Efficacy of Adjuvant Sublingual Immunotherapy After Septomeatoplasty.

BACKGROUND: The efficacy of adjuvant sublingual immunotherapy (SLIT) in correcting structural problems in patients with allergic rhinitis (AR) caused by mite who have undergone septomeatoplasty (SMP) has not been studied. METHODS: This non-randomized controlled study recruited patients with AR (caused by mite) and concurrent septal deviation and inferior turbinate hypertrophy, at a tertiary hospital in Taiwan. SMP was performed on all patients as a surgical intervention. The patients were then divided into two groups: the control group, which underwent surgery only, and the experimental group, which received SLIT as an adjuvant treatment. Demographic data and rhinitis control assessment test (RCAT) results were analyzed. RESULTS: A total of 96 patients were enrolled in the study (SMP + SLIT group, n = 52; SMP only group, n = 44). No significant differences were observed in any of the variables between the two groups before and one month after surgery. However, during evaluations at the third and sixth month, the SMP + SLIT group showed significant improvement in the total RCAT scores compared to the SMP only group (28.6 ± 1.56 vs. 24.5 ± 3.66, p < 0.001; 27.1 ± 2.87 vs. 19.9 ± 5.56, p < 0.001). In addition, significantly better control of all RCAT sub-categories was observed in the SMP + SLIT group at the third and sixth month evaluations. CONCLUSIONS: SLIT may serve as an ideal adjuvant therapy after SMP in patients with AR. LEVEL OF EVIDENCE: Level 3 Laryngoscope, 2024.

Video Didactic Preparation Augments Problem-Based Learning for First Year Medical Students.

Problem-based learning (PBL) utilizes a self-directed strategy. This process relies on group participation to succeed. Students without a background in biology or medicine can feel overwhelmed by the complexity of the subject matter and unable to participate in the group learning process. We incorporated curated educational videos in the PBL curriculum to help address this situation. First year medical students participated in this study in the form of a typical PBL session. They were then assessed on basic and clinical science knowledge and their learning experience. Student basic science and clinical knowledge were similar between the student groups. However, the students given a list of suggested videos scored higher in their learning experience, perception of feeling prepared, and participating in the group PBL experience than students who were not given the video list. Results from this study indicate that videos can be utilized to enhance the PBL process.

An aerosol deposition based MEMS piezoelectric accelerometer for low noise measurement.

Potentially applied in low-noise applications such as structural health monitoring (SHM), a 1-axis piezoelectric MEMS accelerometer based on aerosol deposition is designed, fabricated, simulated, and measured in this study. It is a cantilever beam structure with a tip proof mass and PZT sensing layer. To figure out whether the design is suitable for SHM, working bandwidth and noise level are obtained via simulation. For the first time, we use aerosol deposition method to deposit thick PZT film during the fabrication process to achieve high sensitivity. In performance measurement, we obtain the charge sensitivity, natural frequency, working bandwidth and noise equivalent acceleration of 22.74 pC/g, 867.4 Hz, 10-200 Hz (within ±5% deviation) and 5.6 µ g / Hz (at 20 Hz). To demonstrate its feasibility for real applications, vibrations of a fan are measured by our designed sensor and a commercial piezoelectric accelerometer, and the results match well with each other. Moreover, shaker vibration measurement with ADXL1001 indicates that the fabricated sensor has a much lower noise level. In the end, we show that our designed accelerometer has good performance compared to piezoelectric MEMS accelerometers in relevant studies and great potential for low-noise applications compared to low-noise capacitive MEMS accelerometers.

Mobile learning: Pre-service teachers' perceptions of integrating iPads into future teaching.

This study investigated pre-service teachers' perceptions of using iPads in teaching, with a focus on motivation to adopt iPads, iPad-integration self-efficacy, and intention to adopt iPads for future teaching. Changes of pre-service teachers' perceptions of using iPads over time as well as the relationships of motivation, self-efficacy, and intention for iPad adoption were examined. Participants were pre-service teachers from a university in the northeastern United States. Data were collected using online pre- and post-surveys. Quantitative and qualitative approaches were performed to analyze the data. Results indicated that there were significant changes in pre-service teachers' motivation and intention to adopt iPads before and after their participation in a mobile learning project. Motivation and iPad-integration self-efficacy were significant predictors of pre-service teachers' intention for future adoption. iPad ownership and prior experience with iPad-integrated lesson plans were potential factors that had a significant impact on pre-service teachers' perceptions of using iPads in future teaching. Pre-service teachers' perceived advantages and disadvantages of using iPads were reported and discussed. The findings of this study not only contribute to the understanding of iPad integration among pre-service teachers, but also provide an evidence on the positive influence of iPad-integrated activities on pre-service teachers' perceptions of using iPads for future teaching.

Advanced Medication Alert System Decreased Hospital-Based Outpatient Duplicated Medications: A Longitudinal Hospital Cohort Study.

OBJECTIVES: This study aimed to examine the associations between adoption of an advanced medication alert system and decreases in hospital-based outpatient duplicated medication rates in Taiwan. METHODS: The unit of analysis was the hospital. We merged the hospital medication alert system adoption survey data and Taiwan National Health Insurance outpatient claims data. The observation time was 1998 to 2011, divided into 5 periods (T1-T5). The analysis included 216 hospitals, and outcome variable was hospital-based outpatient duplicated medication rates. The system adoption time frame, hospital accreditation level, and number of drugs per prescription were defined as predicted variables. A generalized estimating equation regression model was used. RESULTS: Adoption of the advanced medication alert system gradually increased, such that 100% of medical centers and 84% of regional hospitals, but less than 50% of district hospitals, had systems by T5. The hospital-based outpatient duplicated medication rate continually decreased, from 29.8% to 11.2%. The generalized estimating equation model showed rates of duplicated medications of b = -8.44 at T2 and b = -17.88 at T5 (P < 0.001) compared with T1. Medical centers and regional hospitals demonstrated much lower duplication rates (b = -13.71, b = -6.82; P < 0.001) compared with district hospitals. Hospitals with more medications per prescription had higher duplication rates than did hospitals with fewer items. CONCLUSIONS: Hospitals accredited at higher levels tended to have advanced medication alert systems. Hospitals that implemented advanced systems decreased hospital-based outpatient duplicated medications, avoiding a potential risk due to inappropriate medication use.

Polyaniline Based Pt-Electrocatalyst for a Proton Exchanged Membrane Fuel Cell.

Calcination reduction reaction is used to prepare Pt/EB (emeraldine base)-XC72 (Vulcan carbon black) composites as the cathode material of a proton exchange membrane fuel cell (PEMFC). The EB-XC72 core-shell composite obtained from directly polymerizing aniline on XC72 particles is able to chelate and capture the Pt-ions before calcination. X-ray diffraction spectra demonstrate Pt particles are successfully obtained on the EB-XC72 when the calcined temperature is higher than 600 °C. Micrographs of TEM and SEM illustrate the affluent, Pt nanoparticles are uniformly distributed on EB-XC72 at 800 °C (Pt/EB-XC72/800). More Pt is deposited on Pt/EB-XC72 composite as temperatures are higher than 600 °C. The Pt/EB-XC72/800 catalyst demonstrates typical type of a cyclic voltammograms (C-V) curve of a Pt-catalyst with clear Pt-H oxidation and Pt-O reduction peaks. The highest number of transferred electrons during ORR approaches 3.88 for Pt/EB-XC72/800. The maximum power density of the single cell based on Pt/EB-XC72/800 reaches 550 mW cm-2.

Adoption of medication alert systems in hospital outpatient departments in Taiwan.

OBJECTIVE: The adoption of medication alert systems in the health care sector varies among regions. In Taiwan, the health authority introduced policies in 2005 to encourage the adoption of medication alert systems in hospitals. This study aimed to understand the adoption of medication alert systems in the outpatient departments of hospitals in Taiwan using a nationwide survey. METHODS: A questionnaire was developed and mailed to 380 accredited general hospitals in Taiwan in 2013. The information collected from the questionnaire concerning the outpatient department included (1) the time of adoption of a medication alert system; (2) the operation of individual alert functions: availability, management, and stability; and (3) hospital characteristics: accreditation level, teaching status, ownership, and number of beds. RESULTS: A total of 216 hospitals completed and returned the questionnaire, corresponding to a response rate of 56.8%. The adoption rate of medication alert systems in hospital outpatient departments increased from less than 10% in 1997-95.83% in 2012. Approximately two-thirds of the hospitals developed and maintained the alert systems independently or collaboratively with vendors. Teaching and large hospitals tended to develop more advanced alert functions such as drug-drug interaction functions. Improving the safety and quality of pharmaceutical services and meeting the policy requirements are reasons for hospitals to establish medication alert systems. CONCLUSION: The adoption rate of medication alert systems reached 95% in accredited general hospitals in Taiwan. Government policy and available health information professionals and vendors may somewhat contribute to the high adoption rate.

Interleukin-24 as a target cytokine of environmental aryl hydrocarbon receptor agonist exposure in the lung.

Exposure to environmental aryl hydrocarbon receptor (AhR) agonists, such as halogenated aromatic hydrocarbons and polycyclic aromatic hydrocarbons (PAHs), has great impacts on the development of various lung diseases. As emerging molecular targets for AhR agonists, cytokines may contribute to the inflammatory or immunotoxic effects of environmental AhR agonists. However, general cytokine expression may not specifically indicate environmental AhR agonist exposure. By comparing cytokine and chemokine expression profiles in human lung adenocarcinoma cell line CL5 treated with AhR agonists and the non-AhR agonist polychlorinated biphenyl (PCB) 39, we identified a target cytokine of environmental AhR agonist exposure of in the lungs. Thirteen cytokine and chemokine genes were altered in the AhR agonists-treated cells, but none were altered in the PCB39-treated cells. Interleukin (IL)-24 was the most highly induced gene among AhR-modulated cytokines. Cotreatment with AhR antagonist completely prevented IL-24 induction by AhR agonists in the CL5 cells. Knockdown AhR expression with short-hairpin RNA (shRNA) significantly reduced benzo[a]pyrene (BaP)-induced IL-24 mRNA levels. We further confirmed that gene transcription, but not mRNA stability, was involved in IL-24 upregulation by BaP. Particulate matter (PM) in the ambient air contains some PAHs and is reported to activate AhR. Oropharyngeal aspiration of PM significantly increased IL-24 levels in lung epithelia and in bronchoalveolar lavage fluid of mice 4weeks after treatment. Thus, our data suggests that IL-24 is a pulmonary exposure target cytokine of environmental AhR agonists.

Herbal supplement attenuation of cardiac fibrosis in rats with CCl4-induced liver cirrhosis.

Previously we found carbon tetrachloride (CCl4) induced cirrhosis associated cardiac hypertrophy and apoptosis. The purpose of this study is to determine whether further CCl4 treatment would induce cardiac cell fibrosis. The cardiac tissues were analyzed by H&E. histological staining, Trichrome Masson staining and Western blotting. The results showed that the CCl4-treated-only group exhibits more trichrome staining, meaning that more fibrosis is present. Moreover, CCl4 could further induce cardiac-fibrosis via TGF-ß-p-Smad2/3-CTGF pathway. However, our data showed that the CCl4- indcued cardiac abnormalities were attenuated by Ocimum gratissimum extract (OGE) and silymarin co- treatments. In conclusion, our results indicated that the OGE and silymarin may be a potential traditional herb for the protection of cardiac tissues from the CCl4 induced cirrhosis associated cardiac fibrosis through modulating the TGF-ß signaling pathway.

Herbal Supplement Ameliorates Cardiac Hypertrophy in Rats with CCl(4)-Induced Liver Cirrhosis.

We used the carbon tetrachloride (CCl(4)) induced liver cirrhosis model to test the molecular mechanism of action involved in cirrhosis-associated cardiac hypertrophy and the effectiveness of Ocimum gratissimum extract (OGE) and silymarin against cardiac hypertrophy. We treated male wistar rats with CCl(4) and either OGE (0.02 g/kg B.W. or 0.04 g/kg B.W.) or silymarin (0.2 g/kg B.W.). Cardiac eccentric hypertrophy was induced by CCl(4) along with cirrhosis and increased expression of cardiac hypertrophy related genes NFAT, TAGA4, and NBP, and the interleukin-6 (IL-6) signaling pathway related genes MEK5, ERK5, JAK, and STAT3. OGE or silymarin co-treatment attenuated CCl(4)-induced cardiac abnormalities, and lowered expression of genes which were elevated by this hepatotoxin. Our results suggest that the IL-6 signaling pathway may be related to CCl(4)-induced cardiac hypertrophy. OGE and silymarin were able to lower liver fibrosis, which reduces the chance of cardiac hypertrophy perhaps by lowering the expressions of IL-6 signaling pathway related genes. We conclude that treatment of cirrhosis using herbal supplements is a viable option for protecting cardiac tissues against cirrhosis-related cardiac hypertrophy.

Enhancement between environmental tobacco smoke and arsenic on emphysema-like lesions in mice.

Chronic obstructive pulmonary diseases (COPD) have been the major cause of mortality worldwide. Early identification of populations at risk allows us to prevent the occurrence and to reduce the cost of health care. In human studies, exposure to environmental tobacco smoke (ETS) and arsenic respectively increased the risk of chronic lung diseases, including COPD. We suspected that ETS and arsenic might enhance the risk of COPD. In our present study, we evaluated this hypothesis in mice and tried to identify early biomarkers for chemicals-induced lung lesions. Mice inhaled ETS and/or administrated arsenite via gavage for 4 weeks. At the end of experiment, exposure to ETS or arsenite alone failed to cause lung lesions or inflammation. However, co-exposure to ETS and arsenite significantly induced emphysema-like lesions, characterized with enlarged alveolar spaces and destruction of alveolar structure, although inflammation was not observed. Furthermore, co-exposure to ETS and arsenite significantly increased plasma 8-oxodeoxyguanosine (8-OHdG) levels. Our results indicated that co-exposure to ETS and arsenite induced emphysematous lesions, and plasma 8-OHdG might serve as an early biomarker for co-exposure of ETS and arsenite. With information about ETS and arsenic exposure in human populations, plasma 8-OHdG will help us to identify individuals at risk.

Synergism between 2,3,7,8-tetrachlorodibenzo-p-dioxin and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone on lung tumor incidence in mice.

Although 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is classified as a human carcinogen, TCDD only induced oxidative DNA damages. In our present study, we combined TCDD with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) to investigate their tumorigenic effects on lung tumor formation in A/J mice. Application of NNK at a tumorigenic dose (2 mg/mouse) induced lung adenoma in both male and female A/J mice. Neither application of NNK at a non-tumorigenic dose (1 mg/mouse) nor repeated application of TCDD alone increased tumor incidence. Following the single injection of NNK at a non-tumorigenic dose (1 mg/mouse), repeated application of TCDD significantly increased the lung tumor incidence in female, but not in male, A/J mice 24 weeks later. Utilizing the real-time RT-PCR array, we found that P16 mRNA was significantly reduced in female lung, but not male lung, of NNK/TCDD co-treated A/J mice. With immunohistochemical staining, we confirmed that nuclear P16 protein was reduced in the lungs of NNK/TCDD co-treated female mice. These data suggest that P16 reduction at least partially contributed to synergistic effects of TCDD in lung tumorigenesis.

Dementia care costs and the patient's quality of life (QoL) in Taiwan: home versus institutional care services.

Organizing optimal care for demented older people is a complex health care issue. Controversies of service models for demented patients should be balanced between cost of care, placement, and quality of life (QoL). The main purpose of this study was to explore the optimal model of dementia care in Taiwan by evaluating the care cost, patients' QoL and healthcare settings. Overall, 140 pairs of demented patients and their primary informal caregivers were enrolled (89 community-living and 51 institute-living). Compared to institute-living subjects, community-living subjects were significantly better in cognition, physical function and QoL. The annual direct cost of institutional care was significantly higher than community care (464,193 New Taiwanese Dollar (NTD) vs. 144,047 (NTD), p<0.001), but indirect cost was significantly higher in home care (287,904 NTD vs. 35,665 NTD, p<0.001). The care cost of home care subjects with low physical dependence was significantly lower than institutional care subjects, but the care cost of home care subjects with high physical dependence was significantly higher than institutional care subjects. Physical dependence was the significant determinant of QoL for demented patients in this study. In conclusion, demented patients with low physical dependence may be cared in the communities with support and those who had high physical dependence may be cared in the institutes in terms of the balance of QoL and the care cost.

Effect of taurine supplementation on cytochrome P450 2E1 and oxidative stress in the liver and kidneys of rats with streptozotocin-induced diabetes.

To investigate whether diabetes-induced alterations of CYP2E1 and oxidative stress can be modulated by dietary taurine supplementation, male Wistar rats were divided into non-diabetic, diabetic, and diabetic taurine-supplemented groups (administered at 2% in the drinking water). Increased levels of CYP2E1-catalyzed p-nitrophenol hydroxylation were found in liver and kidney microsomes of rats with STZ-induced diabetes compared to those of non-diabetic control rats. Immunoblot and RT-PCR analyses of CYP2E1 protein and mRNA levels in the liver and kidneys showed the same trend as with enzyme activities. Taurine supplementation significantly decreased the enzyme activity and expression (protein and mRNA) of CYP2E1 in diabetic rat kidneys. Plasma beta-hydroxybutyrate concentration was significantly reduced in taurine-treated diabetic rats. The induction of heme oxygenase-1 mRNA was suppressed by taurine treatment in diabetic rat kidneys. An increase in reduced glutathione (GSH) and a higher ratio of reduced to oxidized glutathione (GSH/GSSG) together with lower values of thiobarbituric acid-reactive substances (TBARS) were observed in the kidneys of taurine-treated diabetic rats. However, taurine supplementation caused only a slight or insignificant effect on these alternations in the liver of diabetic rats. Our results show dietary taurine may reduce CYP2E1 expression and activity, and oxidative stress in kidneys of diabetic rats.

Aryl hydrocarbon receptor activation and overexpression upregulated fibroblast growth factor-9 in human lung adenocarcinomas.

We had previously reported that aryl hydrocarbon receptors (AhRs) are overexpressed in lung adenocarcinomas. Benzo[a]pyrene (BaP), an AhR agonist, increased FGF-9 expression in human lung adenocarcinoma cells. Similarly, several AhR agonists increased FGF-9 mRNA levels, and BaP-induced FGF-9 expression was prevented by cotreatment with AhR antagonist in human lung adenocarcinoma cells. Furthermore, AhR agonists increased transcriptional activity of FGF-9 promoter. Modulation of AhR expression via RNA interference or transient overexpression respectively reduced or increased both constitutive and BaP-induced FGF-9 expression in human lung cells. These results suggested that AhR activation and overexpression increased FGF-9 expression in lung cells. FGF-9 increased growth of lung fibroblasts but not that of lung adenocarcinoma cells. However, conditioned media collected from FGF-9-treated fibroblasts increased cell growth of lung adenocarcinoma cells. Furthermore, lung adenocarcinoma cells expressed FGF receptor 2 and cotreatment with anti-FGF receptor 2 prevented the interaction between fibroblasts and tumor cells. It is likely that FGF-9-stimulated fibroblasts secreted unknown factors, which activated FGF receptor 2 and subsequently promoted growth of lung adenocarcinoma cells. We further compared AhR and FGF-9 expression in 146 non-small cell lung cancer (NSCLC) cases by immunohistochemistry. FGF-9 expression was more common in adenocarcinomas than in squamous cell carcinomas. Furthermore, FGF-9 and AhR expression were well correlated in lung adenocarcinomas. These results suggest that AhR expression correlated positively with FGF-9 expression in lung adenocarcinomas, which might promote tumor growth by modulating communication between tumor cells and fibroblasts. Preventing AhR overexpression or disturbing FGF-9 function may reduce the development of lung adenocarcinomas. (c) 2009 UICC.

Computational and ultrastructural toxicology of a nanoparticle, Quantum Dot 705, in mice.

We conducted pharmacokinetic and toxicology studies on Quantum Dot 705 (QD705) in male ICR mice for up to 6 months after a single intravenous dose. Time-course sacrifices were carried out at 1, 4, and 24 h; 3, 7, 14, and 28 days; and 6 months on groups of six mice per time point. Mass balance studies were also carried out at 24 h, 28 days, and 6 months. Using inductively coupled plasma mass spectrometry, various tissues, urine, and feces were analyzed for cadmium (Cd111), which is a major (46%) component of QD705. On the basis of these experimental studies, a physiologically based pharmacokinetic computer simulation model was developed with excellent predictive capability for the time-dependent kinetic and distributional changes of QD705 in tissues. QD705 persisted and accumulated in the spleen, liver, and kidneys for at least 28 days with little or no disposition but was gradually and partially eliminated by 6 months. Although histological alterations of the spleen, liver, and kidney by light microscopy are unremarkable, investigation using electron microscopy on numerous renal samples revealed definitive mitochondrial alterations in renal tubular epithelial cells at 28 days and 6 months postdosing. Health implications and potential beneficial applications of QD705 are suggested.

Persistent tissue kinetics and redistribution of nanoparticles, quantum dot 705, in mice: ICP-MS quantitative assessment.

BACKGROUND: Quantum dots (QDs) are autofluorescent semiconductor nanocrystals that can be used for in vivo biomedical imaging. However, we know little about their in vivo disposition and health consequences. OBJECTIVES: We assessed the tissue disposition and pharmacokinetics of QD705 in mice. METHODS: We determined quantitatively the blood and tissue kinetics of QD705 in mice after single intravenous (iv) injection at the dose of 40 pmol for up to 28 days. Inductively coupled plasma-mass spectrometry (ICP-MS) measurement of cadmium was the primary method of quantification of QD705. Fluorescence light microscopy revealed the localization of QD705 in tissues. RESULTS: Plasma half-life of QD705 in mice was short (18.5 hr), but ICP-MS analyses revealed QD705 persisted and even continued to increase in the spleen, liver, and kidney 28 days after an iv dose. Considerable time-dependent redistribution from body mass to liver and kidney was apparent between 1 and 28 days postdosing. The recoveries at both time points were near 100%; all QD705s reside in the body. Neither fecal nor urinary excretion of QD705 was detected appreciably in 28 days postdosing. Fluorescence microscopy demonstrated deposition of QD705 in the liver, spleen, and kidneys. CONCLUSION: Judging from the continued increase in the liver (29-42% of the administered dose), kidney (1.5-9.2%), and spleen (4.8-5.2%) between 1 and 28 days without any appreciable excretion, QD705 has a very long half-life, potentially weeks or even months, in the body and its health consequences deserve serious consideration.

Ellipticine induces apoptosis through p53-dependent pathway in human hepatocellular carcinoma HepG2 cells.

Ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole), one of the simplest naturally occurring alkaloids, was isolated from the leaves of the evergreen tree Ochrosia elliptica Labill (Apocynaceae). Here, we reported that ellipticine inhibited the cell growth of human hepatocellular carcinoma cell line HepG2 and provided molecular understanding of this effect. The XTT assay results showed that ellipticine decreased the cell viability of HepG2 cells in a dose- and time-dependent manner, and the IC50 value was 4.1 microM. Furthermore, apoptosis induction by ellipticine in HepG2 cells was verified by the appearance of DNA fragmentation and annexin V-FITC/propidium iodide (PI) staining assay. Ellipticine treatment was found to result in the upregulation of p53, Fas/APO-1 receptor and Fas ligand. Besides, ellipticine also initiated mitochondrial apoptotic pathway through regulation of Bcl-2 family proteins expression, alteration of mitochondrial membrane potential (DeltaPsim), and activation of caspase-9 and caspase-3. Taken together, ellipticine decreased the cell growth and induced apoptosis in HepG2 cell.

The anti-proliferative inhibition of ellipticine in human breast mda-mb-231 cancer cells is through cell cycle arrest and apoptosis induction.

Ellipticine, a cytotoxic plant alkaloid, is known to inhibit topoisomerase II. Here we report the mechanism of apoptosis induction and cell cycle arrest by ellipticine in human breast MDA-MB-231 cancer cells. Ellipticine treatment arrested MDA-MB-231 cells at the G2/M phase after 6 h of treatment. This effect was strongly associated with a concomitant decrease in the level of cyclin B1, Cdc25 and Cdc2, and increase in phospho-Cdc2 (Tyr15). In addition, ellipticine also induced apoptosis in MDA-MB-231 cells, as determined by using both DNA fragmentation and Annexin-V staining assay. Ellipticine increased the expression of Bax, but decreased the level of Bcl-2, Bcl-XL and X-linked inhibitor of apoptosis protein (XIAP), and subsequently triggered the mitochondrial apoptotic pathway (release of cytochrome c, and activation of caspase-9 and -3). In addition, pre-treatment of cells with caspase-9 inhibitor inhibited ellipticine-induced cell proliferation and apoptosis, indicating that caspase-9 activation was involved in MDA-MB-231 cell apoptosis induced by ellipticine. Taken together, our study suggests that the inhibition of cell cycle progression signaling and initiation of the mitochondrial apoptotic system may participate in the anti-proliferative activity of ellipticine in MDA-MB-231 cells.

Apoptotic effects of extract from Antrodia camphorata fruiting bodies in human hepatocellular carcinoma cell lines.

The fruiting body of Antrodia camphorata is well known in Taiwan as a traditional medicine for treating cancer and inflammation. The purpose of this study was to evaluate the apoptotic effects of ethylacetate extract from A. camphorata (EAC) fruiting bodies in two human liver cancer cell lines, Hep G2 and PLC/PRF/5. Treatment with EAC decreased the cell growth of Hep G2 and PLC/PRF/5 cells in a dose dependent manner. In Fas/APO-1 positive-Hep G2 cells, EAC increased the expression level of Fas/APO-1 and its two forms of ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), in a p53-indenpendent manner. In addition, EAC also initiated mitochondrial apoptotic pathway through regulation of Bcl-2 family proteins expression, release of cytochrome c, and activation of caspase-9 both in Hep G2 and PLC/PRF/5 cells. Furthermore, EAC also inhibited the cell survival signaling by enhancing the amount of IkappaBalpha in cytoplasm and reducing the level and activity of NF-kappaB in the nucleus, and subsequently attenuated the expression of Bcl-X(L) in Hep G2 and PLC/PRF/5 cells. EAC therefore decreased the cell growth and induced apoptosis both in Hep G2 and PLC/PRF/5 cells.