Objective: To investigate the value of CT radiomics model for predicting pathologic types of adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and invasive adenocarcinoma (IAC) among lung adenocarinoma. Methods: Data of 542 patients with pathologically confirmed lung adenocarcinoma and clear subtypes were retrospective analyzed. AIS and MIA were classified as group 1 while IAC as group 2. The gender and age were compared between 2 groups. Feature extraction software was used to extract three-dimensional texture feature parameters of each lesion, and the imaging omics features obviously different between 2 groups were retained, then the optimal imaging omics features were selected to build a predictive model. All the data were divided into training set and validation set in a ratio of 2: 1. Six machine learning algorithms were used to classify the five-fold cross-training sets to select the best classifier. Then, the five-fold cross-training data set, training set and validation set were analyzed with the prediction model to obtain the ROC curves of the model in predicting pathological subtypes of lung adenocarcinoma as well as the relative AUC, accuracy, specificity and sensitivity. Results: There were 235 patients in group 1 and 307 in group 2. No statistical difference of gender nor age was found between 2 groups (χ2=0.56, t=-0.19, P=0.63, 0.98). A total of 1 766 three-dimensional texture feature parameters were extracted from the lesions, including 988 imaging omics features significantly different between 2 groups. Finally, 10 optimal imaging omics features were retained to construct the prediction model. Perceptron classifier was the best classifier. AUC of the predictive model in predicting pathological subtypes of validation set was 0.95, and the relative accuracy, specificity and sensitivity was 0.88, 0.87 and 0.84, respectively. Conclusion: CT radiomics medel could effectively predict pathological subtypes of AIS, MIA and IAC among lung adenocarcinoma.

Objective To investigate the effect and the possible mechanism of osthole on proliferation and apopotosis of human cervical carcinoma Hela cells and its passible mechanism.Methods After cervical carcinoma Hela cells were incubated with different concentrations osthole,the cell proliferation activity was examined by MTT assay.The apoptosis rate and cellular ROS level were measured by flow cytometry.The Bcl-2 and Bax mRNA expression was determined by semi-quantitative RT-PCR.Results In comparison with the control group,osthole with different concentrations could obviously inhibit the Hela cells proliferation and accelerated the cellular apoptosis,lowered the expression rate of Bcl-2/Bax,raise the cellular ROS level in a osthole dose-dependent manner.Conclusion Osthole may inhibit Hela cell proliferation and accelerates the cells apoptosis,which might be associated with the increasing the cellular ROS level,promoting Bax expression and inhibiting Bcl-2 expression.

AIM: To study the effect of fructose-1, 6-diphosphate (FDP) on adriamycin(ADM)-induced cardiomyocyte apoptosis in rats. METHODS: Twenty-four Wistar rats were randomly divided into three groups: control group, ADM treated group and FDP intervention group. The contents of malondialdehyde (MDA) and NO - 2/NO - 3, the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were determined by colorimetric method in myocardial tissue, and the cardiomyocyte apoptosis was detected by TUNEL method in myocardial tissue, and the expression of inducible nitric oxide synthase (iNOS) mRNA, Bcl-2 mRNA and Bax mRNA in myocardial tissue were detected by in situ hybridization. RESULTS: The contents of NO - 2/NO - 3 and MDA in myocardial tissue, the expressive levels of iNOS mRNA and Bax mRNA in cardiomyocyes and its apoptotic amounts in FDP intervention group were significantly lower than those in ADM treated group ( P

Objective To investigate the effect of endoplasmic reticulum stress (ER stress) in cisplatin-induced apoptosis of human cervical cancer HeLa cells. Methods HeLa cells were used as the study object which were divided into four groups: TUNI (5mg/L) group, cisplatin (6mg/L) group, TUNI(5mg/L)+cisplatin(6mg/L) group, and negative control group (no drug treatment). MTT assay was employed to examine the growth status of the cells. Hoechst staining was used to observe the morphological change in the nucleus. Immunoblotting was used to detect the activation of apoptotic proteins, caspase-3 and caspase-4. Indirect immunofluorescence was used to assess the expression of the protein disulfide isomerase (PDI) and phosphorylated histone H2AX (γ-H2AX). Results MTT assay showed that the growth inhibition rates were 2.65%±2.71%, 19.60%±4.34%, 44.69%±7.07% and 0% in TUNI group, cisplatin group, TUNI+cisplatin group and control group, respectively (P<0.05). Cisplatin showed a significant inhibitory effect on the growth of HeLa cells, and TUNI enhanced the effect of cisplatin. Statistical significance was found between TUNI+cisplatin group and cisplatin group (P<0.05). Hoechst staining showed that the fluorescence of the nucleus in control group was weak and well-distributed. At 12h after treatment, the nuclei in some HeLa cells in cisplatin group and TUNI+cisplatin group diminished in size, thus showing dense hyperfluorescence, and some of them were broken. The proportion of karyorrhexis cells in TUNI+cisplatin group (44.5%±5.1%) was significantly higher than that in cisplatin group (22.7%±3.9%, P<0.05). Immunoblotting showed the expressions of activated caspase-3 and caspase-4 were up-regulated obviously in cisplatin group. Compared to cisplatin group, the expressions of those proteins significantly increased in TUNI+cisplatin group (P<0.05). Indirect immunofluorescence staining showed no PDI expression and weak fluorescence was found in control group. PDI proteins presented in granular form, distributing around the nuclei with strong fluorescence were found in TUNI group and cisplatin group. PDI proteins showed obviously stronger fluorescence in a large proportion of cells in TUNI+cisplatin group, and the fluorescence intensity was obviously higher than that in TUNI group and cisplatin group. No expression of γ-H2AX protein was found in the nucleus in either control group or TUNI group. However, obvious green fluorescence was observed in nuclei of a part of cells in cisplatin group and TUNI+cisplatin group, no obvious difference existed between the two groups. Conclusion Heightened ER stress by tunicamycin may increase the apoptosis of HeLa cells induced by cisplatin.

Objective To investigate the effect of Huntingtin-interacting protein1 (HIP1) gene silencing on the proliferation of PC-3 cells in a human androgen-independent prostate tumor. Methods pSlience-shHIP1, a shRNA expression vector targeting HIP1, was constructed and transfected into PC-3 cells by liposome. RT-PCR was adopted to detect the silencing effect of HIP1 gene. Western bloting was then used to confirm the effective target point. Moreover, the scratch assay and growth curve assay were performed to analyze the effect of HIP1 on the proliferation of PC-3 cells. Results The efficiency of HIP1 gene silencing was increased to 83% (P<0.01) after PC-3 cell transfection. Western blotting proved that this genetic fragment was the effective target point for the inhibition of HIP1. The scratch assay and growth curve assay showed that the proliferation of PC-3 cells was inhibited by silencing HIP1 gene. Conclusions The pSilence-HIP1 expression vector can specifically suppress the expression of the HIP1 gene. In addition, HIP1 gene silencing can inhibit the proliferation and migration of PC-3 cells.

Aim To study the effect of S-methylisothiourea(SMT) on adriamy ci n (ADM) induced myocardial lipid peroxidation in rats.Methods T hirty-two Wistar rats were randomly divided into four groups: control group;SMT treated group ( SMT5.0 mg?kg -1,iv,only 1 time);ADM treated group (ADM 5.0 mg?kg -1, ip, only 1 time ); ADM with SMT treated group (the dos ageand method of ADM and SMT were similar to ADM treated group and SMT treated g roup, respectively).24 hour after of administration of the drugs, rats of all t he groups were killed.TBA method, DTNB method, nitrate reductase method, pyrogal lol autoxidation method and hemoglobin-oxidation method were used to determine the contents of lipid peroxide(LPO)and nitric oxide (NO), the activities of glut athione peroxidase (GPx) and superoxide dismutase (SOD) in myocardium, respectiv ely. The level of nitrotyrosine (NT) was determined by immunohistochemical metho d in myocardium.Results SMT significantly reduced the contents of LPO and NO, the activity of inducible nitric oxide synthase (iNOS), the level of NT in myocardium (P0.05).Conclusion SMT can inhibit myocardial lipid peroxidation induced by ADM. The mechanism may be that SMT can selective ly inhibited the activity of iNOS in myocardium induced by ADM, reduce productio n of NO in myocardium, thereby reduce production of peroxynitrite and protect the activities of SOD and GPx in myocardium.

OBJECTIVETo investigate the effect of ultrasonic wave on extracting Konjac Glucomannan(KGM) in Konjac refined powder.

METHODFree reduced sugar in Konjac refined powder was removed and Konjac refined powder in the aqueous solution was processed by ultrasonic wave and KGM content was measured by spectrophotometry.

RESULTKGM content in the Konjac refined powder aqueous solution by ultrasonic process at fixed 40 kHz, 100 W, 30-45 min was equal to that by routine method at 4 h; whereas, by 1 h of ultrasonic process, KGM content was significantly enhanced than that by 4 h of routine method(P < 0.01), enhancement rate was 6.5%. Linearity of standard glucose was good (r = 0.9996) in range of 0.2-1.6 mg. The average recovery was 97.8%, RSD of repeatability was 1.27%.

CONCLUSIONUltrasonic extraction in aqueous solution is a reliable and rapid method that can enhance extraction efficiency of KGM in Konjac refined powder.

Amorphophallus ; chemistry ; Mannans ; analysis ; isolation & purification ; Powders ; Ultrasonics

Small cell lung cancer (SCLC) is a highly malignant tumor with a very poor prognosis; therefore, more effective treatments are urgently needed for patients afflicted with the disease. In recent years, emerging molecular classifications based on key transcription factors of SCLC have provided more information on the tumor pathophysiology, metastasis, immune microenvironment, and acquired therapeutic resistance and reflected the intertumoral heterogeneity of the various SCLC phenotypes. Additionally, advances in genomics and single-cell sequencing analysis have further revealed the high intratumoral heterogeneity and plasticity of the disease. Herein, we review and summarize these recent lines of evidence and discuss the possible pathogenesis of SCLC.
Humans ; Small Cell Lung Carcinoma/genetics* ; Lung Neoplasms/genetics* ; Prognosis ; Genomics ; Phenotype ; Tumor Microenvironment

BACKGROUNDColon cancer is one of the major malignancies worldwide and it still remains resistant to much of the currently available chemotherapy. Downregulation of HGF/c-Met signaling pathway is an emerging therapy for cancer treatment.

METHODSIn this study, the inhibitory effects of c-Met phosphorylation were observed with SU11274 on different colon cancer cell lines in vitro.

RESULTSThe results revealed the significant inhibitory effects of SU11274 on cell proliferation and cell survival, in a time and dose-dependent manner. Furthermore, the inhibitory effects of SU11274 on different subgroups of colon cancer cells via the HGF/c-Met signaling pathway were implicated in this study.

CONCLUSIONThe results suggested the possible selective therapeutic effects of c-Met inhibitor on colon cancer.

Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; drug therapy ; pathology ; Hepatocyte Growth Factor ; pharmacology ; Humans ; Indoles ; pharmacology ; Piperazines ; pharmacology ; Proto-Oncogene Proteins c-met ; antagonists & inhibitors ; physiology ; Signal Transduction ; Sulfonamides ; pharmacology