Objective:To explore the effect and mechanism of c-Myc on regulating the expression of immune-related ligands in Y subtype small-cell lung cancer (SCLC) characterized by high expression of immune-related molecules.Methods:The Y subtype SCLC cell line H196 was randomly divided into the control group, c-Myc inhibitor 10058-F4 group, histone deacetylase 1 (HDAC1) inhibitor pyroxamide group, and 10058-F4 plus pyroxamide group. The co-culture system with NK-92MI cells was used to determine the effect of H196 cells on the function of natural killer (NK) cells. Western Blotting and co-immunoprecipitation assays were used to detect the effect of c-Myc on class Ⅰ HDAC, and flow cytometry was used to detect the regulatory effect of c-Mycon CD47, programmed cell death ligand 1 (PD-L1), and CD155, which are highly expressed immune checkpoints in Y subtype SCLC, and major histocompatibility complex classⅠ-related chains A and (MICA/B), which is a poorly expressed immune-activating ligand in SCLC, and the role of HDAC. Chromatin immunoprecipitation (ChIP) assay and real-time quantitative polymerase chain reaction (RT-qPCR) were used to determine the regulatory mechanism of c-Myc-HDAC1 on MICA/B expression.Results:Inhibition of c-Myc decreased the mortality of H196 cells in the co-culture system and down-regulated the expression of MICA/B. Compared with the NK+H196 group [(42.54±2.47)%], the proportion of cells killed by NK-92MI cells in the NK+H196+10058-F4 group was lower [(28.48±3.38)%, P＜0.001]. The mean fluorescence intensity (MFI) of MICA/B on the cells in the 10058-F4 group (36.40±0.82) was lower than that in the control group (91.23±8.60, P＜0.001). And c-Myc could bind to HDAC1, whose protein level was up-regulated by 10058-F4 while the mRNA level was not. Compared with the cells in the control group (90.10±4.91), the MFI of MICA/B on the cells in the pyroxamide group was significantly increased (145.70±5.86, P＜0.001), and the MFI of MICA/B on the cells in the 10058-F4+pyroxamide group (54.60±2.88) was significantly increased compared with the cells in the 10058-F4 group (35.97±1.60, P＜0.001). The percentage of MICA promoter gene fragments in the c-Myc antibody precipitation group (0.125±0.037) was significantly higher than that in the IgG group (0.000 8±0.000 3, P=0.004). MICB had a similar trend, suggesting that the c-Myc-HDAC1 complex could bind to the promoter region of MICA/B. The MFI of CD47 on the cells in the 10058-F4 group (60.07±0.21) was significantly lower than cells in the control group (70.27±1.37, P＜0.001), but the MFIs of PD-L1 (13.50±0.61) and CD155 (829.70±41.19) were significantly higher than those on the cells in the control group (9.23±0.94, P＜0.01; 496.00±4.36, P＜0.001, respectively). Conclusions:c-Myc may promote the expression of MICA/B and CD47 in Y subtype SCLC cells by binding and inhibiting HDAC1, while it may also be involved in inhibiting the expression of PD-L1 and CD155 in SCLC cells.

Objective:To explore the effect and mechanism of c-Myc on regulating the expression of immune-related ligands in Y subtype small-cell lung cancer (SCLC) characterized by high expression of immune-related molecules.Methods:The Y subtype SCLC cell line H196 was randomly divided into the control group, c-Myc inhibitor 10058-F4 group, histone deacetylase 1 (HDAC1) inhibitor pyroxamide group, and 10058-F4 plus pyroxamide group. The co-culture system with NK-92MI cells was used to determine the effect of H196 cells on the function of natural killer (NK) cells. Western Blotting and co-immunoprecipitation assays were used to detect the effect of c-Myc on class Ⅰ HDAC, and flow cytometry was used to detect the regulatory effect of c-Mycon CD47, programmed cell death ligand 1 (PD-L1), and CD155, which are highly expressed immune checkpoints in Y subtype SCLC, and major histocompatibility complex classⅠ-related chains A and (MICA/B), which is a poorly expressed immune-activating ligand in SCLC, and the role of HDAC. Chromatin immunoprecipitation (ChIP) assay and real-time quantitative polymerase chain reaction (RT-qPCR) were used to determine the regulatory mechanism of c-Myc-HDAC1 on MICA/B expression.Results:Inhibition of c-Myc decreased the mortality of H196 cells in the co-culture system and down-regulated the expression of MICA/B. Compared with the NK+H196 group [(42.54±2.47)%], the proportion of cells killed by NK-92MI cells in the NK+H196+10058-F4 group was lower [(28.48±3.38)%, P＜0.001]. The mean fluorescence intensity (MFI) of MICA/B on the cells in the 10058-F4 group (36.40±0.82) was lower than that in the control group (91.23±8.60, P＜0.001). And c-Myc could bind to HDAC1, whose protein level was up-regulated by 10058-F4 while the mRNA level was not. Compared with the cells in the control group (90.10±4.91), the MFI of MICA/B on the cells in the pyroxamide group was significantly increased (145.70±5.86, P＜0.001), and the MFI of MICA/B on the cells in the 10058-F4+pyroxamide group (54.60±2.88) was significantly increased compared with the cells in the 10058-F4 group (35.97±1.60, P＜0.001). The percentage of MICA promoter gene fragments in the c-Myc antibody precipitation group (0.125±0.037) was significantly higher than that in the IgG group (0.000 8±0.000 3, P=0.004). MICB had a similar trend, suggesting that the c-Myc-HDAC1 complex could bind to the promoter region of MICA/B. The MFI of CD47 on the cells in the 10058-F4 group (60.07±0.21) was significantly lower than cells in the control group (70.27±1.37, P＜0.001), but the MFIs of PD-L1 (13.50±0.61) and CD155 (829.70±41.19) were significantly higher than those on the cells in the control group (9.23±0.94, P＜0.01; 496.00±4.36, P＜0.001, respectively). Conclusions:c-Myc may promote the expression of MICA/B and CD47 in Y subtype SCLC cells by binding and inhibiting HDAC1, while it may also be involved in inhibiting the expression of PD-L1 and CD155 in SCLC cells.

Evidence-based medicine (EBM) is a science that uses the best available research data to make decisions, and the core is that clinical decision-making is supported by the best research evidence. Incorporating EBM into traditional standardized residency training in hematology can foster residents' professional theoretical knowledge and clinical skills, improve the quality of standardized training, and provide ideas and methods for standardized training of hematology residents, which is worthy of further research and exploration.

Objective To study the effects of selecting different fixing segments on biomechanical characteristics of the spine during the treatment of early onset scoliosis（EOS） by growing rod technique. Methods By using finite element method, four spine models (C6-S1 segments) fixed by growing rod were established: preoperative model, T1-L4 fixed model, T2-L4 fixed model, T3-L4 fixed model. Then 7 N·m torque load and 1 rad angular displacement load were applied on superior surface of C6 segment to analyze biomechanical characteristics for adjacent structure of the fixed vertebral body. Results The whole spinal range of motion (ROM) decreased significantly after operation. When the T2-L4 segment was fixed, the spine activity was mostly restricted, the compensatory activity of adjacent vertebrae increased significantly, and the intervertebral disc stress increased significantly. Conclusions When T2 segment is selected as the upper instrumented segment, the risk of proximal junctional kyphosis and spinal degeneration is the highest, which should be avoided in clinical surgery.

OBJECTIVE： To study the dose-time-effect relationship of Tibetan medicine Rannasangpei in cerebral ischemic- reperfusion injury model rats with intragastric administration. METHODS： The rats were randomly divided into sham operation group （normal saline， 10 mL/kg）， model control group （normal saline， 10 mL/kg）， positive control group （nimodipine， 30      mg/kg）， Rannasangpei different dose groups （0.52， 1.04， 2.08， 4.17， 8.33， 16.67， 33.34， 66.68， 133.36， 266.72 and 533.44    mg/kg）， with 18 rats in each group. Each group was given relevant medicine intragastrically once； 25 min after intragastric administration， cerebral ischemic-reperfusion injury model was established with suture-occluded method in those groups except for sham operation group. 24， 48， 72 h after cerebral ischemia， neuroethology of rats were graded in each group. The rate of cerebral infraction was detected to evaluate the optimal effective time， the optimal dose （Dmax） and maximal effect （the rate of minimum cerebral infraction， Emax） of Ratnasampil at different periods of cerebral ischemia. Dose-time-effect relationship of Rannasangpei dose with the rate of cerebral infraction was fitted with Thermo Kinetica 5.1 software. The area under curve （AUClast） and retention dose （MRTlast） of dose-effect curve were calculated， and detect the levels of SOD and MDA. RESULTS： Compared with sham operation group， the neurobehavior of model group was significantly abnormal （P＜0.05 or P＜0.01）， and the rate of cerebral infarction was significantly increased （P＜0.01）； the level of SOD was decreased significantly （P＜0.01， 48 h）， and the level MDA was increased significantly （P＜0.05， 48 h）. Compared with model control group， there was no significant change in neurobehavioral abnormalities in the nimodipine group （P＞0.05）， and the rate of cerebral infraction was decreased significantly （P＜0.01， 24， 48 h）. The level of SOD in rats were increased significantly （P＜0.01， 48 h）， while the level MDA decreased significantly （P＜0.05， 48 h）. Rannasangpei 2.08-33.34 mg/kg could significantly improved neurobehavioral abnormalities （P＜0.05， 24 h）； 24 h after cerebral ischemia， the rate of cerebral infraction was decreased significantly in Rannasangpei 4.17-133.36 mg/kg group （the lowest is 33.34 mg/kg group， P＜0.05 or P＜0.01）. The level of SOD in rats were increased significantly in 33.34-533.44 mg/kg groups （P＜0.05）. the level MDA was decreased significantly in 0.52-2.08， 8.33， 33.34， 266.72 and 533.44 mg/kg groups （P＜0.05）. Dmax was 33.34 mg/kg， Emax was 3.02％， AUClast was 5 141.76 mg/kg and MRTlast was 329.161 mg/kg. 48 h after cerebral ischemia， the rate of cerebral infraction was decreased significantly in Rannasangpei 2.08-133.36 mg/kg groups （the lowest is 66.68 mg/kg group， P＜0.05 or P＜0.01）， while the level of SOD was increased significantly in 1.04-533.44（except for 4.17）mg/kg groups （P＜0.05）. The level of MDA was decreased significantly in 16.67-66.68， 533.44 mg/kg groups （P＜0.05）， Dmax was 66.68 mg/kg， Emax was 2.13％， AUClast was    5 219.36 mg/kg and MRTlast was 340.521 mg/kg. 72 h after cerebral ischemia， the rate of cerebral infraction and the level of MDA had no significant decreased in Rannasangpei groups （P＞0.05）， and the levels of SOD had no significant increase （except for 0.52 mg/kg group， P＞0.05）. CONCLUSIONS： The optimal effective time of Rannasangpei for the treatment of cerebral ischemia-reperfusion injury in rats is 48 h， and the Dmax is 66.68 mg/kg. The improvement mechanism may be related to increase the level of SOD and decrease the level of MDA.

Alzheimer's disease (AD)is most common in all dementia types in the elderly.Various researches have been done for studying its pathogenesis,but no single mechanism can explain all its pathological changes.AD is currently incurable and no effective treatment measures are available.So it is of prime importance to prevent the occurrence of AD.In the process of exploring the pathogenesis and treatment of AD,more and more attention is being paid to the role of diet and nutrition in the occurrence and development of AD.Mediterranean diet(MeDi)has been proved to have an unvarying role in the occurrence and development of Alzheimer's disease.This paper reviewed the relevant literatures and summarized the role of MeDi in AD,in order to provide the theoretical supports for dietary intervention and nutritional therapy in AD treatment.

Otbjective:To provide body-mind-spirit-society holistic services for patients,through medical social workers intervening in chronic pain patients and using the professional theory of social work.Methods:By serving the patients and the potential people with community work,group work and case work,this paper explored the tertiary prevention mode for chronic pain patients,and then to intervene in their social psychosocial problems caused by pain and improve their quality of life.Results:Medical social workers intervening in chronic pain patients'social psychosocial problems made a difference.Through combining the prevention model with the three methods of social work,the service scope was expanded and the effectiveness was improved significantly.Conclusion:Under the guidance of tertiary prevention theory,this paperhas explored a set of models to intervene in chronic pain patients' social psychological health,which is of great significance to mitigate chronic pain patients' social psychological problem.

Objective To observe the protective effect of Xiaohuangdecotion against liver damage inα-naphthylisothiocyanate (ANIT)- induced cholestasis in rats and probe the potential mechanisms.Methods Male Wistar rats (40) were randomly divided into a normal group, a model group, aXiaohuangdecotion treatment group, and a UDCA control group (10 for each). Except for rats in the normal group, ANIT solution (6 ml/kg) was administered in other rats by gavages for cholestasis model. After ANIT treated 48 h, rats inXiaohuangdecotion group and UDCA group were treated withXiaohuangdecotion (1.73 g/kg) and UDCA (10 mg/kg) respectively for 1 week. And, rats in the normal group and the model group were given an equal volume of saline. At the end of the experiment, liver function rats were examined. Liver histology was examined by HE staining, and CD68 factor was tested by immunohistochemistry and Western blot.Results Compared with the model group, the content of ALT (164.6 ± 53.4 U/Lvs. 208.4 ± 28.5 U/L), AST (247.6 ± 76.1 U/Lvs. 341.8 ± 32.8 U/L), ALP (601.0 ± 101.1 U/Lvs. 720.6 ± 123.3 U/L), TBiL (96.5 ± 18.1μmol/Lvs. 149.6 ± 30.2μmol/L), DBiL (73.7 ± 16.6μmol/Lvs. 140.3 ± 28.6μmol/L) and TBA (93.4 ± 13.0μmol/Lvs. 146.5 ± 38.9μmol/L) were significantly reduced in the treatment group (P<0.01 orP<0.05). Compared with the model group, CD68 level (7.08 ± 0.19 vs. 17.42 ± 0.48)were significantly reduced by intervention ofXiaohuangdecotion (P<0.01).ConclusionsXiaohuangdecotion could improve liver functions and reduce CD68 expression, leading to a good hepatoprotective and jaundice-relieving effects.

Objective To evaluate the relationship between long non-coding RNAs (LncRNA) in tumor tissues and clinico-pathological features of hepatocllular carcinoma (HCC).Methods Using hepatocellular carcinoma gene database GSE36376,we conducted a study on eight LncRNAs which are associated with liver diseases and analyzed the correlation between these LncRNAs and HCC clinico-pathological characteristics.We also evaluated the potential effect of LncRNAs on HCC development.Results H19 was overexpressed in non-tumorous tissues of HCC (P ＜ 0.05),while MEG3,HOXA13,KCNQ1OT1 were all upregulated in tumorous tissues (all P ＜ 0.05).HULC level in HCC tumorous tissues was negatively correlated with AJCC staging,BCLC staging and tumor size (all P ＜ 0.05).UCA1 was positively correlated with BCLC staging (r =0.135,P ＜ 0.05).Univariate analysis and multivariate logistic analyses showed that UCA1 was a risk factor of intrahepatic metastasis of HCC (OR =6.054,95％ CI =1.429 ～ 25.642,P ＜ 0.05); in contrast,HULC overexpression in tumorous tissues played a positive role in HCC tumor size (OR=0.805,95％CI=0.678 ～0.956,P＜0.05).Conclusion HULC in tumorous tissues suppressed HCC proliferation,while UCA1 was a risk factor of HCC aggressiveness.