Objective To explore intelligence impairment in the patients with idiopathic parkinson's disease(PD) and to investigate whether auditory P300(P3) can be influenced by levodopa therapy. Methods The standard auditory P300 were measured before starting treatment and 6 months after starting treatment in 30 patients with idiopathic parkinson's disease, and 30 healthy subjects with matching age, sex and education levels served as control. Results After levodopa treatment in patients with PD, P300 latency(PL) and amplitude(Amp) did not significantly changes, but reaction time (RT) was significantly shortened(P

AIM:To investigate the molecular mechanism of nontypeable Haemophilus influenzae ( NTHi)-in-duced MUC5AC expression in the human airway NCI-H292 cells.METHODS:Bronchial epithelial NCI-H292 cells were cultured in vitro.The production of MUC5AC and matrix metalloproteinase 9 (MMP-9) after stimulation with NTHi was analyzed by enzyme-linked immunosorbent assay (ELISA).The enzymatic activity of MMP-9 was detected by gelatin zy-mography.In addition, the cells were pretreated with different inhibitors such as AG 1478, LY294002, DPI, NAC and GM6001 before stimulation, which specifically inhibit epidermal growth factor receptor (EGFR), phosphatiadylinositol 3-ki-nase (PI3K), NADPH oxidase, reactive oxygen species (ROS) and MMP-9, respectively, and then the production of MUC5AC or MMP-9 was determined.RESULTS:NTHi-stimulated NCI-H292 cells exhibited a time-dependent increase in MMP-9 secretion and activity .NTHi also increased the activity of Rac 1 and the production of ROS .Pretreatment of AG1478 and LY294002 decreased the Rac1 activity, and preincubation of DPI or Rac 1 inhibitor significantly abrogated ROS production.In addition, secretion of MMP-9 and the enzymatic activity was decreased by treatment of NAC and NSC23766.Furthermore, inhibition of the MMP-9 activity by GM6001 significantly inhibited MUC5AC production.CON-CLUSION:EGFR/PI3K/Rac1/NADPH oxidase/ROS/MMP-9 regulates MUC5AC production in NTHi-challenged NCI-H292 cells.

The metabolic profiles of control and MCF-7 cells treated with luteolin were analyzed separately using gas chromatography/mass spectrometry ( GC/MS ) to study the mechanism of the luteolin treatment on MCF-7 cells. Cell viability assays showed that luteolin had inhibition effect on MCF-7 cells. Partial least square discriminant analysis ( OPLS-DA) was used to process the metabolic data. Since cells in phase of S were increased significantly, we speculated that luteolin had a blocking effect on pentose phosphate pathway of MCF-7 cells, which contributed to its inhibition effect on proliferation of MCF-7 cells.

Objective To investigate the expression of m onocyte chem otactic protein-1 (MCP-1) and its receptor CCchem okine receptor-2 (CCR-2) in coronary atherosclerosis plaques betw een sudden coro-nary death (SCD ) and non-SCD. Methods The expression levels of MCP-1 and CCR-2 in SCD group, coronary atherosclerosis group (non-SCD), control group (norm al coronary artery) w ere detected by im-m unohistochem istry. Results Positive rates of MCP-1 am ong the three groups w ere 78%, 47%, and 0%, respectively, w ith significant expressing differences betw een each tw o groups (P<0.05). Positive rates of CCR-2 am ong three groups w ere 72%, 47%, and 0%, respectively, w ith significant expressing differ-ences betw een the SCD group and coronary atherosclerosis group as w ell as betw een the SCD group and control group (P<0.05), but w ith no significant expressing difference betw een coronary atherosclero-sis group and control group (P>0.05). Conclusion O verexpression of MCP-1 and CCR-2 in coronary atherosclerotic plaques is closely correlated w ith SCD .

OBJECTIVE:To optimize the decolorization condition for polysaccharide extract of Mongolian medicine Vicia amoena,and to establish the method for its extraction and content determination. METHODS:The water extract-alcohol precipita-tion was used to extract polysaccharide from Mongolian medicine V. amoena. Using decolorization rate as index,orthogonal test was designed to investigate the effects of the dosage of activated carbon,decolorization temperature,decolorization time on the de-colorization of polysaccharide,so as to optimize the conditions for the decoloration of polysaccharide. Using glucose as control, phenol sulfuric acid method was adopted,and the content of polysaccharide in crude polysaccharide was determined by UV spectro-photometry at 490 nm. RESULTS:The optimal decoloration condition was as follows as actived carbon of 3%,decoloration time of 40 min,decoloration temperature of 60 ℃. On this basis,the average decolorization rate reached 19.77%(RSD=1.85%,n=3) by the verification test of the decoloration. The average extraction yield for the crude polysaccharide was 4.56%(RSD=2.38%,n=3),of which the polysaccharide content was 1.98%(RSD=2.18%,n=4). CONCLUSIONS:This experiment has relatively good reproducibility in polysaccharide yield;established method for content determination of polysaccharide is stable and feasible.

Objective: To investigate the expression of SnoN in human hypertrophic scar fibroblasts and the mechanism of its participation in hypertrophic scar formation. Methods: Eight patients with hypertrophic scar after burn in need of surgery were admitted in our unit from January to October 2013, and then hypertrophic scar tissue and normal skin tissue of full-thickness skin donor site resected by surgery of the patients were collected. Hypertrophic scar fibroblasts and normal skin fibroblasts of patients were isolated with method of explant culture and then sub-cultured. Cells of the third to fifth passage were used in the following experiments. (1) The protein expressions of SnoN of hypertrophic scar fibroblasts and normal skin fibroblasts were assessed with Western blotting. (2) The mRNA expressions of SnoN of another batch of hypertrophic scar fibroblasts and normal skin fibroblasts were determined with reverse transcription polymerase chain reaction. (3) Another batch of hypertrophic scar fibroblasts and normal skin fibroblasts were treated with 10 ng/mL transforming growth factor beta1 (TGF-β₁) for 30 min, 1 h, 2 h, and 6 h, respectively, and then the protein expressions and mRNA expressions of SnoN of untreated cells and treated cells were detected as above. Data were processed with one way analysis of variance and independent sample t test. Results: (1) The protein expression of SnoN of hypertrophic scar fibroblasts was 0.020±0.003, significantly lower than that of normal skin fibroblasts (0.032±0.005, t=7.19, P<0.05). (2) The mRNA expression of SnoN of hypertrophic scar fibroblasts was 0.407±0.157, with no significant difference from that of normal skin fibroblasts (0.339±0.095, t=-1.29, P>0.05). (3) The protein expression of SnoN of normal skin fibroblasts was increased in a time-dependent fashion with the TGF-β₁ stimulation, and the protein expressions of SnoN of cells treated with TGF-β₁ for 30 min, 1 h, 2 h, and 6 h were significantly higher than those of untreated cells (with t values from 2.27 to 27.89, P values below 0.05). The protein expression of SnoN of hypertrophic scar fibroblasts was decreased in a time-dependent fashion with the TGF-β₁ stimulation, and the protein expressions of SnoN of cells treated with TGF-β₁ for 30 min, 1 h, 2 h, and 6 h were obviously lower than those of untreated cells (with t values from 10.80 to 13.85, P values below 0.05). (4) The mRNA expressions of SnoN of normal skin fibroblasts and hypertrophic scar fibroblasts were both increased in a time-dependent fashion with the TGF-β₁ stimulation, and the mRNA expressions of SnoN of the two types of cells treated with TGF-β₁ for 30 min, 1 h, 2 h, and 6 h were both significantly higher than those of untreated cells (with t values from 18.16 to 58.22, P values below 0.05). Conclusions The protein expression of SnoN in hypertrophic scar fibroblasts is reduced, which weakens its inhibitory effect on TGF-β₁ signal, thus amplifying the TGF-β₁ signal, and it may participate in the formation of hypertrophic scar.

Objective:Percutaneous coronary intervention(PCI)is one of the most important treatments for coronary artery disease(CAD).However,in-stent restenosis(ISR)after PCI is a serious complication without effective measures for prevention and treatment.This study aims to investigate the Ras-related protein 1A(Rap1A)level in ISR patients and in the tumor necrosis factor-α(TNF-α)-induced inflammatory injury model of human umbilical vein endothelial cells(HUVECs),to explore the role of Rap1A in regulating TNF-α-induced inflammation in HUVECs and to provide a new potential target for ISR prevention and treatment. Methods:A total of 60 CAD patients,who underwent PCI between December 2020 and July 2022 from the Department of Cardiovascular Medicine of Xiangya Hospital,Central South University,and re-examined coronary angiography(CAG)1 year after the operation,were included.After admission,27 patients were diagnosed with ISR and 33 patients were diagnosed with non-in-stent restenosis(non-ISR)according to the CAG.Clinical data were collected,and the plasma Rap1A level was determined by enzyme linked immunosorbent assay(ELISA).In cell experiments,an inflammatory injury model was established with TNF-α treatment(10 ng/mL,24 h)in HUVECs.The mRNA and protein expression levels of Rap1A,interlukin-6(IL-6),and vascular cell adhesion molecule-1(VCAM-1)were measured by real-time reverse transcription PCR and Western blotting.Small interfering RNA(siRNA)was used to explore the role of Rap1A in regulating TNF-α-induced inflammation in HUVECs. Results:Compared with the non-ISR patients,a higher proportion of ISR patients had a history of smoking(P=0.005)and diabetes(P=0.028),and higher levels of glycosylated hemoglobin(HbA1c)(P=0.012),low-density lipoprotein cholesterol(LDL-c)(P=0.014),and hypersensitive C-reactive protein(hs-CRP)(P=0.027).The remaining projects did not show significant differences(all P＞0.05).The plasma level of Rap1A in the ISR group was significantly higher than that in the non-ISR group[942.14(873.28 to 1 133.81)μg/mL vs 886.93(812.61 to 930.98)μg/mL;P=0.004].Diabetes,LDL-c,and Rap1A were risk factors for ISR by univariate logistic regression analysis(all P＜0.05).The mRNA and protein expression levels of inflammatory factors IL-6 and VCAM-1 were increased in HUVECs after 10 ng/mL TNF-α treatment for 24 h compared with the control group(all P＜0.05),while the mRNA and protein levels of Rap1A were increased(both P＜0.05).After inhibition of Rap1A in HUVECs,the mRNA and protein expression levels of IL-6 and VCAM-1 were significantly decreased(all P＜0.05). Conclusion:The plasma Rap1A level was significantly elevated in patients with ISR,suggesting that Rap1A may be a potential biomarker for predicting ISR.In the TNF-α-induced HUVECs inflammatory injury model,the expression level of Rap1A was increased.The level of TNF-α-induced endothelial cell inflammation was decreased after inhibition of Rap1A expression,suggesting that Rap1A may be a potential target for the treatment of endothelial cell inflammation in ISR.

Objective To study the composition and concentration of atmospheric particulate pollutants in four seasons in the industrial and clean living areas， and to provide a scientific basis for the strategy of controlling industrial pollution and atmospheric environment. Methods An industrial area dominated by the automobile industry in Shanghai and a relatively clean living area were selected. Samples were collected simultaneously in both areas and continuously for 7 days in the middle of each season. The composition and concentration of PM_2.5 were determined， and the ecological risk of heavy metals in PM_2.5 was evaluated by the potential ecological risk index method. Results We found PM_2.5 concentration was associated with seasonal changes. The PM_2.5 concentration in living areas was the highest in winter， followed by spring， and the lowest in summer. The PM_2.5 concentration in industrial areas was the highest in spring， followed by winter， and the lowest in summer. The heavy metals in PM_2.5 were the same， including Al， Cr， Mn， Ni， As， Cd， Hg and Pb. The content of Cr， Cd and Pb in PM_2.5 in the industrial area is significantly higher than that in the living area. The potential ecological hazard coefficient of PM_2.5 heavy metal Cd in the industrial zone was the highest， up to 189.47， and it was the main component of the total potential ecological hazard index of heavy metals. According to the total potential risk grade of heavy metals， the heavy metal Cd in the industrial area had different degrees of ecological harm with seasonal changes. The ecological harm degree of heavy metal Cd was the highest in winter， high in spring and autumn， and low in summer. Conclusion Although the concentration of PM_2.5 in the industrial area is not higher than that in the living area， the content of Cr， Cd and Pb in the PM_2.5 in the industrial area is significantly higher than that in the living area. The concentration of PM_2.5 in the industrial area is mainly related to seasons， industrial production and human factors. The potential ecological harm coefficient of heavy metal Cd in PM_2.5 is the highest in comparison with other heavy metals such as Cr， Hg and Pb， and it is the main component of the total potential ecological harm index ofheavy metals.

OBJECTIVES: Percutaneous coronary intervention (PCI) is one of the important methods for the treatment of coronary artery disease (CAD). In-sent restenosis (ISR) after PCI for patients suffered from CAD is considered to be an essential factor affecting long-term outcomes and prognosis of this disease. This study aims to investigate the correlation between plasma Quaking (QKI) and cyclooxygenase-2 (COX-2) levels and ISR in patients with CAD. METHODS: A total of 218 consecutive CAD patients who underwent coronary angiography and coronary arterial stenting from September 2019 to September 2020 in the Department of Cardiology of Xiangya Hospital of Central South University were enrolled in this study, and 35 matched individuals from the physical examination center were served as a control group. After admission, clinical data of these 2 groups were collected. Plasma QKI and COX-2 levels were measured by enzyme linked immunosorbent assay (ELISA). Follow-up angiography was performed 12 months after PCI. CAD patients were divided into a NISR group (n=160) and an ISR group (n=58) according to the occurrence of ISR based on the coronary angiography. The clinical data, coronary angiography, and stent features between the NISR group and the ISR group were compared, and multivariate logistic regression was used to explore the factors influencing ISR. The occurrence of major adverse cardiovascular events (MACE) 1 year after operation was recorded. Fifty-eight patients with ISR were divided into an MACE group (n=24) and a non-MACE group (n=34), classified according to the occurrence of MACE, and the plasma levels of QKI and COX-2 were compared between the 2 groups. Receiver operating characteristic (ROC) curves were utilized to analyze the diagnostic value of plamsa levels of QKI and COX-2 for ISR and MACE occurrences in patients after PCI. RESULTS: Compared with control group, plasma levels of QKI and COX-2 in the CAD group decreased significantly (all P<0.001). Compared with the NISR group, the plasma levels of QKI and COX-2 also decreased obviously in the ISR group (all P<0.001), while the levels of high sensitivity C-reactive protein (hs-CRP) and glycosylated hemoglobin (HbAlc) significantly increased (all P<0.001). The level of COX-2 was negatively correlated with hs-CRP (r=-0.385, P=0.003). Multivariate logistic regression analysis showed that high level of plasma QKI and COX-2 were protective factors for in-stent restenosis after PCI, while hs-CRP was a risk factor. ROC curve analysis showed that the sensitivity and specificity of plasma QKI for evaluating the predictive value of ISR were 77.5% and 66.5%, respectively, and the sensitivity and specificity of plasma COX-2 for evaluating the predictive value of ISR were 80.0% and 70.7%, respectively. The sensitivity and specificity of plasma QKI combined with COX-2 for evaluating the predictive value of ISR were 81.3% and 74.1%, respectively. The sensitivity and specificity of plasma QKI for evaluating the prognosis of ISR were 75.0% and 64.7%, respectively. The sensitivity and specificity of plasma COX-2 for evaluating the prognosis of ISR were 75.0% and 70.6%, respectively. The sensitivity and specificity of plasma QKI combined with COX-2 for prognostic evaluation of ISR were 81.7% and 79.4%, respectively. The sensitivity and specificity of plasma COX-2 combined with QKI for evaluating ISR and MACE occurrences in patients after PCI were better than those of COX-2 or QKI alone (P<0.001). CONCLUSIONS High level of plasma QKI and COX-2 might be a protective factor for ISR, which can also predict ISR patient's prognosis.
C-Reactive Protein/analysis* ; Constriction, Pathologic/etiology* ; Coronary Angiography/adverse effects* ; Coronary Artery Disease ; Coronary Restenosis/therapy* ; Cyclooxygenase 2 ; Humans ; Percutaneous Coronary Intervention/adverse effects* ; Risk Factors ; Stents/adverse effects*

AIM: In order to bridge the gap between pharmacogenomic research and its clinical application, we propose the concept of genetic electronic identity, named "GeneFace", and developed an electronic information system which integrated "drug-gene" interactions and recommendations for personalized medicine. METHODS: Based on the self-developed Precision Medicine knowledgebase, which concludes drug directions, guidelines or important literatures with high level of evidence, we developed GeneFace with Java-based open-resource application framework Spring Boot, further developed a mobile App with cross-platform framework Uni-APP. RESULTS: The App includes six modules: genetic testing appointment, genetic knowledge introduction, individualized medication advice, medication records, Geneface interpretation, and Precision Medicine knowledgebase. By detecting the genotype of more than 300 gene loci upon first use, users import the results to form a personal "drug-gene identity card". Then scan or enter the drug name in "GeneFace", the App would automatically give corresponding medication recommendations, including: risks for possible adverse drug reactions, risks for reducing the efficacy or even ineffectiveness, and possibility for dose adjustment, etc., which increase the safety of clinical drug use. People can obtain pharmacogenomics knowledge and basic drug information in the "GeneFace" app. CONCLUSION: Development as a digital therapeutic product, the expanded application of GeneFace can rapidly promote clinical applications of basic pharmacogenomics research and significantly improve drug use safety, which creating a new model for accelerating the clinical application of personalized medicine.