ObjectiveTo evaluate pharmacological effects of Shengmai injection（SMI）on cerebral ischemia and study its neuroprotective mechanism. MethodsMale specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a sham group， a model group， a low-dose SMI group（3 mL·kg^-1）， a middle-dose SMI group（6 mL·kg^-1）， a high-dose SMI group（12 mL·kg^-1）， and a Ginaton group（4 mL·kg^-1）according to the random number table method， with 12 rats in each group. The rat model of cerebral ischemia-reperfusion（MCAO/R）was prepared via the suture method. The administration groups were intraperitoneally injected with corresponding concentrations of SMI or Ginaton injection after reperfusion， which was conducted for 3 consecutive days. The sham group and model group were administered the equivalent volume of physiological saline. The pharmacological effects of SMI on brain injury in MCAO/R rats were evaluated by neurological function scores， cerebral infarction area， hematoxylin-eosin （HE） staining， Nissl staining， terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） staining， and Western blot. The dominant link and key protein of SMI treating cerebral injury were explored using proteomic analysis. The related mechanisms of SMI were further validated using enzyme-linked immunosorbent assay （ELISA）， Western blot， and chloride ion fluorescence probe with oxygen-glucose deprivation/reoxygenation（OGD/R）-treated PC12 cells and MCAO/R rats. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly decreased density of Nissl bodies and neurons（P<0.01）. Compared with the model group， the SMI groups exhibited significantly decreased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly increased density of Nissl bodies and neurons （P<0.05）. The proteomic analysis results showed that oxidative stress and inflammatory response were important processes of SMI intervening in MCAO/R injury， and the chloride intracellular channel protein 1 （CLIC1） was one of key proteins in its action network. The levels of representative indicators of oxidative stress and inflammatory response in the MCAO/R rats of the SMI groups were significantly reduced， compared with those in the model group（P<0.05， P<0.01）， and the expression levels of CLIC1 and downstream NOD-like receptor protein 3 （NLRP3） decreased （P<0.01）. In addition， the experimental results based on the OGD/R PC12 cells showed that SMI significantly increased the cell survival rate（P<0.01） and significantly decreased the intracellular chloride ion concentration（P<0.05）. ConclusionSMI has neuroprotective effects. Oxidative stress and inflammatory response are key processes of SMI intervening in MCAO/R injury. The potential mechanism is closely related to the regulation of CLIC1.

BACKGROUND:Transcranial direct current stimulation(tDCS),as a non-invasive brain stimulation technique,can enhance human muscle strength or improve single-leg landing stability instantly,but no relevant research has demonstrated this yet. OBJECTIVE:To investigate the effect of tDCS on the stability of single-leg landings in human subjects. METHODS:Male undergraduate students from Wuhan Sports University were recruited as study participants.They were divided into two groups,A(n=6)and B(n=5),using a random number table.Group A underwent a sham stimulation session followed by a 3-day washout period,after which they received tDCS.Conversely,Group B received tDCS initially,followed by a 3-day washout period,and subsequently underwent the sham stimulation session.Following the respective stimulation sessions,an immediate single-leg landing test was administered to assess and collect biomechanical parameters.Data resulting from the tDCS intervention were aggregated and analyzed as the experimental group dataset,whereas data stemming from the sham stimulation were consolidated as the control group dataset. RESULTS AND CONCLUSION:Regarding core stability,the tDCS intervention showed a significant interaction with landing height on the maximal trunk flexion angle(P＜0.05).A paired comparison of the data showed a significant decrease in the maximum trunk flexion angle following true stimulation compared to sham stimulation at a 30-cm landing height.Additionally,the tDCS intervention had a significant main effect on the maximum trunk lateral bending angle and the mean trunk lateral bending angular velocity(P＜0.05).Following true stimulation,there was a significant decrease in the maximum trunk lateral bending angle and the mean trunk lateral bending angular velocity compared to sham stimulation.In terms of lower limb joint stability,the tDCS intervention had a significant main effect on the maximum dynamic ankle valgus angle(P＜0.05).This resulted in a significant decrease in the angle following true stimulation compared to sham stimulation.In addition,the tDCS intervention had a significant main effect on the peak muscle activation of the lateral head of the gastrocnemius lateralis(P＜0.05).This showed a significant increase after true stimulation compared to sham stimulation.An interaction between the tDCS intervention and landing height was observed for the peak muscle activation of the tibialis anterior(P＜0.05).Paired comparison analyses revealed a significant increase in muscle activation after true stimulation specifically at a 60-cm landing height.Regarding center of pressure stability,there were no significant interactions or main effects of the tDCS intervention on the mean lateral displacement,mean lateral displacement velocity,mean anterior-posterior displacement,or mean anterior-posterior displacement velocity at the center of pressure(P＞0.05).Furthermore,the tDCS intervention had no significant main effects on any of the center of pressure indicators(P＞0.05).In conclusion,tDCS can immediately improve core stability and lower limb joint stability during single-leg landing,making it an effective warm-up technique for improving single-leg landing stability and reducing the risk of lower limb injuries.

Objective To investigate the distribution and clinical characteristics of TCM syndromes in infertility patients with autoimmune thyroiditis(AIT).Methods By referring to the relevant literature on the distribution of TCM syndromes of AIT and infertility in women of childbearing age,the TCM Syndromes Survey of Infertility Patients with Autoimmune Thyroiditis was formulated.256 cases of infertility patients with AIT who underwent in vitro fertilization-embryo transfer(IVF-ET)at the Reproductive Center of The First Affiliated Hospital of University of Science and Technology of China from June 2019 to December 2020 were retrospectively analyzed.The data of basic information,TCM syndromes,basic thyroid-stimulating hormone(TSH),thyroid peroxidase antibody(TPO-Ab)and thyroglobulin antibody(TG-Ab)were collected.By means of frequency analysis and systematic cluster analysis,the distribution regularity of TCM syndromes in infertility patients with AIT were concluded.Results After analysis,the following 5 common syndrome elements were obtained,namely,qi deficiency,liver depression,spleen deficiency,kidney deficiency and blood stasis.In addition,it was concluded that this disease was more common in complex syndromes.Through systematic clustering analysis,main TCM syndromes of this disease were obtained,which were qi deficiency and liver depression syndrome(69 cases,26.9%),spleen and kidney deficiency syndrome(45 cases,17.6%),spleen qi deficiency syndrome(38 cases,14.8%),qi deficiency and blood stasis syndrome(36 cases,14.1%),kidney deficiency and liver depression syndrome(32 cases,12.5%)and other syndrome types(36 cases,14.1%).The basic TSH level was higher in patients with qi deficiency and liver depression syndrome,spleen qi deficiency syndrome,qi deficiency and blood stasis syndrome than other syndrome types,with statistical significance(P<0.05).There was no significant difference in TPO-Ab and TG-Ab titers among different syndromes(P>0.05).Conclusion TCM syndromes of infertility patients with AIT can be clustered into qi deficiency and liver depression syndrome,spleen and kidney deficiency syndrome,spleen qi deficiency syndrome,qi deficiency and blood stasis syndrome,kidney deficiency and liver depression syndrome and other syndrome.The main element of syndrome is qi deficiency,and the pathological sites involved spleen,kidney and liver.Stasis blood is a main pathological product.It is required to pay close attention to the thyroid function in AIT patients with qi deficiency.

Objective To investigate changes of muscle activation in the lower limbs during landing impact as running fatigue pro-gresses. Methods From November to December,2022,eleven male runners were recruited from Wuhan Sports University.They performed a steady-state run at 75%of their maximum heart rate and continued until Borg rating score≥17 or 90%of their maximum heart rate.Muscle activity data were collected using a Delsys wireless surface electromy-ography system,continuously recording the EMG of the quadriceps(vastus medialis,rectus femoris,vastus later-alis),hamstrings(biceps femoris,semitendinosus),gluteus maximus,lateral head of the gastrocnemius and tibia-lis anterior.The pre-activation,post-activation and co-activation characteristics of these lower limb muscles were analyzed. Results With fatigue accumulation during running,significant differences were observed in the pre-activation level of the tibialis anterior among different fatigue points(F=2.955,P=0.048),with the 100%fatigue point showing significantly higher pre-activation levels than the start(P=0.010);as well as post-activation levels of quadriceps(F=6.609,P=0.001),with higher levels at the 100%point compared to the start(P=0.011),33%(P=0.009)and 67%(P=0.043)fatigue points;co-activation ratios of ankle joint during the pre-activation phase(F=3.287,P=0.034),with a significantly higher co-activation ratio at the 100%fatigue point compared to the start(P=0.023). Conclusion As running fatigue accumulates,the central nervous system adjusts the activation levels of various lower limb muscles to modify impact posture,reducing the risk of injury from accumulated lower limb loads.

Objective:To explore the changes in the synergy mode of human lower limb muscles during the fatigue run-ning,in order to reveal the mechanism by which the central system regulates lower limb movement to adapt to fatigue accumulation. Method:Eleven male runners received constant speed running fatigue intervention,and the electromyograph-ic data of the lower limb muscles was collected during the whole intervention process.The non-negative ma-trix factorization algorithm was used to extract analysis indicators such as the number of lower limb muscle synergists,the peak activation time of muscle synergists,and the muscle relative weight at different interven-tion times. Result:A total of six types of muscle synergists were analyzed throughout the entire process of running fa-tigue intervention to dominate human lower limb joint activities,but each subject would only randomly mobi-lize four to five of them at different fatigue moments,and the number of muscle synergists participating in each fatigue moment had no significant change(P＞0.05).The peak activation time of synergy 1 decreased sig-nificantly at 33％、100％time(P＜0.05).The relative weight of semitendinosus of synergy 1 was significantly reduced at 33％、67％and 100％time(P＜0.05).The relative weight of rectus femoris of synergy 2 decreased significantly at 33％time(P＜0.05).The relative weight of biceps femoris of synergy 4 decreased significantly at 67％time(P＜0.05),but increased significantly at 100％time(P＜0.05). Conclusion:In the process of running fatigue,the human central system will regulate the muscle synergy mode of lower limbs to adapt to fatigue accumulation and reduce the risk of lower limb injury.The specific performance of this regulation process includes:stabilizing the number of lower limb muscle synergists in-volved,reducing the peak activation time of muscle synergists in the early stance stage,dynamically adjusting the relative weight of rectus femoris and semitendinosus in the early stance stage and biceps femoris in the middle swing stage.

The purpose of this study was to investigate the damage mechanism of pathogenic E.coli on mouse brain microvascular endothelial cells(BMEC cells)and mouse alveolar macrophages(MH-S cells),as well as the lung and brain of healthy mice.In this study,BMEC cells and MH-S cells were infected with pathogenic E.coli strains,and cell morphological changes were observed.Plate counting method was used to detect the adhesion and invasion ability of the strains to cells and the number of bacteria in the lungs and brains of mice.RT-qPCR was used to detect the ex-pression of TNF-α,IL-1β and IL-6 genes in cells and mouse organs at different time periods.West-ern blot was used to detect the expression of p-NF-κB,p-JAK2 and p-STAT3 proteins related to inflammation in cells and mouse organs after infection.The results showed that the cell culture medium of the infection group was turbid,the cell vision became dark and blurred,some cells shrank and died,and more fragments were produced.The adhesion rate and invasion rate of BMEC cells at 3 h were significantly lower than those at 6 h(P＜0.050),and the adhesion rate and inva-sion rate of MH-S cells at 3 h were significantly higher than those at 6 h(P＜0.010).Infected mice had a large area of swelling and bleeding in the brain,and the lungs had different degrees of swell-ing and bleeding.The bacterial load in the brain and lung was the highest at 12 h.Compared with the control group,the mRNA expression levels of IL-1β,IL-6 and TNF-α in the infection group were significantly increased at 3 h and 6 h(P＜0.050),and the mRNA expression levels of inflam-matory factors in BMEC cells and MH-S cells were the highest at 6 and 3 h,respectively.The mR-NA expression of inflammatory factors in the brain and lung of infected mice showed a trend of in-creasing first and then decreasing with time,with the highest expression at 12 h after infection.The expression levels of p-NF-κB protein in BMEC cells,MH-S cells,lung and brain tissues of mice in the infection group were significantly higher than those in the control group(P＜0.001),and the expression levels of p-JAK2 protein and p-STAT3 protein were significantly lower than those in the control group(P＜0.050).The above results showed that pathogenic E.coli could adhere and invade BMEC cells and MH-S cells,colonize in lung and brain tissues of mice,promote the expres-sion of NF-κB protein in cells and tissues,inhibit the expression of JAK2 protein and STAT3 pro-tein,and then stimulate cells and tissues to produce inflammatory response.

Objective:To observe the relationship between inducible carbon monoxide synthase (iNOS) and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), and explore its mechanism of action in DEACMP.Methods:This study was designed as prospective cohort study. Patients with acute carbon monoxide poisoning who met the diagnostic criteria and were admitted to Emergency Intensive Care Unit(EICU) of our hospital from June 2019 to June 2021 were selected as subjects. Patients were divided into the DEACMP group and non-DEACMP group according to the occurrence of DEACMP. Serum samples were collected on the first 24 h after admission and on day 7 and 14 after admission, and the serum nitric oxide (NO), neuronal nitric oxide synthase (nNOS), inducible carbon monoxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) level were measured by enzyme-linked immunosorbent assay. The generalized estimating equation was used to estimate the difference of NO, nNOS, iNOS and eNOS between DEACMP and non-DEACMP patients.Results:A total of 78 patients with carbon monoxide poisoning were included in our study finally, including 49 (62.82%) males and 29 (37.18%) females, with an average age of (53.96±14.95) years, 20 (25.64%) patients with DEACMP, and 1 (1.28%) death. Univariate analysis showed that patients with DEACMP had an average increase of 3 h (95% CI: 1.00, 5.00) in carbon monoxide exposure time and a 5-point decrease in GCS score (95% CI: 1.00, 6.00) than the patients without DEACMP, and the proportion of patients with severe carbon monoxide poisoning in the DEACMP group was higher than that of the non-DEACMP group (90.00% vs. 32.76%). According to the analysis of generalized estimation equation, on day 7 and 14 after admission, Compared with non-DEACMP patients, neither by performing unadjusted nor adjusted analysis with the iNOS of DEACMP patients was significantly higher than that in non-DEACMP patients regardless of whether exposure time, GCS score, coma time or severity of carbon monoxide poisoning were adjusted or not ( P <0.01 or P <0.05). Except for the level of nNOS in the GEE model adjusted with carbon monoxide exposure time, the levels of NO, nNOS and eNOS showed no significant difference between DEACMP and non-DEACMP patients ( P >0.05). Conclusions:The expression of iNOS level is increased in DEACMP patients, and its continuous expression may be involved in the pathogenesis of DEACMP.

Leukoencephalopathy with vanishing white matter (VWM) is one of the most prevalent inherited childhood white-matter disorders, and the pathogenic gene has been confirmed as EIF2B gene. VWM is characterized by chronic progressive neurological deterioration with cerebellar ataxia, usually less prominent spasticity and relatively mild mental decline. There are episodes of rapid and major neurological deterioration provoked by stresses, such as fever, minor physical trauma and acute fright, which is a characteristic clinical feature of VWM. Brain magnetic resonance imaging findings are diagnostic in almost all patients,and the disappearance of the cerebral white matter occurs in a diffuse "melting away" pattern. The onset of VWM can be at any age from fetal stage to adult stage, and the clinical phenotypes vary immensely. Gene diagnosis is the golden standard for VWM. This article reported a patient with a course of 17 years, who was misdiagnosed as Wilson′s disease because of low serum ceruloplasmin, and was finally diagnosed as VWM by reinterpretation of whole exome sequencing, which is worthy of clinicians′ vigilance and consideration.

OBJECTIVE: To explore the molecular reasons of weak expression of B antigen on the red cell. METHODS: Serological test for blood group was carried out, including red cell and plasma grouping, and anti-A1 and anti-H testing, and confirming weak A or B antigens by adsorption and elution. Exons 1-7 were sequenced directly, and one of them was cloned and sequenced. RESULTS: All of the 23 samples showed the weak B antigen by serological method. The alleles of the subgroups were identified by DNA sequencing, including 2 Bel subgroup, 4 B3 subgroup, 14 Bw subgroup, 2 CisAB subgroup and a novel allele. The novel allele showed a nucleotide substitution 662G>A in the exon 7, and the sequence was submitted to Blood Group Antigen Gene Mutation Database, and the novel allele was named Bel10. CONCLUSION Nucleotide substitution in exon results in blood subgroup, which showed that the antigens were weakened, and Bw phenotype was the most frequently subgroup.
ABO Blood-Group System/genetics* ; Alleles ; Exons ; Genotype ; Humans ; Nucleotides ; Phenotype

Objective:To compare the efficacy and safety of picosecond alexandrite laser and ultrapulsed fractional CO 2 laser for the treatment of facial atrophic acne scars in a prospective, split-face clinical trial. Methods:From October 2015 to October 2017, patients with facial symmetrical atrophic acne scars were enrolled from Department of Cosmetic Laser Surgery, Hospital for Skin Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College. The left side of the face of the patients was treated with ultrapulsed fractional CO 2 laser, and the right side of the face was treated with a 755-nm picosecond alexandrite laser with a diffractive lens array. All patients received 3 sessions of laser treatment at a 2-month interval. The severity of scars was evaluated by 2 dermatologists before and after the treatment according to the ECCA grading scale (échelle d′évaluation clinique des cicatrices d′acné) , and clinical efficacy was self-assessed by the patients according to a 4-point scale. Pain scores and adverse reactions were recorded. Paired t test was used to compare ECCA scores and pain scores between the 2 sides of the face, as well as between pre- and post-treatment values, and Wilcoxon rank sum test was used to compare the 4-point scores between the 2 groups. Results:There was no significant difference in the ECCA score between the picosecond laser side and the fractional laser side before the treatment ( t = 1.06, P = 0.300) , while the ECCA score was significantly higher in the picosecond laser side than in the fractional laser side after 3 sessions of treatment (70.98 ± 21.48 vs. 58.04 ± 17.63, t = 3.76, P = 0.001) . Compared with the pre-treatment severity score of scars, the improvement in severity score was significantly less in the picosecond laser side than in the fractional laser side (2.21 ± 1.09 vs. 2.83 ± 1.11, z = 2.70, P = 0.007) . Compared with the fractional laser side, the picosecond laser side showed significantly lower pain scores (3.71 ± 0.62 vs. 6.23 ± 1.06, t = 11.93, P < 0.001) and less adverse reactions, which mainly manifested as transient erythema and edema. Conclusions:Both picosecond alexandrite laser and fractional CO 2 laser can effectively improve atrophic acne scars. Fractional CO 2 laser is more effective, but picosecond alexandrite laser has less adverse effects.