Locomotion, a fundamental motor function encompassing various forms such as swimming, walking, running, and flying, is essential for animal survival and adaptation. The mesencephalic locomotor region (MLR), located at the midbrain-hindbrain junction, is a conserved brain area critical for controlling locomotion. This review highlights recent advances in understanding the MLR’s structure and function across species, from lampreys to mammals and birds, with a particular focus on insights gained from optogenetic studies in mammals. The goal is to uncover universal strategies for MLR-mediated locomotor control. Electrical stimulation of the MLR in species such as lampreys, salamanders, cats, and mice initiates locomotion and modulates speed and patterns. For example, in lampreys, MLR stimulation induces swimming, with increased intensity or frequency enhancing propulsive force. Similarly, in salamanders, graded stimulation transitions locomotor outputs from walking to swimming. Histochemical studies reveal that effective MLR stimulation sites colocalize with cholinergic neurons, suggesting a conserved neurochemical basis for locomotion control. In mammals, the MLR comprises two key nuclei: the cuneiform nucleus (CnF) and the pedunculopontine nucleus (PPN). Both nuclei contain glutamatergic and GABAergic neurons, with the PPN additionally housing cholinergic neurons. Optogenetic studies in mice by selectively activating glutamatergic neurons have demonstrated that the CnF and PPN play distinct roles in motor control: the CnF drives rapid escape behaviors, while the PPN regulates slower, exploratory movements. This functional specialization within the MLR allows animals to adapt their locomotion patterns and speed in response to environmental demands and behavioral objectives. Similar to findings in lampreys, the CnF and PPN in mice transmit motor commands to spinal effector circuits by modulating the activity of brainstem reticular formation neurons. However, they achieve this through distinct reticulospinal pathways, enabling the generation of specific behaviors. Further insights from monosynaptic rabies viral tracing reveal that the CnF and PPN integrate inputs from diverse brain regions to produce context-appropriate behaviors. For instance, glutamatergic neurons in the PPN receive signals from other midbrain structures, the basal ganglia, and medullary nuclei, whereas glutamatergic neurons in the CnF rarely receive inputs from the basal ganglia but instead are strongly influenced by the periaqueductal grey and inferior colliculus within the midbrain. These differential connectivity patterns underscore the specialized roles of the CnF and PPN in motor control, highlighting their unique contributions to coordinating locomotion. Birds exhibit exceptional flight capabilities, yet the avian MLR remains poorly understood. Comparative studies suggest that the pedunculopontine tegmental nucleus (PPTg) in birds is homologous to the mammalian PPN, which contains cholinergic neurons, while the intercollicular nucleus (ICo) or nucleus isthmi pars magnocellularis (ImC) may correspond to the CnF. These findings provide important clues for identifying the avian MLR and elucidating its role in flight control. However, functional validation through targeted experiments is urgently needed to confirm these hypotheses. Optogenetics and other advanced techniques in mice have greatly advanced MLR research, enabling precise manipulation of specific neuronal populations. Future studies should extend these methods to other species, particularly birds, to explore unique locomotor adaptations. Comparative analyses of MLR structure and function across species will deepen our understanding of the conserved and evolved features of motor control, revealing fundamental principles of locomotion regulation throughout evolution. By integrating findings from diverse species, we can uncover how the MLR has been adapted to meet the locomotor demands of different environments, from aquatic to aerial habitats.

Objective To construct and validate a risk prediction model for in-hospital death af-ter successful resuscitation in patients with cardiac arrest.Methods A retrospective study was con-ducted on 295 patients with cardiac arrest who successfully restored spontaneous circulation after car-diopulmonary resuscitation and were further treated in hospital.The patients were divided into training and validation sets using K-fold cross-validation and then grouped and compared based on whether in-hospital death occurred.A binary Logistic regression analysis was used to screen risk prediction fac-tors,and a nomogram prediction model was constructed.The model performance was evaluated and validated in the training and validation sets,respectively.Results The results of the multivariate Logistic regression analysis showed that hospitalization duration(OR=1.180;95％CI,1.080 to 1.280;P＜0.001),norepinephrine dose(OR=0.980;95％CI,0.970 to 0.990;P=0.002),ini-tial respiratory rate after resuscitation(OR=1.090;95％CI,1.030 to 1.150;P=0.004),and sinus rhythm recovery after resuscitation(OR=4.280;95％CI,1.670 to 10.980;P=0.003)were inde-pendent influencing factors for in-hospital death.A nomogram model was constructed based on these in-dependent influencing factors,and it was verified that the model had good discrimination,calibration,applicability,and rationality.Conclusion The influencing factors for in-hospital death after successful resuscitation in patients with cardiac arrest include hospitalization duration,norepinephrine dose,initial respiratory rate after resuscitation,and sinus rhythm recovery after resuscitation.The nomo-gram model constructed based on these factors can provide a reference for clinical decision-making.

Objective To explore the role of sevoflurane(SEV)in sepsis-induced acute lung injury(ALI)and observe its impact on the Wnt/β-catenin signaling pathway.Methods Forty C57 mice were randomly divided into 4 groups(n=10 each):Sham,CLP,SEV,and SEV+XAV(β-catenin inhibitor).A sepsis model was established via cecal ligation and puncture.Lung injury was evaluated using HE staining,lung wet/dry weight ratio,and TUNEL staining.Levels of inflammatory factors(TNF-α,IL-1β,IL-6)were detected by ELISA.Oxidative stress indices(SOD,MDA,ROS)were measured by colorimetry and flow cytometry.Hindlimb blood perfusion and oxygenation were assessed with laser speckle flowmetry.Expressions of key Wnt pathway molecules and down-stream target genes(c-Myc,Cyclin D1)were detected by RT-qPCR and Western blot.Co-localization of β-catenin and SP-C(a marker of type Ⅱ alveolar epithelial cells)in lung tissues was determined by immunofluorescence staining.Results Compared with the Sham group,the CLP group exhibited significant increases in sepsis severity,lung pathological damage including alveolar structure destruction,inflammatory infiltration,and apoptosis,elevation in pro-inflammatory cytokine levels,and significant decrease in SOD and increase in MDA and ROS.Additionally,lower limb blood flow and oxygenation levels were significantly reduced,while the expression of β-catenin and its downstream target genes,as well as the co-localization signal and fluorescence intensity of β-catenin with SP-C,were significantly downregulated(all P<0.05).Compared with the CLP group,the SEV group showed significant improvements in all these indicators.However,compared with the SEV group,the SEV+XAV group demon-strated a reversed protective effect,with all indicators approaching the levels observed in the CLP group(all P<0.05).Conclusion Sevoflurane alleviates sepsis-induced ALI by activating Wnt/β-catenin signaling pathway,exerting anti-inflammatory and antioxidant effects,and enhancing the expression and localization of β-catenin in type Ⅱ alveolar epithelial cells.

Objective:To quantitatively evaluate the effects of left bundle branch block（LBBB）on left ventricular structure，function and myocardial perfusion using left ventricular pressure-strain loop and single photon emission computed tomography（SPECT），and to investigate the relationship between myocardial work，myocardial perfusion and pathological changes of left ventricular remodeling in left bundle branch block induced cardiomyopathy（LBBB-CM）.Methods:Fourteen male beagle dogs were selected，and the main trunk of the left bundle branch was ablated to create an LBBB dog model. Electrocardiogram（ECG），transesophageal echocardiography and arterial blood pressure data of LBBB dogs were collected before and 12 months after the ablation of left bundle branch trunk. Global and segmental myocardial work parameters were obtained by left ventricular pressure-strain loop. The differences of above parameters between baseline and 12 months after the ablation of left bundle branch were compared. SPECT was performed in LBBB dogs 12 months after the creation of LBBB. The hearts were harvested for anatomy observation and histopathological analysis in LBBB dogs and another 7 male beagle dogs（normal control group）matched by age and weight. The correlation between myocardial perfusion（percentage of regional tracer uptake）and myocardial work parameters，myocardial fibrosis in LBBB dogs were analyzed.Results:Compared with baseline，the left ventricular end-diastolic volume of 12 months after the ablation increased［（20.78 ± 5.32）ml vs（26.71 ± 7.94）ml， P = 0.003］，left ventricular ejection fraction decreased［（59.17 ± 5.67）% vs（47.69 ± 5.45）%， P<0.001］；left ventricular global/segmental longitudinal strain，global/segmental constructive work and global/segmental work efficiency decreased（all P<0.05），left ventricular global/segmental wasted work increased（all P<0.001）. Heterogenous perfusion defect was observed in LBBB dogs by SPECT，compared with lateral wall segments，the percentage of regional tracer uptake of septum was decreased（all P<0.05）. Gross anatomical and myocardial pathological changes were manifested as cardiomegaly，flaky or focal grayish thickening of endocardium，cardiomyocyte degeneration and fibrosis. Compared with normal control group，the collagen fiber volume fraction（CVF）in all segmental endocardium and partial segmental myocardium of LBBB dogs were significantly increased（all P<0.05）. Percentage of regional tracer uptake was positively correlated with segmental myocardial work（SMW）and segmental myocardial efficiency（SWE）（ r s = 0.49，0.31；both P<0.001），and negatively correlated with CVF and segmental wasted work（SWW）（ r s = -0.51，-0.49；both P<0.001）. Conclusions:Isolated LBBB is not benign，which can result in left ventricular remodeling，decreased cardiac constructive function，abnormal myocardial perfusion，endocardial fibrosis and myocardial fibrosis.The parameters of myocardial work assecsed by echocardiograpgy and myocardial perfusion，as non-invasive examination，can to some extent reflect the degree of left ventricular remodeling in LBBB-CM.

Objective To explore the role of sevoflurane(SEV)in sepsis-induced acute lung injury(ALI)and observe its impact on the Wnt/β-catenin signaling pathway.Methods Forty C57 mice were randomly divided into 4 groups(n=10 each):Sham,CLP,SEV,and SEV+XAV(β-catenin inhibitor).A sepsis model was established via cecal ligation and puncture.Lung injury was evaluated using HE staining,lung wet/dry weight ratio,and TUNEL staining.Levels of inflammatory factors(TNF-α,IL-1β,IL-6)were detected by ELISA.Oxidative stress indices(SOD,MDA,ROS)were measured by colorimetry and flow cytometry.Hindlimb blood perfusion and oxygenation were assessed with laser speckle flowmetry.Expressions of key Wnt pathway molecules and down-stream target genes(c-Myc,Cyclin D1)were detected by RT-qPCR and Western blot.Co-localization of β-catenin and SP-C(a marker of type Ⅱ alveolar epithelial cells)in lung tissues was determined by immunofluorescence staining.Results Compared with the Sham group,the CLP group exhibited significant increases in sepsis severity,lung pathological damage including alveolar structure destruction,inflammatory infiltration,and apoptosis,elevation in pro-inflammatory cytokine levels,and significant decrease in SOD and increase in MDA and ROS.Additionally,lower limb blood flow and oxygenation levels were significantly reduced,while the expression of β-catenin and its downstream target genes,as well as the co-localization signal and fluorescence intensity of β-catenin with SP-C,were significantly downregulated(all P<0.05).Compared with the CLP group,the SEV group showed significant improvements in all these indicators.However,compared with the SEV group,the SEV+XAV group demon-strated a reversed protective effect,with all indicators approaching the levels observed in the CLP group(all P<0.05).Conclusion Sevoflurane alleviates sepsis-induced ALI by activating Wnt/β-catenin signaling pathway,exerting anti-inflammatory and antioxidant effects,and enhancing the expression and localization of β-catenin in type Ⅱ alveolar epithelial cells.

Objective:To quantitatively evaluate the effects of left bundle branch block（LBBB）on left ventricular structure，function and myocardial perfusion using left ventricular pressure-strain loop and single photon emission computed tomography（SPECT），and to investigate the relationship between myocardial work，myocardial perfusion and pathological changes of left ventricular remodeling in left bundle branch block induced cardiomyopathy（LBBB-CM）.Methods:Fourteen male beagle dogs were selected，and the main trunk of the left bundle branch was ablated to create an LBBB dog model. Electrocardiogram（ECG），transesophageal echocardiography and arterial blood pressure data of LBBB dogs were collected before and 12 months after the ablation of left bundle branch trunk. Global and segmental myocardial work parameters were obtained by left ventricular pressure-strain loop. The differences of above parameters between baseline and 12 months after the ablation of left bundle branch were compared. SPECT was performed in LBBB dogs 12 months after the creation of LBBB. The hearts were harvested for anatomy observation and histopathological analysis in LBBB dogs and another 7 male beagle dogs（normal control group）matched by age and weight. The correlation between myocardial perfusion（percentage of regional tracer uptake）and myocardial work parameters，myocardial fibrosis in LBBB dogs were analyzed.Results:Compared with baseline，the left ventricular end-diastolic volume of 12 months after the ablation increased［（20.78 ± 5.32）ml vs（26.71 ± 7.94）ml， P = 0.003］，left ventricular ejection fraction decreased［（59.17 ± 5.67）% vs（47.69 ± 5.45）%， P<0.001］；left ventricular global/segmental longitudinal strain，global/segmental constructive work and global/segmental work efficiency decreased（all P<0.05），left ventricular global/segmental wasted work increased（all P<0.001）. Heterogenous perfusion defect was observed in LBBB dogs by SPECT，compared with lateral wall segments，the percentage of regional tracer uptake of septum was decreased（all P<0.05）. Gross anatomical and myocardial pathological changes were manifested as cardiomegaly，flaky or focal grayish thickening of endocardium，cardiomyocyte degeneration and fibrosis. Compared with normal control group，the collagen fiber volume fraction（CVF）in all segmental endocardium and partial segmental myocardium of LBBB dogs were significantly increased（all P<0.05）. Percentage of regional tracer uptake was positively correlated with segmental myocardial work（SMW）and segmental myocardial efficiency（SWE）（ r s = 0.49，0.31；both P<0.001），and negatively correlated with CVF and segmental wasted work（SWW）（ r s = -0.51，-0.49；both P<0.001）. Conclusions:Isolated LBBB is not benign，which can result in left ventricular remodeling，decreased cardiac constructive function，abnormal myocardial perfusion，endocardial fibrosis and myocardial fibrosis.The parameters of myocardial work assecsed by echocardiograpgy and myocardial perfusion，as non-invasive examination，can to some extent reflect the degree of left ventricular remodeling in LBBB-CM.

Objective:To explore therapeutic effect of cardiac rehabilitation based on traditional exercise on heart failure(HF).Methods:We searched databases including CNKI,Wanfang,VIP,Pubmed and Cochrane library for literature about application of cardiac rehabilitation exercise based on traditional exercises in HF patients before Mar 2023.Literature were screened according to inclusion and exclusion criteria,while article quality assessment and da-ta extraction were performed,and RevMan 5.3 software was used to perform Meta analysis.Results:Meta analysis indicated that compared with control group,there were significant increase in LVEF[MD=4.51,95％CI(1.70,7.33),P=0.002]and 6 min walking distance[6MWD,MD=51.90,95％CI(39.24,64.57),P=0.001],and sig-nificant reductions in left ventricular end-systolic diameter[MD=-1.64,95％CI(-3.18,-0.11),P=0.040],left ventricular end-diastolic diameter[MD=-2.49,95％C1(-3.28,-1.69),P=0.001],score of Minnesota living with heart failure questionnaire[MD=-6.89,95％CI(-8.64,-5.33),P=0.001]and level of N-ter-minal pro-brain natriuretic peptide[MD=-151.46,95％CI(-208.21,-94.70),P=0.001]in observation group.Conclusion:Cardiac rehabilitation based on traditional exercise can significantly improve heart function,in-crease 6 min walking distance and improve quality of life in patients with heart failure.

Innate immunity is the first line of defense against viral infection.Hepatitis E virus(HEV)infection usually cau-ses acute self-limiting diseases in immunocompetent patients,but results in chronic infection in immunocompromised patients or pregnant people.After HEV infects host cells,pattern recognition receptors(PRRs)recognize the viral genome,thus indu-cing rapid activation of multiple antiviral signal pathways in the host immune system,and the expression of interferons(IFNs)and interferon stimulated genes(ISGs),and consequently inhibiting viral replication.To escape host antiviral responses,HEV encoded proteins regulate host antiviral signal pathways and subsequently inhibit antiviral responses,such as those involving cytokines or chemokines.The regulation of host signal pathways by HEV infection and the escape of HEV from host innate im-munity are reviewed herein.

A 5-year-old girl was admitted due to one episode of melena and one episode of hematemesis.Upon admission,gastroscopy revealed esophageal and gastric varices.Abdominal CT scan,MRI,and color Doppler ultrasound suggested cirrhosis,intrahepatic bile duct dilation,and bilateral kidney enlargement.Genetic testing identified compound heterozygous mutations in the PKHD1 gene:c.2264C>T(p.Pro755Leu)and c.1886T>C(p.Val629Ala).The c.2264C>T(p.Pro755Leu)mutation is a known pathogenic variant with previous reports,while c.1886T>C(p.Val629Ala)is a novel mutation predicted to have pathogenic potential according to Mutation Taster and PolyPhen2.The child was diagnosed with autosomal recessive polycystic kidney disease.In children presenting with gastrointestinal bleeding without obvious causes,particularly those with liver or kidney disease,consideration should be given to the possibility of autosomal recessive polycystic kidney disease,and genetic testing should be conducted for definitive diagnosis when necessary.

Objective To explore the effect of emodin on inflammatory response in preeclampsia(PE)rats by regulating the AMP activated protein kinase(AMPK)/thioredoxin-interacting protein(TXNIP)/NOD-like receptor pyrin domain-containing protein 3(NLRP3)signaling pathway.Methods PE rat model was established by subcutaneous injection of L-arginine methyl ester(100 mg·kg-1).Sixty female rats were randomly divided into control group,model group,emodin group(40 mg·kg-1 emodin),Compound B10 group(100 mg·kg-1 Compound B10),emodin+Compound B10 group(40 mg·kg-1 emodin+100 mg·kg-1 Compound B10),with 12 rats in each group.The control group and the model group were intraperitoneally injected with the same amount of 0.9％NaCl.The 24 h urine was collected,and the total urinary protein content was determined by Coomassie brilliant blue method.The protein levels of AMPK/TXNIP/NLRP3 signaling pathway were detected by Western blot.Results The total urinary protein levels of control group,model group,emodin group,Compound B10 group and emodin+Compound B10 group were(54.34±6.26),(136.37±15.43),(76.38±8.61),(215.39±25.14)and(110.93±13.92)g·L-1,respectively;urine volume were(10.59±0.92),(15.38±1.49),(11.51±1.13),(21.49±2.50)and(14.71±1.49)mL,respectively;AMPK protein levels were 0.63±0.06,1.57±0.18,0.81±0.09,2.34±0.23 and 1.38±0.15,respectively;TXNIP protein levels were 0.33±0.04,0.79±0.08,0.49±0.10,1.13±0.12 and 0.82±0.09,respectively;NLRP3 protein levels were 0.46±0.05,0.83±0.09,0.56±0.07,1.25±0.14 and 0.78±0.08,respectively.The above indexes:Model group was compared with control group,emodin group and Compound B10 group,emodin+Compound B10 group was compared with emodin group,the differences were statistically significant(all P＜0.05).Conclusion Emodin may alleviate inflammatory reaction in PE rats by inhibiting AMPK/TXNIP/NLRP3 signal axis,thereby improving placental injury.