Ectopia Cordis ; surgery ; Humans ; Infant, Newborn ; Male

Objective To evaluate the blood supply features and effectiveness of arterial chemoembolization for pedunculated hepatocellular carcinoma.Methods Angiography and chemoembolization via supplying blood arteries of tumor were performed in five patients with pedunculated hepatocellular carcinoma.Interventional procedure was carried out with tumor vascular infusion of 350 mg hot elemene emulsion and tumor embolization by cisplantin-lipidol emulsion(cisplantin 60-80 mg+lipidol 8-15 ml)and glutin.Results Ten interventional procedures(TACE)were undertaken in 5 patients.Angiography showed that tumor blood supply mainly coming from collateral circulation adjacent to the tumors,but partially from hepatic artery.Tumor sizes decreased from 30% to 50% in 5 cases,and AFP declined in 4 cases after the treatment. Conclusion Pedunculated hepatocellular carcinoma possessing different blood supply features from intrahepatocellular carcinomas.But transarterial ehemoembolization is still an effective method of choice for this treatment.

This study was to investigate the effect of peoniflorin on the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream signal molecules in the hippocampus of Alzheimer's disease (AD) rats for exploring the mechanism of peoniflorin protecting hippocampal neurons. AD model rats were established by bilateral intrahippocampal injection of beta-amyloid(1-42) (Abeta(1-42)) and divided randomly into 3 groups: AD model group, peoniflorin low-dose (15 mg x kg(-1)) group and peoniflorin high-dose (30 mg x kg(-1)) group. The vehicle control rats were given bilateral intrahippocampal injection of solvent with the same volume. After peoniflorin or saline was administered (ip) once daily for 14 days, the hippocampuses of all animals were taken out for measuring the expressions of Nrf2, heme oxygenase-1 (HO-1) and gamma-glutamylcysteine synthethase (gamma-GCS) mRNA by reverse transcription PCR, determining the contents of glutathione (GSH), malondialdehyde (MDA) and carbonyl protein (CP) using colorimetric method, and for assaying the expressions of neuronal apoptosis inhibitory protein (NAIP) and Caspase-3 by immunohistochemical staining method. The results showed that peoniflorin markedly increased the expressions of Nrf2, HO-1 and gamma-GCS mRNA, enhanced the level of GSH and decreased the contents of MDA and CP in the hippocampus, as compared with the model group. Peoniflorin also improved the NAIP expression and reduced the Caspase-3 expression in the hippocampus neurons. In conclusion, peoniflorin protects against the Abeta(1-42)-mediated oxidative stress and hippocampal neuron injury in AD rats by activating the Nrf2/ARE pathway.
Alzheimer Disease ; chemically induced ; metabolism ; physiopathology ; Amyloid beta-Peptides ; Animals ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Caspase 3 ; metabolism ; Glucosides ; pharmacology ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Glutathione ; metabolism ; Heme Oxygenase (Decyclizing) ; genetics ; metabolism ; Hippocampus ; metabolism ; Male ; Malondialdehyde ; metabolism ; Monoterpenes ; pharmacology ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Neuronal Apoptosis-Inhibitory Protein ; metabolism ; Neurons ; metabolism ; Oxidative Stress ; drug effects ; Peptide Fragments ; RNA, Messenger ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Child ; Humans ; Lupus Nephritis ; complications ; Male ; Nephritis, Interstitial ; etiology ; Prognosis

OBJECTIVETo study the influence of human cytomegalovirus (HCMV) infection on cell cycle and the expression of replication licensing factor Cdt1 in human embryonic lung fibroblastic (HEL) cells and to explore the pathogenesis of HCMV infection.

METHODSHEL cells were synchronized in the G0/G1 phase by the serum starvation method. The synchronized HEL cells were infected with HCMV, and those that were not subjected to HCMV infection were used as the control group. The HEL cells were harvested at 12, 24, 48, 72 and 96 hrs of HCMV infection. The cell cycle of HEL cells was detected by the flow cytometry. The expression of Cdt1 mRNA in HEL cells was determined by reverse transcription-polymerase chain reaction (RT-PCR).

RESULTSThe cells in the G1 phase in the control group was significantly more than in the HCMV-infected group 12 and 24 hrs after infection (P < 0.01). The expression of Cdt1 mRNA in the HCMV-infected group was significantly lower 12 and 24 hrs after infection but increased significantly 48 hrs after infection compared with the control group (P < 0.05). The expression of Cdt1 mRNA reached a peak at 12 hrs of infection in the control group, but at 48 hrs of infection in the HCMV-infected group, which markedly lagged behind the control group.

CONCLUSIONSHCMV infection arrests the cell cycle of HEL cells at the G1 phase. HCMV infection makes Cdt1 expression delay. HCMV infection can interfere cell cycle of HEL cells possibly through affecting the expression of Cdt1.

Cell Cycle ; Cell Cycle Proteins ; genetics ; Cells, Cultured ; Cytomegalovirus ; pathogenicity ; Embryo, Mammalian ; cytology ; Fibroblasts ; cytology ; metabolism ; Humans ; Lung ; cytology ; metabolism ; RNA, Messenger ; analysis

The purpose of this study was to determine whether the Ca2+ signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-kappaB ligand (RANKL) to stimulate osteoclastogenesis and then treated with different concentrations of OPG, an inhibitor of osteoclast differentiation. The intracellular Ca2+ concentration [Ca2+]i and phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the different treatment groups were measured by flow cytometry and Western blotting, respectively. The results confirmed that M-CSF + RANKL significantly increased [Ca2+]i and CaMKII phosphorylation in osteoclasts (p < 0.01), and that these effects were subsequently decreased by OPG treatment. Exposure to specific inhibitors of the Ca2+ signaling pathway revealed that these changes varied between the different OPG treatment groups. Findings from the present study indicated that the Ca2+ signaling pathway is involved in both the regulation of osteoclastogenesis as well as inhibition of osteoclast differentiation and activation by OPG.
Animals ; Calcium/*metabolism ; *Calcium Signaling ; *Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Gene Expression Regulation/drug effects ; Macrophage Colony-Stimulating Factor/metabolism ; Mice ; Osteoclasts/*cytology/*drug effects/*metabolism ; Osteoprotegerin/*pharmacology ; RANK Ligand/metabolism

OBJECTIVETo investigate the protective effect of paeonol on amyloid beta1-42 (Abeta1-42)-induced neurotoxicity and its mechanism.

METHODHippocampal neurons of well-grown newborn SD rats and differentiated SH-SY5Y cell lines were cultured with various concentrations of paeonol (1, 5, 10 micromol x L(-1), respectively) for 6 hours and then incubated with Abeta1-42 oligomer (30 micromol x L(-1)) for 24 hours and 48 hours, respectively. The neuron apoptosis was observed by Heochst33258. Annexin V/PI double stain flow cytometry assay was adopted for determining SH-SY5Y cell apoptosis rate. And the expression of BDNF and Bcl-2 mRNA was detected by RT-PCR.

RESULTCompared with the model group, various concentrations of paeonol (1, 5, 10 micromol x L(-1)) significantly reduced the hippocampal neurons karyopycnosis, decreased the rate of SH-SY5Y cell apoptosis to 22.4%, 18.1% and 16.4%, respectively, and improved the expressions of BDNF and Bcl-2 mRNA.

CONCLUSIONPaeonol relieves Abeta1-42 oligomer-induced neuron injury by increasing BDNF and Bcl-2 expressions.

Acetophenones ; pharmacology ; Alzheimer Disease ; drug therapy ; genetics ; metabolism ; physiopathology ; Amyloid beta-Peptides ; toxicity ; Animals ; Apoptosis ; drug effects ; Cell Line ; Cells, Cultured ; Hippocampus ; cytology ; drug effects ; Humans ; Neurons ; drug effects ; Neuroprotective Agents ; pharmacology ; Peptide Fragments ; toxicity ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVEThe aim of this study was to investigate the expression and significance of P311 and ITGB4BP in non-small cell lung cancer (NSCLC).

METHODSTissue microarrays were prepared from 80 NSCLC specimens and examined by immunohistochemistry.

RESULTSThe positive rates of P311 and ITGB4BP expression were 77.5% (62/80) and 82.5% (66/80), respectively. The double positive expression rate was 73.8% (59/80). The consistency rate was 87.5%, and there was a significant consistency between P311 and ITGB4BP expressions (Kappa = 0.611, P < 0.001).

CONCLUSIONThere may be a new signaling pathway P311-ITGB4BP in NSCLC, and it may regulate the lung cancer cell migration.

Adenocarcinoma ; metabolism ; Carcinoma, Non-Small-Cell Lung ; metabolism ; Carcinoma, Squamous Cell ; metabolism ; Eukaryotic Initiation Factors ; metabolism ; Humans ; Immunohistochemistry ; Lung Neoplasms ; metabolism ; Nerve Tissue Proteins ; metabolism ; Oncogene Proteins ; metabolism ; Paraffin Embedding ; Signal Transduction ; Tissue Array Analysis

OBJECTIVETo investigate the cytotoxic mechanism of cadmium (Cd) on cerebral cortical neurons.

METHODSThe primary cultures of rat cerebral cortical neurons were treated with different concentrations of cadmium acetate (0, 5, 10, and 20 micromol/L), and then the cell viability, apoptosis, ultrastructure, intracellular [Ca2+], and reactive oxygen species (ROS) levels, mitochondrial membrane potential (delta psi), activities of catalase (CAT) and superoxide dismutase (SOD) were measured.

RESULTSA progressive loss in cell viability and an increased number of apoptotic cells were observed. In addition, Cd-induced apoptotic morphological changes in cerebral cortical neurons were also demonstrated by Hoechst 33258 staining. Meanwhile, ultrastructural changes were distortion of mitochondrial cristae and an unusual arrangement. Simultaneously, elevation of intracellular [Ca2+]i and ROS levels, depletion of Delta Psi were revealed in a dose-dependent manner during the exposure. Moreover, CAT and SOD activities in the living cells increased significantly.

CONCLUSIONExposure of cortical neurons to different doses of Cd led to cellular death, mediated by an apoptotic mechanism, and the apoptotic death induced by oxidative stress may be a potential reason. And the disorder of intracellular homeostasis caused by oxidative stress and mitochondrial dysfunction may be a trigger for apoptosis in cortical neurons.

Animals ; Apoptosis ; drug effects ; Cadmium ; toxicity ; Cerebral Cortex ; cytology ; drug effects ; metabolism ; In Vitro Techniques ; Neurons ; drug effects ; metabolism ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; metabolism

OBJECTIVETo detect the serum proteomic fingerprints in patients with hypopharyngeal squamous cell carcinoma (HPSCC) by surface enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS) protein chip array technique.

METHODSThe serum samples were obtained from 58 HPSCC patients for protein expression analysis using SELDI-TOF Protein Chip technique and cation-exchange (CM10) protein array. All the spectra were compared and the qualified mass peaks with mass-to-charge ratios (m/z) between 1 and 70 kD were autotimatically detected. The tree analysis pattern was generated using Biomarker Patterns Software.

RESULTSThe protein profiles of HPSCC serum were analyzed according to the clinical and pathological features of the patients and their treatment response. No significant difference was noted in the serum proteins between HPSCC patients with different statuses of cervical lympha node metastasis (P>0.05), and the difference between well differentiated and poorly differentiated HPSCC was only minor. No significant difference was found in the serum proteins between chemotherapy-sensitive patients and the insensitive patients (P>0.05), but 5 proteins were identified to be overexpressed in the sensitive patients (P < / = 0.05). Radiotherapy-sensitive HPSCC patients were segregated from the insensitive group with a sensitivity of 86.67% and specificity of 100%.

CONCLUSIONThe serum protein at the m/z value of 6115.74 is overexpressed in radiotherapy-sensitive HPSCC patients. Serum protein profiling allows the prediction of radiotherapy response in HPSCC patients, and the identified proteins may serve as candidate biomarkers for predicting the radiotherapy sensitivity of HPSCC.

Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor ; analysis ; Carcinoma, Squamous Cell ; genetics ; radiotherapy ; Female ; Humans ; Hypopharyngeal Neoplasms ; genetics ; radiotherapy ; Male ; Middle Aged ; Models, Biological ; Proteome ; analysis ; Radiation Tolerance ; Sensitivity and Specificity ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; methods