Objective To study the genes which simultaneously participate in different carcinogenesis progression in lung adenocarcinoma for biomarkers identification. Methods 10 lung adenocarcinoma samples including pathologic stage Ⅰ,Ⅱ,Ⅲ were chosen for experiment and their matched normal tissues for control. After hybridization on 20 slides of microarray with 13824 genes, we analyze the expression profiles combined with pathologic stage and clinical prognosis by data mining. The genes differentially coexpressed in different stage and different prognosis samples were the target. Results 119 genes were identified. Among these targets, 26 genes have known to be related to lung cancer, 46 genes were unreported and 47 gene were new. Conclusions The 119 genes were very important during cancer occurrence and development and were the candidate biomarkers in lung adenocarcinoma.

Objective To observe the effect of astaxanthin on radiotherapy sensitivity of lung cancer A549 cells transplanted in nude mice. Methods Twenty BALB/c nude mice were divided into four groups:control group (mice were gavaged with pure water containing with 10% DMSO), astaxanthin group (mice were gavaged with astaxanthin suspension containing with 10%DMSO, astaxanthin was given to mice with the dose of 50 mg/kg on the first day, and every other day in the following days with a total of 7 times), radiotherapy group (mice were gavaged with pure water containing with 10%DMSO, the tumor site was given local radiotherapy with a dose of 5 Gy per time and the total dose was 15 Gy) and combination group (mice were given 50 mg/kg astaxanthin and radiotherapy with 15 Gy total irradiated dose). When the minor axis of the tumor reached 5 mm we began experiment. Tumor growth curve was measured by detecting the line of apsides every other day. Mice were killed on the second day after the last time of astaxanthin administration. Weights of tumor were measured by a balance and then tumor mass was processed into paraffin sections. Expressions of proliferating tumor cell antigen Ki-67, phosphorylated-signal transducers and activators of transcription (p-STAT3), and cell apoptosis (measured by terminal deoxynucleotidyl transferase mediated dUTP nick- end labeling, Tunnel) were detected by immunohistochemistry. Results Compared with control group, the transplanted tumor growth rate slowed down in other three groups (P<0.05), and tumor growth was the most slowly in the combination group. Tumor weight, Ki-67 and p-STAT3 expressions were decreased gradually in turn in control group, astaxanthin group, radiotherapy group and combination group. The anti-tumor rate and percentage of cell apoptosis were increased gradually in turn. There was significant difference between groups by multiple comparison statistics(P<0.05). Conclusion Astaxanthin enhances radiotherapy sensitivity of human lung cancer A549 cells in nude mice by down-regulating the expression of p-STAT3.

Objective To explore the efficacy of noninvasive continuous positive airway pressure (nCPAP) on infants with degree Ⅲ laryngeal obstruction.Methods Sixty-two infants of acute laryngitis with degree Ⅲ laryngeal obstruction were divided into observation group (n =32) and control group (n =30),which were admitted to our PICU from Jan 2007 to Dec 2012.Thirty-two cases in the observation group were treated using the nCPAP.Thirty infants in the control group received regular mouth-nose mask oxygen therapy.The infants in both groups were given small-dose intravenous injection of methylprednisolone and inhalation of oxygen-driven nebulized epinephrine.Results In a hour after treatments,the effective rate in observation group was 100％,and the average duration for the treatments to take effect was (43.65 ±10.34) min.In control group,symptoms of 13 infants were improved within one hour (the effective rate was 43.3 ％),and symptoms of 22 infants were improved within two hours (the effective rate was 73.3 ％).The average duration for the treatments to take effect in control group was (73.70 ± 15.86) min.The differences of effective rates and take-effect duration between the two groups were statistically significant (P ＜ 0.01).After two hours' treatments,hypoxic symptoms of all infants in the observation group were obviously improved.The average heart rate[(172.24 ± 7.80) times per minute],the average oxygen saturation (90.16％ ±2.58％),the average arterial partial pressure of oxygen [(65.33 ±6.27) mm Hg],and the average partial pressure of carbon dioxide [(48.60 ± 4.39) mm Hg] were improved significantly compared with those before treatment [(146.39 ± 10.61) times per minute,98.53 ％ ± 0.42 ％,(93.64 ± 5.68) mm Hg,(44.25 ±5.76) mm Hg)].The differences were statistically significant (P ＜ 0.01).Conclusion The nCPAP auxiliary treatment is effective for infants with degree Ⅲ laryngeal obstruction,more effective than the regular oxygen therapy.

BACKGROUNDTo explore the experience of gefitinib molecular target therapy for Chinese patients with non-small cell lung cancer (NSCLC).

METHODSThe unpublished data of gefitinib for advanced NSCLC in 7 hospitals were collected. The detailed data from Guangdong Provincial People's Hospital were analyzed.

RESULTSA total of 282 patients with advanced NSCLC was treated with gefitinib from July 2001 to December 2003. Response rate was 22.2%-47.7%, disease control rate 62.6%-81.8%. No severe side effects were surveyed.

CONCLUSIONSGefitinib can be used safely and effectively in Chinese patients with advanced NSCLC.

Carcinoma, Non-Small-Cell Lung ; classification ; therapy ; China ; Humans ; Lung Neoplasms ; classification ; therapy ; Practice Guidelines as Topic ; Receptor Protein-Tyrosine Kinases ; metabolism

Excessive microglial activation and subsequent neuroinflammation lead to synaptic loss and dysfunction as well as neuronal cell death, which are involved in the pathogenesis and progression of several neurodegenerative diseases. Thus, the regulation of microglial activation has been evaluated as effective therapeutic strategies. Although dieckol (DEK), one of the phlorotannins isolated from marine brown alga Ecklonia cava, has been previously reported to inhibit microglial activation, the molecular mechanism is still unclear. Therefore, we investigated here molecular mechanism of DEK via extracellular signal-regulated kinase (ERK), Akt and nicotinamide adenine dinuclelotide phosphate (NADPH) oxidase-mediated pathways. In addition, the neuroprotective mechanism of DEK was investigated in microglia-mediated neurotoxicity models such as neuron-microglia co-culture and microglial conditioned media system. Our results demonstrated that treatment of anti-oxidant DEK potently suppressed phosphorylation of ERK in lipopolysaccharide (LPS, 1 microg/ml)-stimulated BV-2 microglia. In addition, DEK markedly attenuated Akt phosphorylation and increased expression of gp91(phox), which is the catalytic component of NADPH oxidase complex responsible for microglial reactive oxygen species (ROS) generation. Finally, DEK significantly attenuated neuronal cell death that is induced by treatment of microglial conditioned media containing neurotoxic secretary molecules. These neuroprotective effects of DEK were also confirmed in a neuron-microglia co-culture system using enhanced green fluorescent protein (EGFP)-transfected B35 neuroblastoma cell line. Taken together, these results suggest that DEK suppresses excessive microglial activation and microglia-mediated neuronal cell death via downregulation of ERK, Akt and NADPH oxidase-mediated pathways.
Adenine ; Cell Death* ; Cell Line ; Coculture Techniques ; Culture Media, Conditioned ; Down-Regulation ; Microglia ; NADP* ; NADPH Oxidase ; Neuroblastoma ; Neurodegenerative Diseases ; Neurons* ; Neuroprotective Agents ; Niacinamide ; Phosphorylation ; Phosphotransferases ; Reactive Oxygen Species

Mitochondrial calcium overload is a crucial event in determining the fate of neuronal cell survival and death, implicated in pathogenesis of neurodegenerative diseases. One of the driving forces of calcium influx into mitochondria is mitochondria membrane potential (ΔΨ(m)). Therefore, pharmacological manipulation of ΔΨ(m) can be a promising strategy to prevent neuronal cell death against brain insults. Based on these issues, we investigated here whether nobiletin, a Citrus polymethoxylated flavone, prevents neurotoxic neuronal calcium overload and cell death via regulating basal ΔΨ(m) against neuronal insult in primary cortical neurons and pure brain mitochondria isolated from rat cortices. Results demonstrated that nobiletin treatment significantly increased cell viability against glutamate toxicity (100 µM, 20 min) in primary cortical neurons. Real-time imaging-based fluorometry data reveal that nobiletin evokes partial mitochondrial depolarization in these neurons. Nobiletin markedly attenuated mitochondrial calcium overload and reactive oxygen species (ROS) generation in glutamate (100 µM)-stimulated cortical neurons and isolated pure mitochondria exposed to high concentration of Ca²⁺ (5 µM). Nobiletin-induced partial mitochondrial depolarization in intact neurons was confirmed in isolated brain mitochondria using a fluorescence microplate reader. Nobiletin effects on basal ΔΨ(m) were completely abolished in K⁺-free medium on pure isolated mitochondria. Taken together, results demonstrate that K⁺ influx into mitochondria is critically involved in partial mitochondrial depolarization-related neuroprotective effect of nobiletin. Nobiletin-induced mitochondrial K⁺ influx is probably mediated, at least in part, by activation of mitochondrial K⁺ channels. However, further detailed studies should be conducted to determine exact molecular targets of nobiletin in mitochondria.
Animals ; Brain ; Calcium* ; Cell Death ; Cell Survival ; Citrus ; Fluorescence ; Fluorometry ; Glutamic Acid ; Membrane Potential, Mitochondrial ; Membrane Potentials ; Membranes* ; Mitochondria ; Neurodegenerative Diseases ; Neurons ; Neuroprotective Agents ; Rats ; Reactive Oxygen Species