Objective To construct a risk prediction model for post-stroke dysphagia(PSD)based on clinical and laboratory indicators of elderly stroke patients with explainable machine learning.Methods A retrospective analysis was conducted on 3994 stroke patients hospitalized in Depart-ment of Neurology of First Medical Center of Chinese PLA General Hospital from October 2010 to December 2021.Among them,the 1390 cases admitted during January 2019 and December 2021 were assigned into an external validation set,and the 2604 cases admitted during October 2010 to January 2019 were into a training group.Those from the training group were further divided into a training set(1823 cases)and an internal validation set(781 cases)in a 7∶3 ratio,and also grouped into a PSD subgroup(773 cases)and a non-PSD group(1831 cases).With occurrence of swallowing difficulties as an endpoint,risk prediction models were constructed using random for-est(RF),eXtreme Gradient Boosting(XGBoost),Support Vector Machine(SVM),and logistic regression.ROC curve analysis was employed to evaluate the performance of our models.After the optimal model was selected,SHAP was employed to interpret feature contributions.Results There were significant differences in muscle strength,right/left-sided stroke,and area of brain in-jury between the PSD and the non-PSD groups(P＜0.01).The PSD group had obviously larger proportions of hypertension,diabetes,and drinking history,increased neutrophil counts,and de-creased levels of potassium and albumin when compared with the non-PSD group(P＜0.05,P＜0.01).Multivariate logistic regression analysis showed that age,drinking history,diabetes,hyper-tension,muscle strength grade,area of brain injury,hemispheric stroke,neutrophil count,and al-bumin and potassium levels were risk factors for PSD(P＜0.05,P＜0.01).The external validation results showed that the area under curve value of the RF model,XGBoost model,SVM model,and our logistic model was 0.883,0.902,0.877,and 0.868,respectively.The distribution of SHAP value showed that drinking history,hypertension and diabetes were positively correlated with PSD risk;Muscle strength was negatively correlated with the risk;Age growth was positively correlated with the risk;Subtentorial lesions showed stronger predictive efficacy than supratentorial lesions and entire lesions;The bilateral and right-sided stroke had higher risk for PSD than the left-sided stroke.Conclusion The model based on the XGBoost model shows best performance in predicting the risk for swallowing disorders in elderly patients after stroke.

Objective To construct a risk prediction model for post-stroke dysphagia(PSD)based on clinical and laboratory indicators of elderly stroke patients with explainable machine learning.Methods A retrospective analysis was conducted on 3994 stroke patients hospitalized in Depart-ment of Neurology of First Medical Center of Chinese PLA General Hospital from October 2010 to December 2021.Among them,the 1390 cases admitted during January 2019 and December 2021 were assigned into an external validation set,and the 2604 cases admitted during October 2010 to January 2019 were into a training group.Those from the training group were further divided into a training set(1823 cases)and an internal validation set(781 cases)in a 7∶3 ratio,and also grouped into a PSD subgroup(773 cases)and a non-PSD group(1831 cases).With occurrence of swallowing difficulties as an endpoint,risk prediction models were constructed using random for-est(RF),eXtreme Gradient Boosting(XGBoost),Support Vector Machine(SVM),and logistic regression.ROC curve analysis was employed to evaluate the performance of our models.After the optimal model was selected,SHAP was employed to interpret feature contributions.Results There were significant differences in muscle strength,right/left-sided stroke,and area of brain in-jury between the PSD and the non-PSD groups(P＜0.01).The PSD group had obviously larger proportions of hypertension,diabetes,and drinking history,increased neutrophil counts,and de-creased levels of potassium and albumin when compared with the non-PSD group(P＜0.05,P＜0.01).Multivariate logistic regression analysis showed that age,drinking history,diabetes,hyper-tension,muscle strength grade,area of brain injury,hemispheric stroke,neutrophil count,and al-bumin and potassium levels were risk factors for PSD(P＜0.05,P＜0.01).The external validation results showed that the area under curve value of the RF model,XGBoost model,SVM model,and our logistic model was 0.883,0.902,0.877,and 0.868,respectively.The distribution of SHAP value showed that drinking history,hypertension and diabetes were positively correlated with PSD risk;Muscle strength was negatively correlated with the risk;Age growth was positively correlated with the risk;Subtentorial lesions showed stronger predictive efficacy than supratentorial lesions and entire lesions;The bilateral and right-sided stroke had higher risk for PSD than the left-sided stroke.Conclusion The model based on the XGBoost model shows best performance in predicting the risk for swallowing disorders in elderly patients after stroke.

Objective By analyzing the characteristics of PI system in the US,especially its advantages,to learn the ways and means in the cultivation of postgraduates' innovative ability.Combined with the current situation of medical postgraduate training in China,some countermeasures in line with the actual situation of our country and the cultivation characteristics of medical graduate students' innovative ability were proposed.Methods Conducting literature review by using the CNKI and logging on to the official website of relevant agencies to collect and summarize related research data.Results Concrete suggestions from four aspects were proposed:Encourage medical graduate students to participate in scientific and technological research,well-planning of scientific research resources,optimizing and perfecting the mentor-mentee system and constructing a reasonable mechanism for achievement distribution.Conclusions The PI system in American scientific research field can be used for reference in the form and content of cultivating the innovative ability of medical postgraduates in China.

[Objective]To forecast the sponge mechanism mediated by LOC389023 in patients with intractable temporal lobe epilepsy(TLE),through investigating the expression of microRNA interacted with dipeptidyl peptidase 10(DPP10)and LOC389023.[Methods]The expression of DPP10 and Kv4.3 were detected in 15 temporal neocortex from patients with brain trauma (control group)and in 26 temporal neocortex from patients with intractable TLE(epilepsy group)by western blot(WB)and immunohisto?chemical(IHC)staining. The location of DPP10 and voltage dependent potassium channel 4.3(Kv4.3)was detected by immunofluo?rescent(IF)staining. The interaction between DPP10 and Kv4.3 was testified by co-immunoprecipitation(Co-IP). The expression of microRNA obtained by softwares(miRanda,Pita,TargetScan and miRDB)was detected by qPCR.[Results]IHC and WB showed an increased expression of DPP10(P<0.05)and a decreased expression of Kv4.3(P<0.05)in the epilepsy group. IF showed that the DPP10 and the Kv4.3 co-expressed in the membrane and the cytoplasm of neurons. Co-IP showed obvious interaction between the DPP10 and the Kv4.3.Five microRNA(miR-32-5p,miR-140-5p,miR-367-3p,miR-25-3p,miR-4325)were obtained by soft?wares. No significant differences in the expression of miR-32-5p and miR-4325 were found between epilepsy group and control group by qPCR(P>0.05). But decreased expression of LOC389023 and miR-140-5p and increased expression of miR-25-3p and miR-367-3p were found in epilepsygroup compared to control group (P < 0.05).[Conclusion]miR-25-3p and miR-367-3p may be regulated by LOC389023 through the sponge mechanism followed by altered expression of DPP10 in intractable temporal lobe epilepsy.

Objective To investigate the effects of hydrochloride fasudil on inflammation and secondary brain injury in rats after intracerebral hemorrhage (ICH).Methods One hundred and seventeen male Wistar rats were randomly divided into normal group (n=9),sham-operated group (n=36),ICH group (n=36) and hydrochloride fasudil treatment group (ICH/HF,n=36).ICH was caused by injecting non-anticoagulant autologous arterial blood into the right caudate nucleus,3 mg HF was dissolved in 2 mL 0.9％ saline solution and administrated intraperitioneally once daily (12 mg/kg/d) since 12 h ofICH onset.Rats in the sham-operated group and ICH group received an equal volume of normal saline.On one,3,7 and 14 d ofICH induction,Bederson method was used to score neurological deficits in rats;interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels in serum were detected by enzyme-linked immunosorbent assay (ELISA).Brain edema was measured by comparing wet and dry brain weights.Inflammatory cell infiltration around the hematoma was visualized using hematoxylin and eosin,and changes in neuronal morphology were detected by Nissl staining.Immunohistochemistry method was used to detect the expressions of Caspase-3 and Bcl-2.Results (1) The neurological deficit scale scores on one and 3 d ofICH in the ICH/HF group were significantly decreased as compared with those in the ICH group (P＜0.05).(2) Serum IL-6 (except 14 d of ICH) and TNF-α levels in ICH/HF group were significantly decreased as compared with those in the ICH group (P＜0.05).(3) Brain water contents at each time point in ICH/HF group were significantly decreased as compared with those in the ICH group (P＜0.05).(4) HE staining showed the sizes of hematoma on one and 3 d ofICH in the ICH/HF group and ICH group were consistent;but ICH/HF group had smaller hematomas on 7 d of ICH,and disappeared hematoma and glial cell hyperplasia on 14 d of ICH.Mass neutrophils infiltration developed in the perihematomal areas of the ICH and ICH/HF groups;however,neutrophils infiltration in the ICH/HF group ([20.56±6.37] cells/field) was significantly decreased as compared with that in the ICH group ([41.50±8.91] cells/field) on one d of ICH (P＜0.05).(5) Nissl staining showed neuron death and loss in the perihematomal areas on one,3 and 7 d of ICH in the ICH group;but ICH/HF group had significantly increased neuron number as compared with the ICH group (P＜0.05).(6) The Caspase-3 expression on 3 and 7 d ofICH in the ICH/HF group was significantly decreased as compared with that in the ICH group (P＜0.05);the Bcl-2 expressions at each time point in the ICH/HF group was significantly increased as compared with that in the ICH group (P＜0.05).Conclusion HF exerts neuroprotective effects in ICH rat models by decreasing serum IL-6 and TNF-α levels,reducing neutrophils infiltration and neuronal necrosis around the hematoma,restraining the cell apoptosis through down-regulating Caspase-3 and up-regulating expression of Bcl-2,alleviating the brain edema,and improving the neurological outcome.

OBJECTIVE: To investigate the effect of bactericidal/permeability-increasing protein(BPI) on the outcome of sepsis in mice and its possible mechanism. METHODS: Sepsis was induced by injection of 2x10(6) colony-formed unit E. coli J5 via the tail vein. BPI of 5 mg/kg or equal volume of normal saline(NS) were injected intravenously at the same time. Endotoxin and TNFalpha levels in serum were assayed using a chromogenic limulus amebocyte lysate test and ELISA respectively. RESULTS: Seventy-two hour survival rate of septic mice was significantly higher in the BPI group (15/18) than in the NS group(8/18, P<0.01). Serum endotoxin levels in the BPI group (1.3+/-0.3 and 0.7+/-0.4 &mgr;g/L) were significantly lower than those in the NS group (3.9+/-0.8 and 2.5+/-0.9 &mgr; g/L, P<0.01) 0.5 and 1 hour following injection of bacteria respectively. The peak levels of serum tumor necrosis factor-alpha(TNFalpha)in the BPI group (1.9+/-0.6 &mgr;g/L) were also markedly lower than those in the NS group (3.8+/-0.8 &mgr;g/L, P<0.01) 1.5 hours following bacterial injection. But there was no significant difference in blood bacterial count between the BPI and NS groups 0.5, 1.5 and 3.0 hours after injection of bacteria. CONCLUSIONS: BPI has a marked protective effect on E. coli sepsis, which might be related to its action against bacterial endotoxin and its inhibition of TNFalpha production in sepsis.

Objective To systemically investigate 1) distribution of endogenous endotoxin (ET) in tissues and circulation; 2) its relationship with shock duration and organ damage; and 3) its possible mechanism after hemorrhagic shock.Methods To further elucidate the intrinsic relationship between endogenous endotoxin translocation and hemorrhagic shock, the present study systematically investigated the distribution of endogenous ET into the liver, lungs, kidneys and circulation, and the relationship between ET levels and the corresponding organ dysfunction with limulus amebocyte lysate (LAL) chromogenic assay following hemorrhagic shock in rats. Results It was found that ET levels in hepatic homogenate markedly increased (P=0.09) 1.5 hours following shock compared with that in the sham group. After resuscitation, ET levels in hepatic, pulmonary and renal tissues were all significantly elevated. The levels kept increasing with the prolonged experimental time, and reached as high as 3.88±0.95 EU (endotoxin unit)/g in the livers, 2.53±1.46 EU/g in the lungs and 2.51±0.89 EU/g in the kidneys 12 hours after shock. ET levels in plasma reached a peak of 1.13±0.42 EU/ml at 1 hour following resuscitation, then rapidly decreased to the sham levels 3 hours following resuscitation. There was a close relationship between endotoxin translocation and shock duration. Correlation analysis further indicated that the changes in glutamic-pyruvic transaminase (GPT), blood urea nitrogen (BUN) in plasma and angiotensin Ⅰ-converting exzyme (ACE) in pulmonary homogenate were significantly and positively correlated with the ET levels in the liver, kidneys and lungs after hemorrhagic shock. Conclusions Hemorrhagic shock can induce obvious endogenous ET translocation, which is closely related to the shock duration. Although only transient endotoxemia occurs after hemorrhagic shock, ET can massively accumulate in tissues (liver, lungs and kidneys), and may play an important role in the development of shock.