Aim To compare the cytotoxicity of geni-poside (GS)and its metabolite genipin (GP)on hu-man hepatocelluar HepG2 cells and explore the sub-stance and mechanism of hepatotoxicity induced by Fructus Gardeniae.Methods The cytotoxic effect of GS and GP was analyzed by MTT method;the antioxi-dant enzyme activities of manganese superoxide dis-mutase (Mn-SOD),catalase (CAT)and levels of glu-tathione (GSH)were detected by respective kits;the change of intracellular reactive oxygen species (ROS ) was measured by 2′,7′-dichlorofluorescin diacetate (DCFH-DA)staining method;multiparameter cytotox-icity analysis (cell loss,nuclear size and morphologi-cal changes,DNA content,cell membrane permeabili-ty,mitochondrial membrane potential changes,cyto-chrome C release ) were measured simultaneously by high content screening (HCS)assays.Results No cytotoxicity was found in GS (20~1 000 μmol·L-1 ) groups (P>0.05 ),but GP was found to exert obvi-ous cytotoxic effect,and 50μmol·L-1 GP could obvi-ously inhibit HepG2 cell proliferation (P<0.05 ),and the IC50 value was (450.00 ±26.15)μmol·L-1;GS showed no obvious effects on Mn-SOD, CAT, GSH ,ROS (P >0. 0 5 ),GP could significantly decrease the activity of Mn-SOD,CAT and the level of GSH,and obviously increase the content of ROS (P<0.05 or P <0.01 );treatment with 50,500,1 000μmol·L-1 GP resulted in loss of mitochondrial mem-brane potential,cytochrome C release and increased cell permeability (P<0.05 or P<0.01),500,1 000μmol· L-1 GP could also show abvious nuclear con-densation,increased total nuclear intensity and cell loss (P<0.0 1 ).Opposed with GP,GS had no signif-icant effect on the cytotoxic parameters (P>0.05 ). Conclusion GP is the direct substance of hepatotox-icity induced by Fructus Gardeniae,and the mecha-nism might be associated with oxidative stress,mito-chondria injury and apoptosis.

Objective To evaluate the correlations between CT features and histopathologic subtypes of lung adenocarcinomas presenting as pure ground-glass nodules (pGGN) of 1 cm or less in maximal diameter. Methods CT appearances, pathology and clinical data of 95 patients (97 lesions) who underwent curative resection of lung adenocarcinomas presenting as pGGN≤1 cm in diameter from March 2011 to February 2015 were retrospectively analyzed. Of the 97 lung adenocarcinomas, there were 19 atypical adenomatous hyperplasia (AAH) (19.6%), 31 adenocarcinoma in situ (AIS) (31.9%), 19 minimally invasive adenocarcinoma (MIA) (19.6%) and 28 invasive pulmonary adenocarcinoma (IPA) (28.9%). Fifty (51.5%) were preinvasive (AAH+AIS) and 47 (48.5%) were invasive (MIA+IPA). Lesion size and density were compared among pathologic subtypes using analysis of variance (ANOVA). Lesion size were compared between preinvasive and invasive lesions using 2?independent samples t?test. Lesion location, presence of bubble?like sign, air bronchogram, vessel changes, margin, and tumor?lung interface were compared among histopathologic subtypes using chi?square test. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the cut-off point of size in discriminating preinvasive lesions from invasive lesions. Results Of the 97 lesions, there were no statistically significant differences among histopathologic subtypes in terms of lesion density, presence of bubble?like sign, air?bronchogram, and margin (P>0.05). Mean size of AAH, AIS, MIA and IPA was (0.72 ± 0.19), (0.82 ± 0.14), (0.84 ± 0.11) and (0.85 ± 0.16) cm respectively. There were statistically significant differences among histopathologic subtypes in terms of lesion size (F=3.16, P=0.028). The vessel changes occurred in 2 of AAH, 11 of AIS, 10 of MIA and 17 of IPA. There were statistically significant differences among histopathologic subtypes in terms of vessel changes (χ2=13.22, P=0.004). Lesions with clear tumor?lung interface were in 10 of AAH, 24 of AIS, 17 of MIA, and 26 of IPA. There were statistically significant differences among histopathologic subtypes in terms of tumor?lung interface (χ2=12.67, P=0.005). The optimal cutoff value of lesion size for differentiating preinvasive lesions from invasive lesions was 0.82 cm (sensitivity, 61.7%;specificity, 62.0%). Conclusion Lesion size, vessel changes, and lung?tumor interface may indicate the invasiveness of lung adenocarcinoma presenting as pGGNs of≤1 cm in diameter.

OBJECTIVETo investigate whether myocardial bridging (MB) is an independent risk factor for coronary atherosclerosis proximal to the bridge site in the left anterior descending coronary artery (LAD) in diabetic patients.

METHODSFrom March 2011 to December 2012, 9862 patients with suspected coronary disease underwent coronary computed tomography angiography (CCTA) using a dual-source CT scanner. The baseline clinical characteristics (age, gender, smoking history, presence of hypertension, dyslipidemia, diabetes mellitus, family history of heart attack and body mass index) and the results of CCTA were reviewed. Two radiologists evaluated the MB and coronary atherosclerosis stenosis (CAS) over 50% in the LAD and made a diagnosis by consensus. Significant independent risk factors for CAS were investigated by logistic regression analysis.

RESULTSOf the 2345 patients identified to have diabetes mellitus, 1373 had MB, among whom 827 had coronary atherosclerosis proximal to the bridge site; 972 of the diabetic patients were free of MB, among whom 254 had coronary atherosclerosis at the equivalent site. None of the patients had CAS in the tunneled segment. After adjusted for clinical data, logistic regression analysis showed that MB in the LAD was significantly correlated with coronary atherosclerosis in the proximal LAD in diabetic patient (OR=3.91) and non-diabetic patients (OR=2.69) (P<0.05).

CONCLUSIONIn diabetic patients, atherosclerosis occurred frequently in the segment proximal to MB in the LAD, and MB in the mid-LAD is an independent risk factor for CAS in the proximal LAD.

Angiography ; Atherosclerosis ; Coronary Artery Disease ; Coronary Stenosis ; Diabetes Mellitus ; Humans ; Myocardial Bridging ; Myocardium ; pathology ; Risk Factors

Objective:To observe the lipid-lowering effect of atorvastatin on patients with acute cerebral infarction with different ATP-binding cassette subfamily B member 1(ABCB1) genotypes, and thus to provide clinical research evidence for individual application of atorvastatin in patients with acute cerebral infarction.Methods:From March 2021 to December 2021, 131 patients with acute cerebral infarction admitted to the Department of Neurology of Xuchang Central Hospital were included. The ABCB1 G2677T gene polymorphism rs2032582 of patients was detected by fluorescence staining in situ hybridization.Based on the detection results, patients were divided into GG group, GT group and TT group.All patients were given atorvastatin (20 mg/d) for lipid-lowering treatment.The levels of low density lipoprotein cholesterol(HDL-C), high density lipoprotein cholesterol(HDL-C), total cholesterol(TC)and triglyceride(TG) in serum of patients in the three groups before and 2 months after treatment were recorded and analyzed.The adverse drug reactions in the three groups were recorded. When the serum LDL-C level was less than 1.8 mmol/L, it was considered that the lipid-lowering treatment was effective.The binary Logistic regression analysis was used to explore the influencing factors of atorvastatin lipid lowering therapy.The software of SPSS 25.0 was used for statistical analysis.Results:There were 50 (38.17%), 49 (37.40%) and 32 (24.43%) patients in GG group, GT group and TT group, respectively. The serum TC levels of patients in GG group, GT group and TT group after treatment were (3.47±0.70) mmol/L, (3.59±1.09) mmol/L and (3.48±1.02) mmol/L, respectively, which were lower than those before treatment ((4.27± 0.99) mmol/L, (4.02±0.98) mmol/L and (4.03±1.31) mmol/L), all of which were statistically significant ( t=7.652, 3.092, 5.593, all P<0.01). The serum LDL-C levels in GG group, GT group and TT group after treatment were (1.89±0.53) mmol/L, (2.07±0.92) mmol/L and (1.96±0.79) mmol/L, respectively, which were lower than those before treatment ((2.87±0.92) mmol/L, (2.56±0.89) mmol/L and (2.55±1.11) mmol/L) ( t=9.896, 4.055, 5.980, all P<0.001). The differences of serum LDL-C level before and after treatment in GG group, GT group and TT group were (-0.97±0.69) mmol/L, (-0.50±0.86) mmol/L and (-0.59±0.56) mmol/L, respectively. The difference of serum LDL-C level before and after treatment in the three groups was statistically significant ( F=5.614, P=0.005). The difference of TC, TG and HDL-C before and after treatment was not statistically significant( F=2.783, 0.490, 1.677, all P>0.05). The binary Logistic regression analysis showed that ABCB1 G2677T gene type and staying up late were independent influencing factors for atorvastatin lipid-lowering therapy. The probability of effective lipid-lowering in GT patients with ABCB1 G2677T gene was 27.9% of that in GG patients ( OR=0.279, 95% CI: 0.110-0.709, P=0.007), and the probability of TT type patients was 33.8% of GG type patients ( OR=0.338, 95% CI: 0.121-0.943, P=0.038). The probability of effective lipid-lowering in patients who had the habit of staying up late was 26.4% of the patients who did not stay up late ( OR=0.264, 95% CI: 0.118-0.591, P=0.001). There was no significant difference in the total incidence of adverse drug reactions among the three groups( χ2=0.868, P=0.648). Conclusion:The lipid-lowering effect in patients with GG type of ABCB1 G2677T is better than that of GT type and TT type when atorvastatin is used to treat patients with acute cerebral infarction.