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ABSTRACT: Diallyl sulfide (DAS) is a component of garlic (Alliaceae family). Although diallyl polysulfide has been shown to exhibit anticancer activities, no report explored DAS-affected cell death in human cervical cancer cells in vitro. This study investigated DAS affected on cell-cycle regulation and apoptosis in human cervical cancer Ca Ski cells. DAS at 25-100 μM decreased the viability of Ca Ski cells by increasing G0/G1 phase arrest followed by induction of apoptosis in concentration- and time-dependent effects. Flow cytomteric assay indicated that DAS (75 μM) promoted the production of Ca(2+) accumulation and decreased the level of mitochondrial membrane potential in Ca Ski cells. Western blotting showed that 75 μM of DAS-induced G0/G1 phase arrest was mediated through the increased expression of p21, p27, and p53 with a simultaneous decrease in CDK2, CDK6, and CHK2 expression. The characteristics of apoptosis, such as morphological changes and DNA condensation, altered the ratio of Bax/Bcl-2 and sub-G1 phase occurred in Ca Ski cells after exposure to DAS. Furthermore, DAS induced mitochondrial dysfunction, leading to the release of cytochrome c for causing apoptosis in Ca Ski cells. These findings suggest that DAS might be a potential chemotherapeutic agent for the treatment of cervical cancer.
Nutrition and Cancer 04/2013; 65(3):505-14. · 2.78 Impact Factor
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ABSTRACT: This study evaluated the incidence, nature, and seriousness of adverse drug reactions (ADRs) occurring after AdimFlu-S(®) influenza A (H1N1) vaccination in pregnant women was administered.
This is a retrospective cohort study. Between October 2009 and February 2010, 198 pregnant women who had received the AdimFlu-S(®) influenza A (H1N1) vaccine during pregnancy and 198 age-matched pregnant women who had not received influenza vaccine were included and recorded. The pregnancy outcome and maternal adverse effects were extracted from chart reviews. Infant health status data were followed up until 8 weeks post-partum.
During the observation period of each cohort, four subjects (2.0%) in the exposed group experienced vaccine-related adverse events that were mild in severity. A total of 17 women (8.6%) in the vaccine exposed group and 40 women (20.2%) in the unexposed group underwent at least one adverse effect during their pregnancy. A total of 72 infants (35.6%) in the exposed group and 101 infants (49%) in the unexposed group had at least one adverse event within 8 weeks after they were born (p<0.05). The adverse events experienced by the women and their infants were not increased when the vaccine was administered during the first trimester. There were no significant differences between these two groups with regard to preterm delivery rate and stillbirth rate.
AdimFlu-S (®) influenza A (H1N1) vaccine is safe for pregnant women and their infants.
Vaccine 02/2012; 30(16):2671-5. · 3.77 Impact Factor
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ABSTRACT: Vinorelbine tartrate (VNR), a semi-synthetic vinca alkaloid acquired from vinblastine, has extensively been used as an anticancer agent. However, VNR-induced oxidative damage may cause several side effects, such as venous irritation, vascular pain, and necrotizing vasculitis, thereby repressing clinical treatment efficiency. The molecular mechanisms underlying the induced oxidative stress in endothelial cells are still largely unknown. This study was designed to test the hypothesis that VNR induces oxidative injury through modulation of AMP-activated protein kinase (AMPK) and possible mechanisms were then explored. Human umbilical vein endothelial cells (HUVECs) were treated with VNR (5-0.625 μM) to produce oxidative damage. The VNR-mediated AMPK, PKC, and NADPH oxidase expressions were investigated by western blotting. Furthermore, several oxidative stress-induced oxidative damage markers as well as pro-inflammatory responses were also investigated. VNR treatment resulted in dephosphorylation of AMPK, which in turn led to an activation of NADPH oxidase by PKC; however, the phenomena were repressed by AICAR (an agonist of AMPK). Furthermore, VNR suppressed Akt/eNOS and enhanced p38 mitogen-activated protein kinase (MAPK), which in turn activated the NF-κB pathway. Furthermore, VNR facilitated several pro-inflammatory events, such as the adherence of monocytic THP-1 cells to HUVECs, pro-inflammatory cytokines release, and overexpression of adhesion molecular. Our results highlight a possible molecular mechanism for VNR-mediated endothelial dysfunction.
Cell biochemistry and biophysics 12/2011; 62(3):467-79. · 3.34 Impact Factor
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ABSTRACT: Epidemic prevention policies in hospitals address issues such as, indoor air quality control, cleanliness of medical staff clothing and employee hand-washing procedures. Our hospital employed Bio-Kil to treat air-conditioning filters and nursing staff uniforms. We also assessed the efficacy of different detergents. Using Bio-Kil technology, the mean bacterial count in the air was reduced from 108.8 CFU/h/plate (n=420) to 68.6 CFU/h/plate (n=630). On the lower hems of the Bio-Kil-treated gowns, the mean bacterial count was 1,201 CFU/100 cm(2), markedly lower than the bacterial count of 7,753 CFU/100 cm(2), found on the parts of the gowns not treated with Bio-Kil (p=0.0401). On the cuffs of sleeves treated with Bio-Kil, the mean count was 1,165 CFU/100 cm(2), markedly lower than that of 2,131 CFU/100 cm(2), found on the cuffs not treated with Bio-Kil (p=0.0073). With regard to the mean bacterial eradication rates of antimicrobial solutions, Steridal Solution, 75% alcohol and Bio-Kil (3rd generation) were shown to be the most effective, with rates exceeding 80%. Hibiscrub with paper towels and Fresh Protect Skin were the second most effective. Bio-Kil (1st generation), tap water with paper towels, liquid hand soap with paper towels and ozone water were the least effective. One important observation was that hand-washing without the use of paper towels increased the bacterial count by as much as 84% . Bio-Kil is effective in reducing bacterial counts in the air, on nursing staff uniforms and is an effective detergent.
Molecular Medicine Reports 12/2011; 5(3):859-65. · 0.42 Impact Factor
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Kun-Ling Tsai,
Li-Hsin Chen,
Shih-Hwa Chiou,
Guang-Yuh Chiou,
Yu-Chih Chen,
Hsiang-Yun Chou,
Liang-Kung Chen,
Hsiao-Yun Chen, Tsan-Hung Chiu,
Chiou-Sheng Tsai,
Hsiu-Chung Ou,
Chung-Lan Kao
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ABSTRACT: The lectin-like oxidized low-density lipoprotein receptor (LOX-1) is one pivot receptor for oxidized low-density lipoprotein (oxLDL) in human endothelial cells. Co-enzyme Q10 (Co Q10) has been widely used in clinical intervention. However, the molecular mechanisms underlying its protective effects against oxidative stress in endothelial cells are still largely unknown. This study was designed to test the hypothesis that Co Q10 mitigates oxLDL-induced endothelial oxidative injuries via modulation of LOX-1-mediated reactive oxygen species (ROS) generation and explored the role of AMP-activated protein kinase (AMPK), a negative regulator of NADPH oxidase.
Human umbilical vein endothelial cells (HUVECs) were pretreated with Co Q10 and then incubated with oxLDL for 24 h. Co Q10 attenuated oxLDL-elicited LOX-1 expression and ROS generation by suppression of NADPH oxidase activation. Co Q10 rescued dephosphorylation of AMPK caused by oxLDL that in turn led to an activation of NADPH oxidase by PKC. The results were confirmed using AMPK siRNA. Moreover, oxLDL-suppressed Akt/eNOS and enhanced p38 phosphorylation, which in turn activated NF-κB pathway. These detrimental events were ameliorated by Co Q10.
These results provide new highlight onto the possible molecular mechanisms of how Q10 suppresses oxLDL-induced endothelial oxidative injuries by the modulation of LOX-1-mediated ROS generation via the AMPK/PKC/NADPH oxidase signaling pathway.
Molecular Nutrition & Food Research 08/2011; 55 Suppl 2:S227-40. · 4.30 Impact Factor
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ABSTRACT: Severe steroid-resistant acute graft-versus-host disease (aGVHD) is associated with high mortality. Bone marrow-derived mesenchymal stem cells (BMMSC) have been found to be immunosuppressive, and intravenous infusion of BMMSC is an effective therapy for steroid-resistant aGVHD. However, acquiring BMMSC requires an invasive procedure.
We compared umbilical cord-derived mesenchymal stem cells (UCMSC) and BMMSC for morphology, surface markers expression, differentiation, proliferative potential, and their suppressive effects on peripheral blood mononuclear cell proliferation. After institutional review board approved, we intravenously infused ex vivo expanded third-party UCMSC into two patients with severe steroid-resistant aGVHD. Adverse effects and patient responses of UCMSC were monitored. All procedures for UCMSC processing complied with current good tissue practice requirements.
We found that UCMSC had superior proliferative potential and more suppressive effects on peripheral blood mononuclear cell proliferation compared with BMMSC. The aGVHD improved dramatically after each of four infusions of UCMSC into the two patients. No adverse effects were noted. Both patients are doing well now. CONCLUSIONS. Considering that acquiring UCMSC is noninvasive, these cells would appear to be the ideal candidates for clinical cell-based therapies. This is the first report of UCMSC in a human clinical application, and this procedure seems both feasible and safe. These findings suggested that UCMSC were effective for treating aGVHD.
Transplantation 06/2011; 91(12):1412-6. · 4.00 Impact Factor
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Kun-Ling Tsai,
Yi-Hsiang Huang,
Chung-Lan Kao,
De-Ming Yang,
Hsin-Chen Lee,
Hsiang-Yun Chou,
Yu-Chih Chen,
Guang-Yuh Chiou,
Li-Hsin Chen,
Yi-Ping Yang, Tsan-Hung Chiu,
Chiou-Sheng Tsai,
Hsiu-Chung Ou,
Shih-Hwa Chiou
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ABSTRACT: Atherosclerosis is a chronic inflammatory disease of the vessel wall associated with oxidized low-density lipoprotein (oxLDL)-induced apoptosis of endothelial cells. Coenzyme Q10 (CoQ10), a potent antioxidant and a critical intermediate of the electron transport chain, has been reported to inhibit LDL oxidation and thus the progression of atherosclerosis. However, its molecular mechanisms on endothelial cells remain still unclarified.
In this study, primary human umbilical vein endothelial cell cultures treated with oxLDL were used to explore the protective effects of CoQ10.
Our results showed that CoQ10 attenuated the oxLDL-induced generation of reactive oxygen species and improved the antioxidant capacity. CoQ10 also attenuated the oxLDL-mediated down-regulation of endothelial nitric oxide synthase (eNOS) and up-regulation of inducible nitric oxide synthase (iNOS). In addition, CoQ10 suppressed oxLDL-activated NF-κB and downstream inflammatory mediators, including expression of adhesion molecules, release of proinflammatory cytokines and the adherence of monocytic THP-1 cells. Moreover, CoQ10 attenuated oxLDL-altered proapoptotic responses. The inhibitor of eNOS (L-NIO 10 μM) and iNOS (1400W 10 μM) as well as NO enhancer (SNP 10 μM) were used to clean up the mechanism.
These results provide new insight into the possible molecular mechanisms by which CoQ10 protects against atherogenesis by NO-related pathways.
The Journal of nutritional biochemistry 06/2011; 23(5):458-68. · 4.29 Impact Factor
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Mei-Ying Kuo,
Hsiu-Chung Ou,
Wen-Jane Lee,
Wei-Wen Kuo,
Ling-Ling Hwang,
Tuzz-Ying Song,
Chih-Yang Huang, Tsan-Hung Chiu,
Kun-Ling Tsai,
Chiou-Sheng Tsai,
Wayne Huey-Herng Sheu
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ABSTRACT: Previous studies have shown that vascular endothelium-derived matrix metalloproteinases (MMPs) contribute to the destabilization of atherosclerotic plaques, a key event triggering acute myocardial infarction. In addition, studies have reported that the PKC-MEK-PPARγ signaling pathway is involved in oxidized low-density lipoprotein (oxLDL)-induced expression of MMPs. Ellagic acid, a phenolic compound found in fruits and nuts, has potent antioxidant, anti-inflammatory, and anticancerous properties. However, the molecular mechanisms underlying its antiatherogenic effects remain to be clarified. This study aimed to assess whether the effects of ellagic acid on the fibrotic markers MMP-1 and MMP-3 are modulated by the PKC-ERK-PPAR-γ signaling pathway in human umbilical vein endothelial cells (HUVECs) that have been exposed to oxLDL. It was found that ellagic acid significantly inhibited oxLDL-induced expressions of MMP-1 and MMP-3. Pretreatment with ellagic acid and DPI, a well-known ROS inhibitor, attenuated the oxLDL-induced expression and activity of PKC-α. In addition, ellagic acid as well as pharmacological inhibitors of ROS, calcium, and PKC strongly suppressed the oxLDL-induced phosphorylation of extracellular signal-regulated kinase (ERK) and NF-κB activation. Moreover, ellagic acid ameliorated the oxLDL-induced suppression of PPAR-γ expression. In conclusion, the data suggest that ellagic acid elicits its protective effects by modulating the PKC-α/ERK/PPAR-γ/NF-κB pathway, resulting in the suppression of ROS generation and, ultimately, inhibition of MMP-1 and MMP-3 expression in HUVECs exposed to oxLDL.
Journal of Agricultural and Food Chemistry 05/2011; 59(9):5100-8. · 2.82 Impact Factor
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ABSTRACT: It is well known that the response of cancer cells to chemotherapeutic drugs involves the activation of apoptotic pathways. Benzyl isothiocyanate (BITC) is an important compound found in plant food and has been shown to have anti-cancer effects on human cancer cells, but its effect on prostate cancer cells in vitro remains unknown. The aim of the present study was to investigate the effects of BITC on DU 145 human prostate cancer cells in order to clarify whether a time/concentration range for optimal BITC-induced apoptosis exists and to find the associated signaling pathway. Cell morphological changes, percentage of cell viability, DNA damage and apoptosis in DU 145 cells were examined by phase-contrast microscopy, flow cytometric assay, 4',6-diamidine-20-phenylindole dihydrochloride staining, comet assay and Western blotting analysis. The results indicate that BITC induces cell morphological changes, decreases the percentage of viable cells (induction of cell cytotoxicity), and induces DNA damage and apoptosis in DU 145 cells in a time- and dose-dependent manner. Flow cytometric assays indicated that BITC promoted reactive oxygen species and Ca2+ productions and decreased the levels of mitochondrial membrane potential (ΤYm), while the pre-treatment with N-acetylcysteine caused an increase in the percentage of viable cells. BITC also promoted caspase-3, -8 and -9 activities. Furthermore, when cells were pre-treated with the caspase-3 inhibitor and then treated with BITC, this led to an increase in the percentage of viable cells. Confocal laser microscopy examination indicated that BITC promoted the expression of AIF and Endo G, which were released from the mitochondria in DU 145 cells. In conclusion, BITC induces apoptosis in DU 145 cells through the release of AIF and Endo G from the mitochondria and also promotes caspase-3 activation.
International Journal of Oncology 03/2011; 38(3):787-96. · 2.40 Impact Factor
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ABSTRACT: The authors report a case of congenital hepatoblastoma that was diagnosed in the antenatal period at 39 weeks' gestation. The infant was delivered vaginally without rupture of the tumor. The neonate then received chemotherapy and underwent surgical excision of the tumor. After 1 year, no tumor recurrence has been noted.
Pediatric Hematology and Oncology 03/2011; 28(2):150-4. · 0.89 Impact Factor
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ABSTRACT: Our earlier studies showed that DATS induced apoptosis in human colon cancer HT29 and colo 205 cell lines in vitro. However, there is no report to show that DATS induced apoptosis in vitro and inhibited CT26 cancer cells in vivo on a murine allograft animal model. In vitro studies, the results indicated that DATS induced morphological changes and induction of apoptosis in CT26 cells. In vivo studies, CT26 cancer cells were implanted into BALB/c mice and groups of mice were treated with vehicle, DATS (10 and 50 mg/kg of body weight). DATS were injected once per four days intraperitoneally (i.p.), with treatment starting 4 weeks prior to cells inoculation. Treatment with vehicle or with 10 and 50 mg/kg of DATS resulted in a reduction in tumor volume and weight. Tumor volume and total hemoglobin in allograft mice treated with 50 mg/kg DATS were significantly smaller than that in the control group. These findings indicated that DATS inhibits tumor growth in an allograft animal model. Thus, DATS may represent a colon cancer preventive agent and can be used in the future.
Phytomedicine: international journal of phytotherapy and phytopharmacology 02/2011; 18(8-9):672-6. · 2.17 Impact Factor
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ABSTRACT: Endothelial apoptosis is a driving force in atherosclerosis development. Oxidized low-density lipoprotein (oxLDL) promotes inflammatory and thrombotic processes and is highly atherogenic, as it stimulates macrophage cholesterol accumulation and foam cell formation. Previous studies have shown that the phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase/nitric oxide (PI3K/Akt/eNOS/NO) pathway is involved in oxLDL-induced endothelial apoptosis. Ellagic acid, a natural polyphenol found in berries and nuts, has in recent years been the subject of intense research within the fields of cancer and inflammation. However, its protective effects against oxLDL-induced injury in vascular endothelial cells have not been clarified. In the present study, we investigated the anti-apoptotic effect of ellagic acid in human umbilical vein endothelial cells (HUVECs) exposed to oxLDL and explored the possible mechanisms. Our results showed that pretreatment with ellagic acid (5-20μM) significantly attenuated oxLDL-induced cytotoxicity, apoptotic features, and generation of reactive oxygen species (ROS). In addition, the anti-apoptotic effect of ellagic acid was partially inhibited by a PI3K inhibitor (wortmannin) and a specific eNOS inhibitor (cavtratin) but not by an ERK inhibitor (PD98059). In exploring the underlying mechanisms of ellagic acid action, we found that oxLDL decreased Akt and eNOS phosphorylation, which in turn activated NF-κB and downstream pro-apoptotic signaling events including calcium accumulation, destabilization of mitochondrial permeability, and disruption of the balance between pro- and anti-apoptotic Bcl-2 proteins. Those alterations induced by oxLDL, however, were attenuated by pretreatment with ellagic acid. The inhibition of oxLDL-induced endothelial apoptosis by ellagic acid is due at least in part to its anti-oxidant activity and its ability to modulate the PI3K/Akt/eNOS signaling pathway.
Toxicology and Applied Pharmacology 10/2010; 248(2):134-43. · 4.45 Impact Factor
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Hung-Yi Chen,
Hsu-Feng Lu,
Jai-Sing Yang,
Sheng-Chu Kuo,
Chyi Lo,
Mei-Due Yang, Tsan-Hung Chiu,
Fu-Shin Chueh,
Heng-Chien Ho,
Yang-Ching Ko,
Jing-Gung Chung
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ABSTRACT: 20-Fluoro-6,7-methylenedioxy-2-phenyl-4-quino-lone (CHM-1) has been reported to induce cell cycle arrest and apoptosis in many types of cancer cells. However, there is no available information to show CHM-1 affecting DNA damage and expression of associated repair genes. Herein, we investigated whether or not CHM-1 induced DNA damage and affected DNA repair gene expression in U-2 OS human osterogenic sarcoma cells. The comet assay showed that incubation of U-2 OS cells with 0, 0.75, 1.5, 3 and 6 μM of CHM-1 led to a longer DNA migration smear (comet tail). DNA gel electrophoresis showed that 3 μM of CHM-1 for 24 and 48 h treatment induced DNA fragmentation in U-2 OS cells. Real-time PCR analysis showed that treatment with 3 μM of CHM-1 for 24 h reduced the mRNA expression levels of ataxia telangiectasia mutated (ATM), ataxia-telangiectasia and Rad3-related (ATR), breast cancer 1, early onset (BRCA1), 14-3-3sigma (14-3-3σ), DNA-dependent serine/threonine protein kinase (DNA-PK) and O(6)-methylguanine-DNA methyltransferase (MGMT) genes in a time-dependent manner. Taken together, the results indicate that CHM-1 caused DNA damage and reduced DNA repair genes in U-2 OS cells, which may be the mechanism for CHM-1-inhibited cell growth and induction of apoptosis.
Anticancer research 10/2010; 30(10):4187-92. · 1.73 Impact Factor
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Hsiu-Chung Ou,
Tuzz-Ying Song,
Yueh-Chiao Yeh,
Chih-Yang Huang,
Shun-Fa Yang, Tsan-Hung Chiu,
Kun-Ling Tsai,
Kai-Ling Chen,
Yun-Jhen Wu,
Chiou-Sheng Tsai,
Li-Yun Chang,
Wei-Wen Kuo,
Shin-Da Lee
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ABSTRACT: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), originally identified as the major receptor for oxidized low-density lipoprotein (oxLDL) in endothelial cells, plays a major role in the pathology of vascular diseases. Green tea consumption is associated with reduced cardiovascular mortality in some epidemiological studies. In the present study, we hypothesized that the most abundant polyphenolic compound in tea, epigallocatechin-3-gallate (EGCG), can downregulate parameters of endothelial dysfunction by modulating LOX-1-regulated cell signaling. In cultured human umbilical vein endothelial cells (HUVECs), exposure to oxLDL (130 microg/ml), which led to an increase in LOX-1 expression at the RNA and protein levels, was abrogated by addition of EGCG or DPI, a well-known inhibitor of flavoproteins, suggesting the involvement of NADPH oxidase. Furthermore, oxLDL rapidly activated the membrane translocation of Rac-1 and p47phox and the subsequent induction of ROS generation, which was suppressed markedly by pretreatment with EGCG or anti-LOX-1 monoclonal antibody. OxLDL also increased p38 MAPK phosphorylation and decreased phosphorylation of the amino-terminal region of Akt, with maximal induction at about 30 min, and NF-kappaB phosphorylation within 1 h, resulting in redox-sensitive signaling. In addition, oxLDL diminished the expression of endothelial nitric oxide synthase (eNOS), enhanced the expression of endothelin-1 and adhesion molecules (ICAM, E-selectin, and monocyte chemoattractant protein-1), and increased the adherence of monocytic THP-1 cells to HUVECs. Pretreatment with EGCG, however, exerted significant cytoprotective effects in all events. These data suggest that EGCG inhibits the oxLDL-induced LOX-1-mediated signaling pathway, at least in part, by inhibiting NADPH oxidase and consequent ROS-enhanced LOX-1 expression, which contributes to further ROS generation and the subsequent activation of NF-kappaB via the p38 MAPK pathway. Results from this study may provide insight into a possible molecular mechanism by which EGCG suppresses oxLDL-mediated vascular endothelial dysfunction.
Journal of Applied Physiology 03/2010; 108(6):1745-56. · 3.75 Impact Factor
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ABSTRACT: Prenatal genetic diagnosis plays an important role in eugenics. Early detection of embryo and fetus abnormalities allows preventive precautions to be taken and treatment to begin early in order to reduce the severity and extent of congenital deformities. Advancements in genetic diagnostic techniques infer that nurses are increasingly likely to deal with prenatal genetic diagnosis cases. This essay introduces a few prevalent prenatal genetic diagnosis methods used at different stages of pregnancy; describes in a comprehensive manner the potential physical and psychological responses of the client; and introduces principles of administering prenatal genetic diagnosis to healthcare clients. Ethical issues related to prenatal genetic diagnosis are also discussed.
Hu li za zhi The journal of nursing 12/2009; 56(6):11-5.
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Tsan-Hung Chiu,
Wan-Wen Lai,
Te-Chun Hsia,
Jai-Sing Yang,
Tung-Yuan Lai,
Ping-Ping Wu,
Chia-Yu Ma,
Chin-Chung Yeh,
Chin-Chin Ho,
Hsu-Feng Lu,
W Gibson Wood,
Jing-Gung Chung
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ABSTRACT: Aloe-emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of aloe-emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that aloe-emodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 microM of aloe-emodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. Aloe-emodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (DeltaPsi(m)) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N-acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-emodin-induced apoptosis. Aloe-emodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. Aloe-emodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.
Anticancer research 11/2009; 29(11):4503-11. · 1.73 Impact Factor
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ABSTRACT: Oxidized low-density lipoprotein (oxLDL) is a proatherogenic molecule that accumulates in the vascular wall and contributes to the pathogenesis of vascular dysfunction early in the development of atherosclerosis. The whole plant of Solanum lyratum is a traditional Chinese medicine that has been used for centuries to treat cancer, tumors, and herpes. However, the cellular and molecular mechanisms of its antioxidant effects are still largely unknown. This study tested the hypothesis that Solanum lyratum Thunberg extract (SLE) could block oxLDL-induced endothelial dysfunction in cultured human umbilical vein endothelial cells (HUVECs). Possible mechanisms were explored.
Antioxidative activities of SLE were assayed by measuring the scavenging of 1,1-diphenyl-2-picryl-hydrazyl (DPPH) free radical and the inhibition of copper-mediated or cell-mediated LDL oxidation. Production of reactive oxygen species (ROS) and the expression of adhesion molecules were evaluated in HUVECs after exposure to oxLDL and treatment with SLE. Several apoptotic signaling pathways were investigated.
SLE scavenged DPPH and also delayed the kinetics of LDL oxidation in a dose-dependent manner. SLE attenuated the level of oxLDL-induced ROS generation, diminished the expression of endothelial NO synthase (eNOS), and enhanced the expression of adhesion molecules (vascular cellular adhesion molecule-1, E-selectin, and monocyte chemotactic protein-1) and the adherence of monocytic THP-1 cells to HUVECs. OxLDL increased the concentration of intracellular calcium, disturbed the balance of the Bcl-2 protein family, destabilized the mitochondrial membrane potential, increased the amount of cytochrome c released into the cytosol, and increased the activation of caspase 3. These detrimental effects were ameliorated dose-dependently by SLE (P < .05).
Crude extracts of Solanum lyratum protect against oxLDL-induced injury in endothelial cells by direct antioxidant action.
Atherosclerosis is a chronic inflammatory disease characterized by lipid-laden lesions within arterialblood vessel walls. Inhibiting the oxidation of low-density lipoprotein may be an effective way to prevent or delay theprogression of atherosclerosis. This study underscores the potential clinical benefits and application of Solanum lyratumextract in controlling oxidized low-density lipoprotein-associated vascular injury and cardiovascular disease.
Journal of vascular surgery: official publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter 08/2009; 50(4):849-60. · 3.52 Impact Factor
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Hung-chien Wu,
Yu-chi Liu,
Keng-liang Ou,
Yung-hsien Chang,
Ching-liang Hsieh,
Angela Hsin-chieh Tsai,
Hong-te Tsai, Tsan-hung Chiu,
Chih-jen Hung,
Chien-chung Lee,
Jaung-geng Lin
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ABSTRACT: Post-operation pain is a very subjective phenomenon. The aim of this study was to find out the effects of acupuncture or electro-acupuncture on post-cesarean pain.
Sixty women, who had had spinal anesthesia during cesarean section at the Department of Obstetrics of China Medical University Hospital, were randomly assigned to the control group, the acupuncture group, and the electro-acupuncture group. After the operation, we applied subjects with acupuncture or electro-acupuncture on the bilateral acupuncture point, San Yin Jiao (Sp6), and the patient controlled analgesia (PCA). The first time of requesting morphine, the frequency of PCA demands in 24 hours, and the doses of PCA used were recorded double blindly. In addition, monitoring the subjects' vital signs, the opioid-related side effects, and the pain scores was done.
The results showed that the acupuncture group and the electro-acupuncture group could delay the time of requesting morphine up to 10 - 11 minutes when compared with the control group. The total dose of PCA used within the first 24 hours was 30% - 35% less in the acupuncture group and the electro-acupuncture group when compared with the control group, which was indicated in statistical significance. However, there was no significant difference between the acupuncture group and the electro-acupuncture group. The electro-acupuncture group's and the acupuncture group's pain scores were lower than the control group's within the first 2 hours. Both were statistically significant. However, two hours later, there were no significant differences of the visual analogue scale (VAS) scores between either of the treatment groups and the control group. Finally, the incidence of opioid-related side effects, such as dizziness, was less in the acupuncture group and electro-acupuncture group than in the control group.
This study shows that the application of acupuncture and electro-acupuncture could definitely delay the time of requesting pain relief medication after cesarean section and decrease the PCA doses used within the first 24 hours.
Chinese medical journal 08/2009; 122(15):1743-8. · 0.86 Impact Factor
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Ting-Ching Chen,
Kuang-Chi Lai,
Jai-Sing Yang,
Ching-Lung Liao,
Te-Chun Hsia,
Guang-Wei Chen,
Jen-Jyh Lin,
Hui-Ju Lin, Tsan-Hung Chiu,
Yih-Jing Tang,
Jing-Gung Chung
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ABSTRACT: The cytotoxicity of berberine on C6 rat glioma cells indicated that berberine induced morphological changes and caused cell death through G2/M arrest and apoptosis. While undergoing apoptosis, there was a remarkable accumulation of G2/M cells with the upregulatoin of Wee1 but it also inhibited cyclin B, CDK1 and Cdc25c that led to G2/M arrest. Along with cytotoxicity in C6 cells, several apoptotic events including mitochondrial cytochrome c release, activation of caspase-9, -3 and -8 and DNA fragmentation were induced. Berberine increased the levels of GADD153 and GRP 78 in C6 cells based on the examination of Western blotting and this is a major hallmark of endoplasmic reticulum (ER) stress. We also found that berberine promoted the production of reactive oxygen species and Ca2+ in C6 cells. Western blotting assay also showed that berberine inhibited the levels of anti-apoptotic protein Bcl-2 but increased the levels of pro-apoptotic protein Bax before leading to a decrease in the levels of mitochondrial membrane potential (DeltaPsim) followed by cytochrome c release that caused the activations of capase-9 and -3 for apoptotic occurrence. The caspase-8, -9 and -3 were activated by berberine in C6 cells based on the substrate solution (PhiPhiLux-G1D1, CaspaLux 8-L1D2, CaspaLux 9-M1D2 for caspase-3, -8 and -9, respectively) and analyzed by flow cytometer and each inhibitor of caspase-8, -9 and -3 led to increase the percentage of viable C6 cells after exposure to berberine. This finding was also confirmed by Western blot assay which showed that berberine promoted the active form of caspase-8, -9 and -3. These results demonstrate that the cytotoxicity of berberine in C6 rat glioma cells is attributable to apoptosis mainly through induced G2/M-arrested cells, in an ER-dependent manner, via a mitochondria-dependent caspase pathway regulated by Bax and Bcl-2.
International Journal of Oncology 07/2009; 34(6):1681-90. · 2.40 Impact Factor
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ABSTRACT: Atherosclerosis is a chronic inflammatory process with increased oxidative stress in vascular endothelium. Ginkgo biloba extract (GbE), extracted from Ginkgo biloba leaves, has commonly been used as a therapeutic agent for cardiovascular and neurological disorders. The aim of this study was to investigate how GbE protects vascular endothelial cells against the proatherosclerotic stressor oxidized low-density lipoprotein (oxLDL) in vitro. Human umbilical vein endothelial cells (HUVECs) were incubated with GbE (12.5-100 microg/ml) for 2 h and then incubated with oxLDL (150 microg/ml) for an additional 24 h. Subsequently, reactive oxygen species (ROS) generation, antioxidant enzyme activities, adhesion to monocytes, cell morphology, viability, and several apoptotic indexes were assessed. Our data show that ROS generation is an upstream signal in oxLDL-treated HUVECs. Cu,Zn-SOD, but not Mn-SOD, was inactivated by oxLDL. In addition, oxLDL diminished expression of endothelial NO synthase and enhanced expression of adhesion molecules (ICAM, VCAM, and E-selectin) and the adherence of monocytic THP-1 cells to HUVECs. Furthermore, oxLDL increased intracellular calcium, disturbed the balance of Bcl-2 family proteins, destabilized mitochondrial membrane potential, and triggered subsequent cytochrome c release into the cytosol and activation of caspase-3. These detrimental effects were ameliorated dose dependently by GbE (P < 0.05). Results from this study may provide insight into a possible molecular mechanism underlying GbE suppression of the oxLDL-mediated vascular endothelial dysfunction.
Journal of Applied Physiology 03/2009; 106(5):1674-85. · 3.75 Impact Factor
