models of ischaemic stroke through enhancing vascular endothelial growth factor- (VEGF-) mediated neuroprotection accompanied by angiogenesis in the ischaemic hemisphere. Whether EEs also promote VEGF-mediated neuroprotection and angiogenesis in the contralateral hemisphere remains unclear. Here, we explored the effect of EEs on VEGF expression and angiogenesis within the contralateral cerebral cortex in a rat middle cerebral artery occlusion/reperfusion (MCAO/r) model. We assessed the expression levels of platelet endothelial cell adhesion molecule-1 (CD31), VEGF, and endothelial nitric oxide synthase (eNOS) in the whole contralateral cerebral cortex using Western blotting assay but did not find an increase in the expression of CD31, VEGF, or eNOS in MCAO/r rats housed in EEs, which suggested that EEs did not enhance the overall expression of VEGF and eNOS or angiogenesis in the entire contralateral cortex. We further analysed the local effect of EEs by immunohistochemistry and found that in and around the bilateral cingulum in MCAO/r rats housed in EEs, haematopoietic progenitor cell antigen- (CD34-) positive endothelial progenitor cells were significantly increased compared with those of rats housed in standard cages (SCs). Further experiments showed that EEs increased neuronal VEGF expression surrounding the cingulum in MCAO/r rats and robustly upregulated eNOS expression. These results revealed that EEs enhanced angiogenesis, VEGF expression, and activation of the VEGF-eNOS pathway in and/or around the cingulum in MCAO/r rats, which were involved in the functional recovery of MCAO/r rats.

OBJECTIVE:The study aims to investigate the after-effect of three sessions of intermittent theta-burst stimulation (iTBS) on motor cortical excitability. The iTBS was induced over the primary motor cortex (M1) at different time intervals.METHODS:The study has a crossover design. Sixteen participants were assigned to three groups and received different accelerated iTBS (aiTBS) protocols during each visit: (1) three continuous sessions with no interval (iTBS18000); (2) three iTBS sessions with 10-min intervals (iTBS600 × 3∗10); and (3) three iTBS sessions with 30-min intervals (iTBS600 × 3∗30). As washout period, each visit is separated by at least 7 days. We measured the motor cortical excitability changes and intracortical inhibition.RESULTS:A dose of 1,800 pulses of aiTBS per day is tolerable. The iTBS1800 led to a reduced cortical excitability; whereas iTBS600 × 3∗10 and iTBS600 × 3∗30 enhanced cortical excitability to a differential extent. After a total dose of 1,800 pulses, iTBS600 × 3∗30 exhibited the longer effect and highest percentage of individuals with enhanced cortical excitability.CONCLUSION:The results suggest that aiTBS protocols at different time intervals result in different motor cortical excitability after-effects.

Objective: To study differential post-stroke changes of excitability of spinal motor neurons innervating a group of antagonist muscles of ankle and their effects on foot inversion. Methods: F waves in tibialis anterior (TA) and peroneus muscles (PN) were recorded. The condition of spasticity and foot inversion in stroke patients were also evaluated. The differences of F wave parameters between patients and healthy controls (HC), as well as TA and PN, were investigated. Results: There were natural differences in the persistence of the F waves (Fp) and F/M amplitude ratio (F/M) between TA and PN in HC. Stroke patients showed significantly higher F/M in TA and PN, while there was no difference in Fp comparing to HC. The natural differences in F wave parameters between TA and PN were differentially retained after stroke. The natural difference of the two muscles in Fp remained unchanged and the F/M difference disappeared in those without spasticity or foot inversion, while the Fp difference disappeared and the F/M difference remained in those with spasticity or foot inversion. Conclusion: Based on the natural difference of the number and size of spinal motor neurons innervating TA and PN, their excitability may change differently according to the severity of the stroke, which may be the reason of foot inversion.

Brain has limited capacity for spontaneous recovery of lost function after stroke. Exposure to enriched environment (EE) can facilitate functional recovery, but mechanisms underlying this effect are poorly understood. Here, we used a middle cerebral artery occlusion (MCAO) model to investigate the impact of EE on angiogenesis in the post-ischemic brain in adult male Sprague Dawley rats, and examined whether blood-borne factors may contribute. Compared with standard cage (SC), exposure to EE was associated with greater improvement in neurological function, higher peri-infarct vascular density, and higher chronic post-ischemic cerebral blood flow assessed by laser speckle imaging. The effect persisted for at least 28 days. EE also enhanced the expression of hepatocyte growth factor in the peri-ischemic cortex when measured 15 days after MCAO. Interestingly, serum from rats exposed to EE after MCAO showed elevated levels of hepatocyte growth factor, and plasma or serum from rats exposed to EE after MCAO enhanced the survival and proliferation of cultured endothelial cells, in vitro, when compared with control plasma or serum from SC group after MCAO. Together, our data suggest that exposure to EE promotes angiogenesis in the ischemic brain that may in part be mediated by blood-borne factors.

BACKGROUND:Spasticity commonly occurs in hemiplegic patients with stroke, and clinical experience indicates that upper limb spasticity is more apparent when patients are standing than when they are lying down. Few reports have investigated how positional changes impact the spasticity of the upper limb and trigger a combined movement called the "hemiplegic posture". OBJECTIVE:The objective of this study was to explore the influence of different body positions on the spasticity of the upper extremity. METHODS:Eighty-four poststroke patients with upper limb spasticity were recruited for this study. We measured the spasticity of hemiplegic upper limbs involving elbow flexors, wrist flexors and digitorum flexors using the Modified Ashworth Scale (MAS), Modified Tardieu Scale (MTS) and Triple Spasticity Scale (TSS) in three positions, i.e., supine, sitting and standing. The results were obtained by comparing one position with another for each muscle. RESULTS:All the MAS, MTS and TSS scores of all the muscles of the upper limb were significantly lower in the supine position than in the other positions (all P < 0.05), and the MTS and TSS scores were statistically higher while standing than while sitting (P < 0.05). CONCLUSION:High modulation of spasticity in the upper limbs measured using the MAS, MTS and TSS when transitioning to the standing position from either the supine or sitting position demonstrated that posture plays a role in modulating the spasticity of the hemiplegic upper limb in poststroke patients.

Olfactory ensheathing cells (OECs) has been widely studied in stroke. The present study was aimed at examining the role of wheel-running treatment (WR) on rat olfactory ensheathing cells (rOECs) functions. Thirty adult male Sprague Dawley rats were randomly divided into two groups: the middle cerebral artery occlusion (MCAO) group and WR + MCAO group. Motor behavior was assessed through the footfault test, and the results showed that WR training markedly improved the neurobehavioral outcome. The glucose metabolic status of the brain was assessed with the micro-PET. This training significantly enhanced the glucose uptake of olfactory bulb in the early stage of WR treatment. The function of rOECs mitochondrial was significantly enhanced after 10 days of treatment. Body weight of rats in both of the two groups decreased and then increased slowly following the days. But the growth trend of the WR + MCAO group was no significantly higher than that of the WR group. This training significantly enhanced the glucose uptake, improved the proliferation of rOECs and increased the expression level of cytochrome C (Cyt-c). The mechanism may be associated with the facilitation of mitochondrial function of rOECs cells. Including facilitation of mitochondrial fusion, fission, and accompanying increased quantities of mitochondria. Obtained results indicate that early WR treatment may exert enhanced function on rOECs in vivo and increased mitochondrial amounts, and improved the expression level of Cyt-c after ischemic stroke.

Objective: In this study, we explored whether laminar shear stress (LS) had an effect on the apoptosis of rat brain microvascular endothelial cells (rBMECs) during the course of cerebral ischaemia-reperfusion injury (CIRI). Methods: First, blood flow changes in CIRI were studied by Laser Doppler flowmetry in vivo. Then, the oxygen/glucose deprivation (OGD) model was adopted to cause ischaemia in rBMECs for 6 hours in vitro. Flow intervention without nutrition and an LS force magnitude of 0.8 +/- 0.05 dynes/cm(2) were delivered for the last 2 hours to simulate the single factor effect of LS on reperfusion. Results: We found that cell apoptosis was significantly relieved under haemodynamic intervention with Annexin V-FITC/PI and Hoechst 33258 analysis. In terms of molecular mechanisms, it is possible that LS could activate the cytomembrane surface receptor Tie-2 and cause downstream inhibition of the caspase-3 apoptosis pathway. Conclusion: LS should be a protective factor for CIRI.

Hypoperfusion is one of the common causes of ischemic stroke. In this study, decreased blood perfusion and neurological damage were confirmed in ischemic rats. Further, the effect of different perfusion was researched in vivo. We found that hypoperfusion promoted the apoptosis of rats brain microvascular endothelial cells, and the more serious of hypoperfusion, the more obvious of apoptosis. At the same time, this process was related to Tie-2 receptor on cell membranes and Caspase-3 apoptotic pathways. Hemodynamics was one factors affecting the cerebral infarction.

Exercise preconditioning is a simple and effective way to prevent ischemia. This paper further provided the mechanism in hemodynamic aspects at the cellular level. To study the anti-apoptotic effects of fluid mechanics preconditioning, Cultured rats brain microvascular endothelial cells were given fluid intervention in a parallel plate flow chamber before oxygen glucose deprivation. It showed that fluid mechanics preconditioning could inhibit the apoptosis of endothelial cells, and this process might be mediated by the shear stress activation of Tie-2 on cells membrane surface and Bcl-2 on the mitochondria surface.