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1
Rakotomanga, M., M. Saint-Pierre-Chazalet, and P. M. Loiseau. "Alteration of Fatty Acid and Sterol Metabolism in Miltefosine-Resistant Leishmania donovani Promastigotes and Consequences for Drug-Membrane Interactions." Antimicrobial Agents and Chemotherapy 49, no. 7 (July 2005): 2677–86. http://dx.doi.org/10.1128/aac.49.7.2677-2686.2005.
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ABSTRACT Miltefosine (hexadecylphosphocholine [HePC]) is the first orally active drug approved for the treatment of visceral leishmaniasis. In order to investigate the biochemical modifications occurring in HePC-resistant (HePC-R) Leishmania donovani promastigotes, taking into account the lipid nature of HePC, we investigated their fatty acid and sterol metabolisms. We found that the content of unsaturated phospholipid alkyl chains was lower in HePC-R parasite plasma membranes than in those of the wild type, suggesting a lower fluidity of HePC-R parasite membranes. We also demonstrated that HePC insertion within an external monolayer was more difficult when the proportion of unsaturated phospholipids decreased, rendering the HePC interaction with the external monolayer of HePC-R parasites more difficult. Furthermore, HePC-R parasite membranes displayed a higher content of short alkyl chain fatty acids, suggesting a partial inactivation of the fatty acid elongation enzyme system in HePC-R parasites. Sterol biosynthesis was found to be modified in HePC-R parasites, since the 24-alkylated sterol content was halved in HePC-R parasites; however, this modification was not related to HePC sensitivity. In conclusion, HePC resistance affects three lipid biochemical pathways: fatty acid elongation, the desaturase system responsible for fatty acid alkyl chain unsaturation, and the C-24-alkylation of sterols.
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Yeh, Kwo-yih, Mary Yeh, Laura Mims, and Jonathan Glass. "Iron feeding induces ferroportin 1 and hephaestin migration and interaction in rat duodenal epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 1 (January 2009): G55—G65. http://dx.doi.org/10.1152/ajpgi.90298.2008.
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Intestinal iron absorption involves proteins located in the brush border membrane (BBM), cytoplasm, and basolateral membrane (BLM) of duodenal enterocytes. Ferroportin 1 (FPN1) and hephaestin (Heph) are necessary for transport of iron out of enterocytes, but it is not known whether these two proteins interact during iron absorption. We first examined colocalization of the proteins by cotransfection of HEK293 cells with pDsRed-FPN1 with pEmGFP-Heph or with the COOH-terminal truncated pEmGFP-HephΔ43 or -HephΔ685 and found that FPN1 and Heph with or without the COOH terminus colocalized. In rat duodenal enterocytes, within 1 h of iron feeding prominent migration of FPN1 from the apical subterminal zone to the basal subnuclear zone of the BLM occurred and increased to at least 4 h after feeding. Heph exhibited a similar though less prominent migration after iron ingestion. Analysis using rat duodenal epithelial cell sheets demonstrated that 1) by velocity sedimentation ultracentrifugation, FPN1 and Heph occupied vesicles of different sizes prior to iron feeding and migrated to similar fractions 1 h after iron feeding; 2) by blue native/SDS-PAGE, FPN1, and Heph interacted to form two complexes, one containing dimeric FPN1 and intact Heph and the other consisting of monomeric FPN1 and a Heph fragment; and 3) by immunoprecipitation, anti-Heph or anti-FPN1 antiserum coimmunoprecipitated FPN1 and Heph. Thus the data indicate that FPN1 and Heph migrate and interact during iron feeding and suggest that dimeric FPN1 is associated with intact Heph.
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Tseng, Chung-Chih, Tah-Wei Chu, Ridha Danata, Yenny Risjani, Hui-Tsu Shih, and Shao-Yang Hu. "Hepcidin-Expressing Fish Eggs as A Novel Food Supplement to Modulate Immunity against Pathogenic Infection in Zebrafish (Danio rerio)." Sustainability 12, no. 10 (May 15, 2020): 4057. http://dx.doi.org/10.3390/su12104057.
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Hepcidin antimicrobial peptides are difficult to produce in prokaryotic expression systems due to their complex structure and antimicrobial activity. Although synthetic hepcidin provides an alternative to solve this issue, its high cost limits its practical application in various industries. The present study used zebrafish eggs as bioreactors to produce convict cichlid (Amatitlania nigrofasciata) hepcidin (AN-hepc) using the oocyte-specific zona pellucida (zp3) promoter. The expression plasmid pT2-ZP3-AN-hepc-ZP3-EGFP, using EGFP as a reporter of AN-hepc expression, was designed to establish the transgenic line Tg(ZP3:AN-hepc:ZP3:EGFP) for the expression of AN-hepc. The AN-hepc peptide was produced successfully in fertilized eggs, as evidenced by RT-PCR and Western blotting. The AN-hepc-expressing eggs exhibited antimicrobial activity against a variety of aquatic pathogens and antibiotic-resistant pathogens, suggesting that the AN-hepc expressed in fish eggs was bioactive. The immunomodulatory effects of AN-hepc-expressing fertilized eggs on zebrafish innate immunity were evaluated by determining the expression of indicator genes after feeding with AN-hepc-expressing fertilized eggs for two months. Zebrafish supplementation with AN-hepc-expressing fertilized eggs significantly increased the expression of innate immunity-related genes, including IL-1β, IL-6, IL-15, TNF-α, NF-κb, complement C3b, lysozyme and TLR-4a. The zebrafish administered AN-hepc-expressing eggs exhibited higher cumulative survival than fish supplemented with wild-type and control eggs after infection with Aeromonas hydrophila and Streptococcus iniae. In conclusion, the present results showed that supplementation with AN-hepc-expressing fish eggs enhanced zebrafish innate immunity against pathogenic infections, suggesting that fertilized eggs containing AN-hepc have the potential to be developed as a food supplement for improving health status in aquaculture.
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Li, Jie, Xuelan Shang, Yan Liang, Wenjie Yang, Zhe Wang, and Hezhao Ji. "Assessment of the Hepatitis C Surveillance System in Henan, China: 2014~2016." BioMed Research International 2018 (September 26, 2018): 1–8. http://dx.doi.org/10.1155/2018/8942152.
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Objectives. To access the Hepatitis C (HepC) surveillance program in Henan, China, 2014~2016. Methods. A total of 8,448 HepC-relevant cases were reviewed and this data was then inquired against the 6,147 archived HepC reports during the same time period. The performance of the HepC surveillance program was evaluated using parameters including Timely Reporting Rate (TRR), pairs of Report Sensitivity (RS)/Underreporting Rate (UR), and False Report Rate (FRR)/Predictive Value Positive (PVP). Longitudinal comparisons of report quality over the three examined years were conducted to determine the temporal trend of HepC surveillance accountability. Results. All HepC reports were submitted within 24 hours post diagnosis, and TRR rates for all examined years remained at 100%. The RS rates significantly improved overtime for clinically diagnosed HepC cases (CDHC) (2014:60.32%, 2015:68.13%, and 2016:82.83%), whereas the RS for confirmed HepC cases (CHC) remained relatively constant (80.77%, 88.64%, and 85.82%). The FRR rates for CDHC and CHC in 2015~2016 were both approximately 30% but at 23.61% and 51.85%, respectively, in 2014. Conclusions. The HepC surveillance system in Henan remains effective and consistent improvement in report accountability was observed over time. However, some issues concerning especially RS and PVP remained to be addressed for ensuring data accountsbility.
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Rakotomanga, M., S. Blanc, K. Gaudin, P. Chaminade, and P. M. Loiseau. "Miltefosine Affects Lipid Metabolism in Leishmania donovani Promastigotes." Antimicrobial Agents and Chemotherapy 51, no. 4 (January 22, 2007): 1425–30. http://dx.doi.org/10.1128/aac.01123-06.
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ABSTRACT Miltefosine (hexadecylphosphocholine [HePC]) is the first orally active antileishmanial drug. Transient HePC treatment of Leishmania donovani promastigotes at 10 μM significantly reduced the phosphatidylcholine content and enhanced the phosphatidylethanolamine (PE) content in parasite membranes, suggesting a partial inactivation of PE-N-methyltransferase. Phospholipase D activity did not seem to be affected by HePC. In addition, the enhancement of the lysophosphatidylcholine content could be ascribed to phospholipase A2 activation. Moreover, transient HePC treatment had no effect on the fatty acid alkyl chain length or the fatty acid unsaturation rate. Concerning sterols, we found a strong reduction of the C24 alkylated sterol content, and the enhancement of the cholesterol content could be the result of the HePC condensation effect with sterols. Because some of the effects observed after transient HePC treatment were different from those previously observed in HePC-resistant parasites, it could be hypothesized that continuous in vitro drug pressure induces the mechanisms of regulation in Leishmania lipid metabolism.
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Mena, Natalia P., Andrés Esparza, Victoria Tapia, Pamela Valdés, and Marco T. Núñez. "Hepcidin inhibits apical iron uptake in intestinal cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 1 (January 2008): G192—G198. http://dx.doi.org/10.1152/ajpgi.00122.2007.
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Hepcidin (Hepc) is considered a key mediator in iron trafficking. Although the mechanism of Hepc action in macrophages is fairly well established, much less is known about its action in intestinal cells, one of the main targets of Hepc. The current study investigated the effects of physiologically generated Hepc on iron transport in Caco-2 cell monolayers and rat duodenal segments compared with the effects on the J774 macrophage cell line. Addition of Hepc to Caco-2 cells or rat duodenal segments strongly inhibited apical 55Fe uptake without apparent effects on the transfer of 55Fe from the cells to the basolateral medium. Concurrently, the levels of divalent metal transporter 1 (DMT1) mRNA and protein in Caco-2 cells decreased while the mRNA and protein levels of the iron export transporter ferroportin did not change. Plasma membrane localization of ferroportin was studied by selective biotinylation of apical and basolateral membrane domains; Hepc induced rapid internalization of ferroportin in J774 cells but not in Caco-2 cells These results indicate that the effect of Hepc is cell dependent: in macrophages it inhibits iron export by inducing ferroportin degradation, whereas in enterocytes it inhibits apical iron uptake by inhibiting DMT1 transcription. Our results highlight the crucial role of Hepc in the control of intestinal iron absorption.
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Graf v.d. Schulenburg, M. "HEPAC – New Editor-in-chief." European Journal of Health Economics (HEPAC) 2, no. 1 (March 2001): 1. http://dx.doi.org/10.1007/pl00012213.
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Myers, John, Michael Smith, Claudia Espinosa, Charles Woods, and Scott Duncan. "Is there Failure to Screen for Hepatitis C in Newborns Suffering from Neonatal Abstinence Syndrome?" Open Forum Infectious Diseases 4, suppl_1 (2017): S40—S41. http://dx.doi.org/10.1093/ofid/ofx162.098.
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Abstract Background Enormous advances in treating/curing patients suffering from Hepatitis C (HepC) infection have occurred; resulting in many states mandating screening for HepC for older individuals. Unfortunately, no protection of screening exists for newborns. In Kentucky, rates of HepC among pregnant women are the second highest within the U.S., which has been associated to high intravenous drug use. Infants born to those women are at risk of HepC infection and other conditions such as neonatal abstinence syndrome (NAS). The current study examined the rate of HepC screening in a high-risk cohort (newborns suffering from NAS) and it’s impact on policy-making for this vulnerable population. Methods Kentucky Medicaid records, from 2015, were obtained to develop a detailed demographic, behavioral, clinical, and diagnostic data set (n = 152,749). NAS was defined by ICD-9 code 779.5 and ICD-10 code P96.1. HepC screening was defined by CPT codes (CPT 87520 [HCV, direct probe], 87521 [HCV, amplified probe], and 87522 [HCV RNA, Quantitative] or antibody [CPTs 86803–4]). Initially a descriptive study was performed, then multiple logistic regression techniques were used to test what variables impacted the odds of not being screened for HepC. Results A total of 1234 newborns with NAS were identified. The majority showed signs of NAS within 24 hours (64%), were white (68%) and were admitted to the hospital for an average of 24.8 days. Only one-in-three newborns with NAS (n = 412, 33.4%) were screened for HepC. Non-Whites (OR = 1.58, 95% CI 1.45–1.71, P < 0.001) and those living in non-urban areas (OR = 1.42, 95% CI 1.28–1.56, P < 0.001) were the only study variables to significantly impact the odds of not being screened for HepC (for newborns suffering from NAS). Conclusion A high-risk and vulnerable population for HepC may not be getting screened for HepC and thus are being underserved by the health care system. Non-Whites and those in rural areas are the most affected. Solutions and policies need to be focused on this population and area where screening is lacking. Optimization of maternal screening for HepC is crucial in high-risk populations. Disclosures All authors: No reported disclosures.
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Luque-Ortega, Juan Román, and Luis Rivas. "Miltefosine (Hexadecylphosphocholine) Inhibits Cytochrome c Oxidase in Leishmania donovani Promastigotes." Antimicrobial Agents and Chemotherapy 51, no. 4 (February 5, 2007): 1327–32. http://dx.doi.org/10.1128/aac.01415-06.
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ABSTRACT Miltefosine (hexadecylphosphocholine [HePC]) is currently on trial as a first-choice, orally active drug for the treatment of visceral leishmaniasis when resistance to organic pentavalent antimonials becomes epidemic. However, data on the targets involved in its leishmanicidal mechanism have, until now, been only fragmentary. We have carried out a systematic study of the alterations induced on the bioenergetic metabolism of Leishmania donovani promastigotes by HePC. Overnight incubation with HePC caused a significant decline in the intracellular ATP levels of the parasites, together with a reduction in the oxygen consumption rate and mitochondrial depolarization, while the integrity of the plasma membrane remained undamaged. In a further step, the effects of HePC on the respiratory chain were addressed in digitonized parasites. The inhibition of the oxygen consumption rate caused by HePC was not reverted either with the uncoupling agent carbonyl cyanide p-trifluoromethoxyphenylhydrazone or with tetramethyl-p-phenylenediamine plus ascorbate, which feeds the electron transport chain at the level of cytochrome c. These results suggest that cytochrome c oxidase is a likely target in the complex leishmanicidal mechanism of HePC. This was further confirmed from the finding that this enzyme was specifically inhibited in a dose-dependent manner by HePC, but not the cytochrome c reductase, ruling out an unspecific effect of HePC on the respiratory chain.
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Pérez-Victoria, F. Javier, Santiago Castanys, and Francisco Gamarro. "Leishmania donovani Resistance to Miltefosine Involves a Defective Inward Translocation of the Drug." Antimicrobial Agents and Chemotherapy 47, no. 8 (August 2003): 2397–403. http://dx.doi.org/10.1128/aac.47.8.2397-2403.2003.
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ABSTRACT Miltefosine (hexadecylphosphocholine [HePC]) is the first drug approved for the oral treatment of visceral leishmaniasis. As part of a study on the mechanisms of action of this drug and on the rates of resistance to this drug, we have been working in vitro with an Leishmania donovani line that was previously shown to be 15-fold more resistant to HePC. We have studied the accumulation of [14C]HePC by L. donovani promastigotes and have found a drastic reduction (>95%) in the ability of the resistant line to internalize the drug. Binding of HePC to the plasma membrane and drug efflux from preloaded cells were similar in both drug-sensitive and -resistant lines, and no [14C]HePC metabolism was evident in either line. Resistant parasites were also unable to take up other short-chain phospholipid analogs, independently of their polar head group, even though endocytosis remained unaltered. Finally, HePC uptake was temperature and energy dependent and sensitive to the thiol-reactive agent N-ethylmaleimide. We propose that inward translocation of a short-chain phospholipid across the plasma membrane may exist in Leishmania promastigotes and that such activity is defective in the resistant line.
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Filippone, Edward J., Christine Chmielewski, Rakesh Gulati, Eric Newman, and John L. Farber. "De NovoFibrillary Glomerulonephritis (FGN) in a Renal Transplant with Chronic Hepatitis C." Case Reports in Transplantation 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/978481.
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Chronic hepatitis C viremia (HepC) has been associated with numerous renal manifestations both in native kidneys and in the setting of renal transplantation. Glomerulonephritis (GN) of the renal allograft in the setting of HepC most commonly manifests as type 1 membranoproliferative GN (MPGN), either representing recurrence of the original disease or arisingde novo. Other GNs were reported after transplantation in the patient with HepC including membranous nephropathy and thrombotic microangiopathy, as well as an enhanced susceptibility to transplant glomerulopathy. We describe the first case ofde novofibrillary GN in a renal transplant patient with HepC where the primary renal disease was biopsy proven type 1 MPGN. We discuss this relationship in detail.
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Paris, Caroline, Philippe M. Loiseau, Christian Bories, and Jaqueline Bréard. "Miltefosine Induces Apoptosis-Like Death in Leishmania donovani Promastigotes." Antimicrobial Agents and Chemotherapy 48, no. 3 (March 2004): 852–59. http://dx.doi.org/10.1128/aac.48.3.852-859.2004.
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ABSTRACT Miltefosine (hexadecylphosphocholine [HePC]) has proved to be a potent oral treatment for human visceral leishmaniasis due to Leishmania donovani. The molecular mechanisms that contribute to the antileishmanial activity of HePC are still unknown. We report that in wild-type promastigotes of Leishmania donovani HePC is able to induce a cell death process with numerous cytoplasmic, nuclear, and membrane features of metazoan apoptosis, including cell shrinkage, DNA fragmentation into oligonucleosome-sized fragments, and phosphatidylserine exposure. None of these changes were detected in an HePC-resistant clone treated with the same drug concentration. Therefore, HePC does not appear to kill L. donovani promastigotes by a direct toxic mechanism but, rather, kills the promastigotes by an indirect one. Pretreatment of wild-type promastigotes with two broad caspase inhibitors, z-Val-Ala-dl-Asp(methoxy)-fluoromethylketone and Boc-Asp(methoxy)-fluoromethylketone, as well as a broad protease inhibitor, calpain inhibitor I, prior to drug exposure interfered with DNA fragmentation but did not prevent cell shrinkage or phosphatidylserine externalization. These data suggest that at least part of the apoptotic machinery operating in wild-type promastigotes involves proteases. Identification of the death-signaling pathways activated in HePC-sensitive parasites appears to be essential for a better understanding of the molecular mechanisms of action and resistance in these parasites.
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Ménez, Cécile, Marion Buyse, Madeleine Besnard, Robert Farinotti, Philippe M. Loiseau, and Gillian Barratt. "Interaction between Miltefosine and Amphotericin B: Consequences for Their Activities towards Intestinal Epithelial Cells and Leishmania donovani Promastigotes In Vitro." Antimicrobial Agents and Chemotherapy 50, no. 11 (September 11, 2006): 3793–800. http://dx.doi.org/10.1128/aac.00837-06.
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ABSTRACT The aim of this study was to evaluate the potential of a combination of two antileishmanial drugs, miltefosine (HePC) and amphotericin B (AMB), when administered by the oral route. Caco-2 cell monolayers were used as a validated in vitro model of the intestinal barrier and Leishmania donovani promastigotes as a model for evaluating the effect of the drug combination. Spectroscopic measurements demonstrated that HePC and AMB associate, leading to the formation of mixed aggregates in which AMB is solubilized as monomers. The incubation of the association of HePC and AMB with Caco-2 cell monolayers, at a concentration higher than 5 μM, led to (i) a reduction of the HePC-induced paracellular permeability enhancement in Caco-2 cell monolayers, (ii) an inhibition of the uptake of both drugs, and (iii) a decrease in the transepithelial transport of both drugs, suggesting that a pharmacokinetic antagonism between HePC and AMB could occur after their oral administration. However, the combination did not exhibit any antagonism or synergy in its antileishmanial activity. These results demonstrated a strong physicochemical interaction between HePC and AMB, depending on the concentration of each, which could have important consequences for their biological activities, if they are administered together.
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Yalovenko, T. M., I. M. Todor, N. Yu Lukianova, and V. F. Chekhun. "HEPCIDIN AS A POSSIBLE MARKER IN DETERMINATION OF MALIGNANCY DEGREE AND SENSITIVITY OF BREAST CANCER CELLS TO CYTOSTATIC DRUGS." Experimental Oncology 38, no. 2 (June 22, 2016): 84–88. http://dx.doi.org/10.31768/2312-8852.2016.38(2):84-88.
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Aim: To investigate the role of hepcidin (Hepc) in the formation of cells malignant phenotype in vitro and its expression in the dyna mics of growth of Walker-256 carcinosarcoma with different sensitivity to doxorubicin (Dox). Materials and Methods: The cell lines used in the analysis included T47D, MCF-7, MDA-MB-231, MDA-MB-468, MCF/CP, and MCF/Dox. Hepc expression was studied by immunocytochemical method. “Free” iron content was determined by EPR spectroscopy. Determination of Hepc expression in homogenates of tumor tissue and in blood serum of rats with Dox-sensitive and -resistant Walker-256 carcinosarcoma was performed. Results: It was found that Hepc levels in breast cancer (BC) cells with high degree of malignancy (MDA-MB-231, MDAMB-468) and drug-resistant phenotype (MCF/CP, MCF/Dox) were by 1.5–2 times higher (p < 0.05) in comparison with sensitive and less malignant BC cells. The development of drug-resistant phenotype in Walker-256 carcinosarcoma cells was accompanied by increasing of Hepc and “free” iron content (by 2.4 and 1.2 times, respectively). Conclusion: The data of in vitro and in vivo research evidenced on involvement of Hepc in formation of BC cells malignant phenotype and their resistance to Dox.
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Vacchina, P., B. Norris-Mullins, M. A. Abengózar, C. G. Viamontes, J. Sarro, M. T. Stephens, M. E. Pfrender, L. Rivas, and M. A. Morales. "Genomic Appraisal of the Multifactorial Basis forIn VitroAcquisition of Miltefosine Resistance in Leishmania donovani." Antimicrobial Agents and Chemotherapy 60, no. 7 (April 25, 2016): 4089–100. http://dx.doi.org/10.1128/aac.00478-16.
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ABSTRACTProtozoan parasites of theLeishmania donovanicomplex are the causative agents of visceral leishmaniasis (VL), the most severe form of leishmaniasis, with high rates of mortality if left untreated.Leishmaniaparasites are transmitted to humans through the bite of infected female sandflies (Diptera:Phlebotominae), and approximately 500,000 new cases of VL are reported each year. In the absence of a safe human vaccine, chemotherapy, along with vector control, is the sole tool with which to fight the disease. Miltefosine (hexadecylphosphatidylcholine [HePC]), an antitumoral drug, is the only successful oral treatment for VL. In the current study, we describe the phenotypic traits ofL. donovaniclonal lines that have acquired resistance to HePC. We performed whole-genome and RNA sequencing of these resistant lines to provide an inclusive overview of the multifactorial acquisition of experimental HePC resistance, circumventing the challenge of identifying changes in membrane-bound proteins faced by proteomics. This analysis was complemented by assessment of thein vitroinfectivity of HePC-resistant parasites. Our work underscores the importance of complementary “omics” to acquire the most comprehensive insight for multifaceted processes, such as HePC resistance.
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Doguer, Caglar, Jung-Heun Ha, Sukru Gulec, Chris D. Vulpe, Gregory J. Anderson, and James F. Collins. "Intestinal hephaestin potentiates iron absorption in weanling, adult, and pregnant mice under physiological conditions." Blood Advances 1, no. 17 (July 25, 2017): 1335–46. http://dx.doi.org/10.1182/bloodadvances.2017008359.
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Key Points Intestinal Heph may be required to potentiate iron absorption during rapid growth and pregnancy, or when hypoxia stimulates erythropoiesis. Here, the physiological conditions in which Heph is required are defined and other, complementary, intestinal ferroxidases are identified.
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Lee, S. H., H. J. Oh, M. J. Kim, G. A. Kim, E. M. N. Setyawan, Y. B. Choi, S. Lee, J. X. Jin, A. Taweechaipaisankul, and B. C. Lee. "174 EFFECT OF HUMAN ENDOTHELIAL PROGENITOR CELLS ON IN VITRO MATURATION OF PORCINE OOCYTES AND PARTHENOGENETIC EMBRYO DEVELOPMENT COMPETENCE." Reproduction, Fertility and Development 29, no. 1 (2017): 195. http://dx.doi.org/10.1071/rdv29n1ab174.
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In oocyte maturation, hepatocyte growth factor and vascular endothelial growth factor (VEGF) contribute to promote granulosa cell proliferation and cumulus cell expansion. It is well known that human endothelial progenitor cells (hEPC), which are isolated from monocytes and macrophages, secrete a variety of growth factors, such as hepatocyte growth factor and VEGF, and improve the process of angiogenesis. Therefore, the aim of this study was to investigate the effects of hEPC on in vitro oocyte maturation and subsequent embryo development in pigs. To isolate and culture hEPC, human peripheral blood sample was collected from a healthy donor and peripheral blood mononuclear cells were separated. The peripheral blood mononuclear cells were seeded into flask with defined Keratinocyte-SFM-based medium and incubated at 37°C, 5% CO2. The hEPC were cultured and cryopreserved until use for co-culturing with porcine oocytes obtained from a local slaughterhouse ovaries. Cumulus-oocyte complexes were randomly cultured in 2 groups; 1) co-culturing with hEPC and 2) culturing without hEPC. Cumulus-oocyte complexes were cultured in the in vitro maturation (IVM) medium containing TCM-199 supplemented with 0.57 mM cysteine, 0.91 mM sodium pyruvate, 5 μL mL−1 of insulin-transferrin-selenium solution 100X (Invitrogen, Seoul, South Korea), 10% porcine follicular fluid, 10 IU mL−1 of eCG, and 10 IU mL−1 of hCG. After IVM, the first polar body extrusion was observed under the microscope. To evaluate embryo development competence, the matured oocytes were activated with electrical stimulus and cultured in porcine zygote medium-5 for 7 days. The cleavage and blastocyst formation rates were observed on Day 2 and 7, respectively. Also, blastocysts were stained with Hoechst 33342 and total blastocyst cell numbers were evaluated under a fluorescence microscope. As a result, the oocyte maturation rate or first polar body extrusion rate of the hEPC co-culture group (90.06 ± 0.75) was significantly higher than the control group (90.06 ± 0.75 v. 85.79 ± 0.59; P < 0.05). There was no significant difference between the hEPC co-cultured and the control groups in cleavage rate. However, a significant difference in blastocyst formation rate was observed between the hEPC co-cultured and the control groups (28.45 ± 4.92 v. 15.87 ± 2.27; P < 0.05), whereas total blastocyst cell numbers did not show significant difference between the 2 groups. The all data were analysed by unpaired t-test using GraphPad Prism 5.0 (GraphPad Software Inc., La Jolla, CA, USA). Values are means ± standard error of mean. In conclusion, the results in the present study demonstrated that co-culturing with hEPC improved the in vitro oocyte maturation and blastocyst formation rate. Also, we are underway in analysing the concentration of VEGF families in the hEPC co-culture medium after IVM. For further study, we will analyse the genes of the VEGF signaling pathway in the cumulus cells and matured oocytes derived from the 2 groups. This research was supported by Nature Cell (#550-20150030), global PH.D Fellowship Program through NRF funded by the Ministry of Education (NRF-20142A1021187), and Research Institute for Veterinary Science, the BK21 plus program.
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Nelson, James E., Virginia R. Mugford, Ellen Kilcourse, Richard S. Wang, and Kris V. Kowdley. "Relationship between gene expression of duodenal iron transporters and iron stores in hemochromatosis subjects." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 1 (January 2010): G57—G62. http://dx.doi.org/10.1152/ajpgi.00175.2009.
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To test the hypothesis that differences in duodenal iron absorption may explain the variable phenotypic expression among HFE C282Y homozygotes, we have compared relative gene expression of duodenal iron transporters among C282Y homozygotes [hereditary hemochromatosis (HH)] with and without iron overload. Duodenal biopsy samples were analyzed using real-time PCR for expression of DMT1, FPN1, DCYTB, and HEPH relative to GAPDH from 23 C282Y homozygotes, including 5 “nonexpressors” (serum ferritin < upper limit of normal and absence of phenotypic features of hemochromatosis) and 18 “expressors.” Four subjects of wild type for HFE mutations without iron overload or liver disease served as controls. There was a significant difference in expression of DMT1 ( P = 0.03) and DMT1(IRE) ( P = 0.0013) but not FPN1, DCYTB, or HEPH between groups. Expression of DMT1(IRE) was increased among HH subjects after phlebotomy compared with untreated ( P = 0.006) and nonexpressor groups ( P = 0.026). A positive relationship was observed among all HH subjects regardless of phenotype or treatment status between relative expression of FPN1 and DMT1 ( r = 0.5854, P = 0.0021), FPN1, and DCYTB ( r = 0.5554, P = 0.0040), FPN1 and HEPH ( r = 0.5100, P = 0.0092), and DCYTB and HEPH ( r = 0.5400, P = 0.0053). In summary, phlebotomy is associated with upregulation of DMT1(IRE) expression in HH subjects. HFE C282Y homozygotes without phenotypic expression do not have significantly decreased duodenal gene expression of iron transport genes compared with HH subjects with iron overload. There is coordinated regulation between duodenal expression of FPN1 and DMT1, FPN1 and DCYTB, and FPN1 and HEPH and also DCYTB and HEPH in HH subjects regardless of phenotype.
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Skill, Nicholas James, and Mary Alice Maluccio. "Apurinic/apyrimidinic endonuclease-1 and hepatocellular carcinoma." Journal of Clinical Oncology 38, no. 4_suppl (February 1, 2020): 563. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.563.
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563 Background: The enzyme apurinic/apyrimidinic endonuclease-1 (APE1) is associated with protection against DNA damage and oxidative damage congruent with cancer. The purpose of this study is to investigate hepatic APE1 levels in association with hepatocellular carcinoma (HCC) in order to better stratify patients with underlying liver disease for the development of HCC and identify novel targets for therapy. Methods: Hepatic APE1 levels were determined by immunohistochemistry staining and ELISA within liver and tumor samples from patients with HepC±HCC. Hepatic APE1 staining was semi-quantitated using a scale of 0-100. Serum APE1 levels were determined by ELISA. In addition, APE1 staining was quantified in hepatic paraffin embedded sections from MDR2−/− mice with HCC and within MDR2−/+ mice controls that do not develop HCC. Results: Hepatocyte APE1 staining was lower in livers from patients with HepC and HCC when compared to patients with HepC without HCC. In a similar manner, hepatic APE1 levels were significantly lower in patients with HepC and HCC patients when compared to HepC controls. In contrast, serum APE1 level was greater in patients with HepC and HCC when compared to patients with HepC and no HCC. Moreover, APE1 levels were greater in HCC tumors when compared to non-malignant liver tissue. Hepatocyte APE1 staining in MDR−/− mice with HCC was lower when compared to MDR2−/+ mice that do not develop HCC. In addition, cytosolic APE1 staining was increased in HCC tumor of MDR2−/− mice when compared to controls. Conclusions: Increased APE1 is a potential biomarker of HCC risk in patients with underlying liver disease and is a novel target for therapy in patients with underlying liver disease whom have a higher risk of developing HCC. Consequently, targeted APE1 inhibition may increase chemotherapy response by reducing tolerance to DNA damage. Additional studies are required to better understand the role of APE1 inhibition in HCC in the face of reduced background hepatic APE1 levels.
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Böser, Dr Sebastian. "HepMCVisual – an interactive browser for HepMC events." Journal of Physics: Conference Series 219, no. 4 (April 1, 2010): 042032. http://dx.doi.org/10.1088/1742-6596/219/4/042032.
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Wieder, T., C. C. Geilen, and W. Reutter. "Antagonism of phorbol-ester-stimulated phosphatidylcholine biosynthesis by the phospholipid analogue hexadecylphosphocholine." Biochemical Journal 291, no. 2 (April 15, 1993): 561–67. http://dx.doi.org/10.1042/bj2910561.
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The antagonization of phorbol 12-myristate 13-acetate (PMA)-stimulated phosphatidylcholine (PtdCho) biosynthesis by the phospholipid analogue hexadecylphosphocholine (HePC) in MDCK cells was investigated and compared with the corresponding influence in HeLa cells. In both cell lines, PMA-stimulated PtdCho biosynthesis was antagonized by 50 microM HePC. However, subsequent experiments provided evidence that PMA enhances PtdCho biosynthesis by at least two mechanisms: (i) by stimulation of choline uptake and (ii) by translocation of CTP:choline phosphate cytidylyltransferase to membranes. In MDCK cells, 5 nM PMA caused a 4-fold increase in [methyl-3H]choline incorporation into PtdCho, which was paralleled by an approx. 2-fold stimulation of choline uptake. These data indicate that choline uptake might play an important role in the regulation of PtdCho biosynthesis in this cell line, especially since we could not detect any significant increase in membrane-bound cytidyltransferase activity in PMA-treated MDCK cells. In contrast, enhanced PtdCho biosynthesis in HeLa cells is achieved by a 2-fold increase in particulate cytidylyltransferase activity after PMA stimulation. Translocation of cytidylyltransferase from the cytosol to membranes is therefore important in HeLa cells. Nevertheless, in both cell lines, the main target of HePC seems to be the translocation process. In MDCK cells, addition of 50 microM HePC decreases membrane-bound cytidylyltransferase activity by about 45%, compared with control cells and PMA-treated cells. In HeLa cells, PMA-induced translocation of cytidylyltransferase to membranes is totally abolished by HePC.
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Huang, Guocun, Qing Fan, Sigal Lechno-Yossef, Elizabeth Wojciuch, C. Peter Wolk, Takakazu Kaneko, and Satoshi Tabata. "Clustered Genes Required for the Synthesis of Heterocyst Envelope Polysaccharide in Anabaena sp. Strain PCC 7120." Journal of Bacteriology 187, no. 3 (February 1, 2005): 1114–23. http://dx.doi.org/10.1128/jb.187.3.1114-1123.2005.
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ABSTRACT As demonstrated with alr2835 (hepA) and alr2834 (hepC) mutants, heterocysts of Anabaena sp. strain PCC 7120, a filamentous cyanobacterium, must have an envelope polysaccharide layer (the Hep+ phenotype) to fix dinitrogen in an oxygen-containing milieu (the Fox+ phenotype). Transpositions presumptively responsible for a Fox− phenotype were localized in open reading frames (ORFs) near hepA and hepC. A mutation in each of nine of these ORFs was complemented by a clone bearing only that single, intact ORF. Heterocysts of the nine mutants were found to lack an envelope polysaccharide layer. Complementation of mutations in alr2832 and alr2840 may have resulted from recombination. However, alr2825, alr2827, alr2831, alr2833, alr2837, alr2839, and alr2841, like hepA and hepC, are required for a Hep+ Fox+ phenotype.
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Zheng, Ling-Ling. "Synthesis, Crystal Structures, and Magnetic Properties of Ternary M(II)-Dicyanamide-hydroxypyridine Complexes." Journal of Inorganic Chemistry 2013 (June 5, 2013): 1–10. http://dx.doi.org/10.1155/2013/206589.
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Three two-dimensional (2D) and 3D supramolecular coordination architectures based on ternary M(II)-dicyanamide-2-hydroxypyridine systems, [Co(hmpH)2(dca)2] (1), [Cu(hmpH)2(dca)2] (2), and [Mn(hepH)2(dca)2] (3) (dca = dicyanamide, hmpH = 2-(hydroxymethyl)pyridine, hepH = 2-(hydroxyethyl)pyridine), have been synthesized. 1 is a mononuclear Co(II) complex. The mononuclear units are interlinked into a 2D (4,4) hydrogen-bonded layer via O–H⋯N hydrogen bonds between the hydroxyl groups and the noncoordinating nitrile ends. These 2D layers are further extended into a 3D supramolecular architecture via the interlayer pyridyl-pyridyl stacking interaction. 2 has a 1D coordination chain structure formed by the double 1,5-dca bridged dinuclear [Cu2(1,5-dca)2(hmpH)2] unit and the 1,3-dca bridges via weak Cu–N coordination, and these 1D coordination chains are further extended into 2D hydrogen-bonded layers via strong O–H⋯N hydrogen-bonding interaction between the hydroxyl groups and the noncoordinating nitrile ends. 3 is a 2D (4,4) coordination network made of 1D [Mn(hepH)(1,5-dca)] helical chain units and interchain double (1,5-dca) bridges. Pairs of [Mn(hepH)(1,5-dca)] helical chains are interlinked by the double (1,5-dca) bridges into a racemic coordination layer structure, which is further extended into a 3D hydrogen-bonded network. Magnetic studies reveal that weak antiferromagnetic exchange occurs in 3.
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Gottfredsson, Magnus, Thorarinn Tyrfingsson, Valgerdur Runarsdottir, Ingunn Hansdottir, Ottar M. Bergmann, Einar S. Bjornsson, Birgir Johannsson, et al. "928. Major Decrease in Prevalence of Hepatitis C Viremia in Key Populations following the Second Year of Treatment as Prevention for Hepatitis C (TraP HepC) Program in Iceland." Open Forum Infectious Diseases 5, suppl_1 (November 2018): S30. http://dx.doi.org/10.1093/ofid/ofy209.069.
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Abstract Background Hepatitis C Virus (HCV) commonly affects people who inject drugs (PWID) and/or with history of injection drug use (IDU). They are also disproportionately represented in addiction treatment centers and the penitentiary system. In order to curtail spread of HCV it is therefore important to approach these groups. PWID and prisoners have been prioritized in the TraP HepC program. The impact can thus be assessed by monitoring HCV prevalence at sentinel sites, such as addiction hospitals and prisons. Methods TraP HepC offers direct-acting antiviral agents (DAAs) to all HCV patients in Iceland, starting in January 2016. HCV PCR is performed at the end of treatment and 12 weeks later (SVR12). PWID and prisoners are monitored for reinfection and retreated if needed. We compared the prevalence of HCV viremia among PWID admitted for treatment at Vogur addiction hospital and inmates of the penitentiary system, before and after 2 years of TraP HepC. Results Two years into the program 667 patients had been evaluated of which 632 were initiated on their first course of DAAs and 7 were pending, representing 80% of the estimated total patient population. Of those who completed first treatment according to guidelines the SVR12 is 95.5%. Drop-out from first treatment was 8.2%; nevertheless, the SVR12 was >40% and most of the remaining viremic patients completed or are undergoing retreatment. In 2012–2015, prior to TraP HepC the prevalence of HCV viremia among actively injecting PWID admitted for addiction treatment was 47.9%, dropping to 39.8% in 2016 and 16.2% in 2017 (P < 0.001). Likewise, the prevalence of viremia among patients with history of IDU but not recently injecting fell from 27.4% (2012–2015) to 19.8% in 2016 and 4.1% in 2017 (P < 0.001). The prevalence of viremia among inmates of the penitentiary system was 29% prior to initiation of TraP HepC, dropping to 7% in 2017 (P < 0.01). These results are not explained by declining IDU in the community. Conclusion On a population level the domestic transmission of HCV can be reduced by DAAs when combined with other efforts. Two years into the TraP HepC program the prevalence of viremia among two of the most important drivers of the epidemic has been markedly reduced. The program is ongoing, with further emphasis on increased intensity of screening, retreatment and harm reduction. Disclosures All authors: No reported disclosures.
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Ledezma Morales, Mónica, Juan Carlos Restrepo Gutierrez, Pedro Amariles Muñoz, Maria Camila Trillos Almanza, and Rubén Darío Vargas Ruiz. "Caracterización de pacientes con hepatitis C crónica tratados en un hospital de alta complejidad de Medellín." Revista Colombiana de Gastroenterología 34, no. 3 (October 7, 2019): 249–60. http://dx.doi.org/10.22516/25007440.328.
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Introducción: la hepatitis C (HepC) representa un problema de salud pública a nivel mundial. Se estima que en Colombia la prevalencia de virus de la hepatitis C (VHC) está entre el 0,5-1 %, y asciende al 2,1 % en pacientes mayores de 50 años. La Unidad de Hepatología del Hospital Pablo Tobón Uribe (HPTU) ha sido un referente en el manejo de la HepC en Medellín y Colombia durante años.
Objetivo: describir las características sociodemográficas/clínicas y los resultados en salud de los pacientes con HepC crónica atendidos en el HPTU entre 2013 y 2018.
Materiales y métodos: estudio observacional, descriptivo, retrospectivo de pacientes con HepC crónica atendidos entre el 1 de enero de 2013 y el 31 de marzo de 2018.
Resultados: se analizaron 108 pacientes. La edad promedio fue de 55,8 años (desviación estándar [DE] 13,7), 51,9 % eran hombres, y 78,7 % pertenecían al régimen contributivo. El mecanismo de transmisión más frecuente fue la hemotransfusión; el genotipo 1 predominó en el grupo de pacientes analizados. La efectividad de los esquemas con interferón fue del 46,9 % y de los antivirales de acción directa (AAD) del 94,6 %. La presencia de reacciones adversas a medicamentos (RAM) fue del 68,2 % en pacientes con esquemas con interferón/ribavirina y del 25,9 % en pacientes con AAD.
Conclusiones: se realiza la caracterización de los pacientes atendidos en el HPTU, en quienes los AAD han mostrado mayor efectividad y seguridad en comparación con esquemas con interferón/ribavirina.
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Müller-Ehmsen, Jochen, Annette Schmidt, Benjamin Krausgrill, Robert H. G. Schwinger, and Wilhelm Bloch. "Role of erythropoetin for angiogenesis and vasculogenesis: from embryonic development through adulthood." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 1 (January 2006): H331—H340. http://dx.doi.org/10.1152/ajpheart.01269.2004.
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Erythropoetin (EPO), a stimulator of erythropoiesis, was previously shown to stimulate angiogenesis and proliferation of endothelial cells. Here, we investigated and compared the influence of EPO on cell number, proliferation, apoptosis, migration, and differentiation of endothelial cells in intact mouse embryoid bodies (EB), isolated endothelial cells from EB (EBEC), and adult human endothelial progenitor cells (hEPC). EB were treated with EPO (0.5 U/ml) immediately after plating was completed ( day 5+0) or 3 days later. EPO treatment was continued until days 5+3 or 5+6. Cultured EBEC were treated 3 days after being plated, and primary hEPC from young healthy adults were treated 5 days after being plated with EPO for 48 h. Immunohistochemistry was performed with anti-PECAM (CD31), anti-Ki67, anti-CD34, anti-CD133, anti-EphB4, and anti-ephrinB2 antibodies. In all, mouse EB and EBEC and hEPC, EPO-treatment resulted in increased number of endothelial cells, increased proliferation, decreased apoptosis, and enhanced migration. In EB, this EPO effect was most pronounced when treatment was begun early ( day 5+0) and was accompanied by an enhanced endothelial tube formation. In EBEC and hEPC, EPO shifted the phenotypic differentiation toward an increased ratio of EphB4-positive cells, i.e., toward a venous phenotype. These results are consistent with an important role of EPO for the number, proliferation, apoptosis, function, and phenotypical development of immature endothelial cells, which persists from early development through adulthood. They provide additional and further evidence for a strong interrelation between hematopoiesis and vasculogenesis/angiogenesis (sharing the same pathways), which may be important in many physiological and pathophysiological conditions.
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Roetto, Antonella, Mariarosa Mezzanotte, and Rosa Pellegrino. "The Functional Versatility of Transferrin Receptor 2 and Its Therapeutic Value." Pharmaceuticals 11, no. 4 (October 23, 2018): 115. http://dx.doi.org/10.3390/ph11040115.
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Iron homeostasis is a tightly regulated process in all living organisms because this metal is essential for cellular metabolism, but could be extremely toxic when present in excess. In mammals, there is a complex pathway devoted to iron regulation, whose key protein is hepcidin (Hepc), which is a powerful iron absorption inhibitor mainly produced by the liver. Transferrin receptor 2 (Tfr2) is one of the hepcidin regulators, and mutations in TFR2 gene are responsible for type 3 hereditary hemochromatosis (HFE3), a genetically heterogeneous disease characterized by systemic iron overload. It has been recently pointed out that Hepc production and iron regulation could be exerted also in tissues other than liver, and that Tfr2 has an extrahepatic role in iron metabolism as well. This review summarizes all the most recent data on Tfr2 extrahepatic role, taking into account the putative distinct roles of the two main Tfr2 isoforms, Tfr2α and Tfr2β. Representing Hepc modulation an effective approach to correct iron balance impairment in common human diseases, and with Tfr2 being one of its regulators, it would be worthwhile to envisage Tfr2 as a therapeutic target.
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Koksharova, Olga A., and C. Peter Wolk. "Novel DNA-Binding Proteins in the Cyanobacterium Anabaena sp. Strain PCC 7120." Journal of Bacteriology 184, no. 14 (July 15, 2002): 3931–40. http://dx.doi.org/10.1128/jb.184.14.3931-3940.2002.
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ABSTRACT As an approach towards elucidation of the biochemical regulation of the progression of heterocyst differentiation in Anabaena sp. strain PCC 7120, we have identified proteins that bind to a 150-bp sequence upstream from hepC, a gene that plays a role in the synthesis of heterocyst envelope polysaccharide. Such proteins were purified in four steps from extracts of vegetative cells of Anabaena sp. Two of these proteins (Abp1 and Abp2) are encoded by neighboring genes in the Anabaena sp. chromosome. The genes that encode the third (Abp3) and fourth (Abp4) proteins are situated at two other loci in that chromosome. Insertional mutagenesis of abp2 and abp3 blocked expression of hepC and hepA and prevented heterocyst maturation and aerobic fixation of N2.
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ARUNA, S., R. THIYAGARAJAN, and A. PANNEERSELVAM. "Ultrasonic Investigation on Hydroxy Ethyl Propyl Cellulose (HEPC) Solution at Different Concentration and pH." Asian Journal of Chemistry 32, no. 9 (2020): 2255–61. http://dx.doi.org/10.14233/ajchem.2020.22765.
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The ultrasonic investigation is one of the most effective and economical technique to analyze the nature of the matter. Ultrasonic techniques provide valuable information about the physico-chemical nature of the aqueous solutions. Thus, the propagation characteristics of an acoustical wave in solutions are used to study the nature of intermolecular interaction. In this work, the ultrasonic velocity, viscosity and density studies were determined to study the effect of concentration and pH in the aqueous hydroxyethyl propyl cellulose (HEPC) solutions at different temperatures (303, 313 and 323 K). From the observed values, the necessary related ultrasonic parameters are calculated and their variations are discussed. The findings from the result say the variations in the velocity and absorption coefficient values are only due to the conformational changes that occur in the HEPC solution.
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Dobbs, Matt, and Jørgen Beck Hansen. "The HepMC C++ Monte Carlo event record for High Energy Physics." Computer Physics Communications 134, no. 1 (February 2001): 41–46. http://dx.doi.org/10.1016/s0010-4655(00)00189-2.
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Roetto, Antonella, Rosa Maria Pellegrino, Ilaria Defilippi, Sonia Carturan, Enrico Bracco, Daniela Cilloni, Clara Camaschella, and Giuseppe Saglio. "TFR2 BETA Isoform Is Differentially Produced Compared to ALFA and Has Specific Function at Young Age." Blood 112, no. 11 (November 16, 2008): 1856. http://dx.doi.org/10.1182/blood.v112.11.1856.1856.
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Abstract The transferrin receptor 2 gene (TFR2) encodes for a transmembrane protein that plays a pivotal role in iron metabolism, since TFR2 mutations are responsible of type 3 Hereditary Hemochromatosis (HH). Together with other HH proteins (Hfe and Rgmc) Tfr2 participates to modulation of Hepcidin (Hepc) production, a small peptide able to regulate body iron availability through its negative effect on cellular iron exporter Ferroportin (Fpn1). Tfr2 protein is a member of the transferrin receptor family, showing moderate homology to transferrin receptor (Tfrc). It is able to bind transferrin even thought at lower affinity compared to TFRC. Two alternative transcripts of TFR2 have been reported, named alfa and beta. TFR2 alfa mRNA is highly expressed in the hepatocytes while TFR2 beta has a low ubiquitous expression (Kawabata et al, 1999). The beta isoform is identical to alfa but it lacks the transmembrane and cytoplasmic domains; it has been considered an alternative splicing form and its role is still poorly understood. Nevertheless, clinical observations support the hypothesis that TFR2 beta has an important functional role since HFE3 patients with mutations not compromising its production have a milder phenotype compared to those unable to synthesize both alfa and beta TFR2 isoforms (Roetto et al,2002; Le Gac et al, 2004). In order to elucidate whether TFR2 beta was differentially expressed and produced during life span its mRNA and translated protein were analyzed in C57BL/6 mice during their growth and adult age. Since Tfr2 beta protein has never been demonstrated to exist before, its cDNA has been cloned in an expression vector and transfected in HEK293T cells. Cells lysates have been electhrophoresed, transferred onto nitrocellulose membrane, decorated with Tfr2 Ab (Santa Cruz Biotechnoloy, Inc) and visualized on Western Blot. A 65 kDa band has been obtained from the transfection, consistent with the aminoacid sequence predicted molecular weight, and used as a positive control for further in vivo experiments. C57BL/6 mice livers from seven different ages, starting from birth until adult age (post natal days 0, 1, 3, 7, 14, 28, 40 and 60) have been analyzed in WB utilizing Tfr2 antibody. At least three mice per point have been analyzed. One band of a molecular weight of approximately 95 KDa has been detected during whole animal life, quantitatively increasing during life time, corresponding to Tfr2 alfa. Meanwhile, the beta isoform appeared to be consistently produced until the 7th day after birth and disappears starting from day 14. To evaluate the possible consequences of this result on iron metabolism, HH proteins (Hfe, Fpn1, Rgmc) mRNA expression pattern has been analyzed in real time PCR at the same points, as well as Hepcidin (Hepc) transcript, in order to evaluate whether TFR2 beta production could in some way influence Hepc modulation. HEPC transcription resulted to be significantly downmodulated from day 0 after birth until day 14 as compared to later stages in mice life (adulthood). HFE transcription resulted to be lower in young animals compared to adults while FPN1 increased significantly between day 3 and 7, according to HEPC decreasing. On the whole, these results suggest a functional role for the Tfr2 beta isoform in iron sensing, since this isoform resulted to be selectively produced during animal growth. At the same life period Hepc transcription resulted to be significantly downmodulated, allowing in this way increased iron absorption. These data are consistent with an higher iron requirement necessary for massive animal body growth.
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Sadeghi, Reza, Seyed Saeed Mazloomy Mahmoodabad, Hossein Fallahzadeh, Mohsen Rezaeian, Reza Bidaki, and Narges Khanjani. "Hookah is the enemy of health campaign: a campaign for prevention of hookah smoking among youth." Health Promotion International 35, no. 5 (November 5, 2019): 1125–36. http://dx.doi.org/10.1093/heapro/daz109.
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Abstract Hookah smoking is now a serious health threat especially for adolescents. Implementation of planned interventions can help reduce hookah smoking. This study was conducted to investigate the effect of a campaign Hookah is the Enemy of Health Campaign (HEHC) based on the protection motivation theory to prevent hookah smoking among the youth in Sirjan city, in 2018. This was a pre- and post-intervention study. Participants were 280 male and female youth who were selected randomly through the health centers of Sirjan. The educational campaign was conducted during 3 months and participants were trained through interpersonal, group, organizational and community channels and mass media. Data were collected by filling out a questionnaire (containing 64 questions) by the participant before the intervention and 3 months after. Data were analyzed by descriptive statistics (frequency and percentage), chi-square and Wilcoxon signed-rank test by SPSS20 software. The prevalence of hookah smoking was 44.3% in the target group. There was a significant change in the mean scores of knowledge and perceived susceptibility, perceived severity, response efficiency, self-efficacy, rewards, fear and protection motivation after the HEHC (p < 0.05), but there was no significant difference in the structure of perceived cost (p > 0.05). Also, the prevalence of hookah smoking among the target group for those who had ever consumed decreased from 8.9 to 4% and for those who used it occasionally decreased from 35 to 19.4%. The HEHC was effective in reducing hookah smoking, raising knowledge and improving the constructs of the protection motivation theory among the youth of Sirjan.
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Zanella, Isabella, Giulia Paiardi, Diego Di Lorenzo, and Giorgio Biasiotto. "Iron Absorption in Celiac Disease and Nutraceutical Effect of 7-Hydroxymatairesinol. Mini-Review." Molecules 25, no. 9 (April 27, 2020): 2041. http://dx.doi.org/10.3390/molecules25092041.
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Anemia is the main extra-gastrointestinal symptom in inflammatory bowel diseases (IBDs). Interleukin-6 (IL-6) and other cytokines are secreted and act in the microenvironment of the small intestine mucous membrane of IBD patients. Iron is essential for multiple cell functions and its homeostasis is regulated by the hepcidin–ferroportin axis. Hepcidin (HEPC) is mainly produced by the liver in response to iron needs but is also an acute phase protein. During inflammation, hepcidin is upregulated by IL-6 and is responsible for iron compartmentalization within cells, in turn causing anemia of inflammation. Tissues other than liver can produce hepcidin in response to inflammatory stimuli, in order to decrease iron efflux at a local level, then acting in an autocrine–paracrine manner. In IBDs and, in particular, in celiac disease (CeD), IL-6 might trigger the expression, upregulation and secretion of hepcidin in the small intestine, reducing iron efflux and exacerbating defective iron absorption. 7-Hydroxymatairesinol (7-HMR) belongs to the family of lignans, polyphenolic compounds produced by plants, and has nutraceutical antioxidant, anti-inflammatory and estrogenic properties. In this mini-review we revise the role of inflammation in IBDs and in particular in CeD, focusing our attention on the close link among inflammation, anemia and iron metabolism. We also briefly describe the anti-inflammatory and estrogenic activity of 7-HMR contained in foods that are often consumed by CeD patients. Finally, considering that HEPC expression is regulated by iron needs, inflammation and estrogens, we explored the hypothesis that 7-HMR consumption could ameliorate anemia in CeD using Caco-2 cells as bowel model. Further studies are needed to verify the regulation pathway through which 7-HMR may interfere with the local production of HEPC in bowel.
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Zhao, Liangliang, Majda Hadziahmetovic, Chenguang Wang, Xueying Xu, Ying Song, H. A. Jinnah, Jolanta Wodzinska, et al. "Cp/Heph mutant mice have iron-induced neurodegeneration diminished by deferiprone." Journal of Neurochemistry 135, no. 5 (September 29, 2015): 958–74. http://dx.doi.org/10.1111/jnc.13292.
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Han, Okhee, and Marianne Wessling-Resnick. "Copper repletion enhances apical iron uptake and transepithelial iron transport by Caco-2 cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 3 (March 1, 2002): G527—G533. http://dx.doi.org/10.1152/ajpgi.00414.2001.
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The influence of copper status on Caco-2 cell apical iron uptake and transepithelial transport was examined. Cells grown for 7–8 days in media supplemented with 1 μM CuCl2had 10-fold higher cellular levels of copper compared with control. Copper supplementation did not affect the integrity of differentiated Caco-2 cell monolayers grown on microporous membranes. Copper-repleted cells displayed increased uptake of iron as well as increased transport of iron across the cell monolayer. Northern blot analysis revealed that expression of the apical iron transporter divalent metal transporter-1 (DMT1), the basolateral transporter ferroportin-1 (Fpn1), and the putative ferroxidase hephaestin (Heph) was upregulated by copper supplementation, whereas the recently identified ferrireductase duodenal cytochrome b (Dcytb) was not. These results suggest that DMT1, Fpn1, and Heph are involved in the iron uptake process modulated by copper status. Although a clear role for Dcytb was not identified, an apical surface ferrireductase was modulated by copper status, suggesting that its function also contributes to the enhanced iron uptake by copper-repleted cells. A model is proposed wherein copper promotes iron depletion of intestinal Caco-2 cells, creating a deficiency state that induces upregulation of iron transport factors.
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Zhu, Jinsong, Renqiu Kong, and C. Peter Wolk. "Regulation of hepA ofAnabaena sp. Strain PCC 7120 by Elements 5′ from the Gene and by hepK." Journal of Bacteriology 180, no. 16 (August 15, 1998): 4233–42. http://dx.doi.org/10.1128/jb.180.16.4233-4242.1998.
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ABSTRACT In Anabaena spp., synthesis of the heterocyst envelope polysaccharide, required if the cell is to fix dinitrogen under aerobic conditions, is dependent on the gene hepA. A transcriptional start site of hepA was localized 104 bp 5′ from its translational initiation codon. A 765-bp open reading frame, denoted hepC, was found farther upstream. Inactivation ofhepC led to constitutive expression of hepA and prevented the synthesis of heterocyst envelope polysaccharide. However, the glycolipid layer of the heterocyst envelope was synthesized. AhepK mutation blocked both the synthesis of the heterocyst envelope polysaccharide and induction of hepA. The predicted product of hepK resembles a sensory protein-histidine kinase of a two-component regulatory system. Analysis of the region between hepC and hepA indicated that DNA sequences required for the induction of hepA upon nitrogen deprivation are present between bp −574 and −440 and between bp −340 and −169 relative to the transcriptional start site ofhepA. Gel mobility shift assays provided evidence that one or more proteins bind specifically to the latter sequence. The Fox box sequence downstream from hepA appeared inessential for the induction of hepA.
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Krawczenko, Agnieszka, Aleksandra Bielawska-Pohl, Maria Paprocka, Honorata Kraskiewicz, Agnieszka Szyposzynska, Elżbieta Wojdat, and Aleksandra Klimczak. "Microvesicles from Human Immortalized Cell Lines of Endothelial Progenitor Cells and Mesenchymal Stem/Stromal Cells of Adipose Tissue Origin as Carriers of Bioactive Factors Facilitating Angiogenesis." Stem Cells International 2020 (June 15, 2020): 1–17. http://dx.doi.org/10.1155/2020/1289380.
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Endothelial progenitor cells (EPCs) and mesenchymal stem/stromal cells (MSCs) are associated with maintaining tissue homeostasis and tissue repair. Both types of cells contribute to tissue regeneration through the secretion of trophic factors (alone or in the form of microvesicles). This study investigated the isolation and biological properties of microvesicles (MVs) derived from human immortalized MSC line HATMSC1 of adipose tissue origin and EPC line. The human immortalized cell line derived from the adipose tissue of a patient with venous stasis was established in our laboratory using the hTERT and pSV402 plasmids. The human EPC line originating from cord blood (HEPC-CB.1) was established in our previous studies. Microvesicles were isolated through a sequence of centrifugations. Analysis of the protein content of both populations of microvesicles, using the Membrane-Based Antibody Array and Milliplex ELISA showed that isolated microvesicles transported growth factors and pro- and antiangiogenic factors. Analysis of the miRNA content of isolated microvesicles revealed the presence of proangiogenic miRNA (miR-126, miR-296, miR-378, and miR-210) and low expression of antiangiogenic miRNA (miR-221, miR-222, and miR-92a) using real-time RT-PCR with the TaqMan technique. The isolated microvesicles were assessed for their effect on the proliferation and proangiogenic properties of cells involved in tissue repair. It was shown that both HEPC-CB.1- and HATMSC1-derived microvesicles increased the proliferation of human endothelial cells of dermal origin and that this effect was dose-dependent. In contrast, microvesicles had a limited impact on the proliferation of fibroblasts and keratinocytes. Both types of microvesicles improved the proangiogenic properties of human dermal endothelial cells, and this effect was also dose-dependent, as shown in the Matrigel assay. These results confirm the hypothesis that microvesicles of HEPC-CB.1 and HATMSC1 origin carry proteins and miRNAs that support and facilitate angiogenic processes that are important for cutaneous tissue regeneration.
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Jończy, Aneta, Rafał Mazgaj, Rafał Radosław Starzyński, Piotr Poznański, Mateusz Szudzik, Ewa Smuda, Marian Kamyczek, and Paweł Lipiński. "Relationship between Down-Regulation of Copper-Related Genes and Decreased Ferroportin Protein Level in the Duodenum of Iron-Deficient Piglets." Nutrients 13, no. 1 (December 30, 2020): 104. http://dx.doi.org/10.3390/nu13010104.
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In mammals, 2 × 1012 red blood cells (RBCs) are produced every day in the bone marrow to ensure a constant supply of iron to maintain effective erythropoiesis. Impaired iron absorption in the duodenum and inefficient iron reutilization from senescent RBCs by macrophages contribute to the development of anemia. Ferroportin (Fpn), the only known cellular iron exporter, as well as hephaestin (Heph) and ceruloplasmin, two copper-dependent ferroxidases involved in the above-mentioned processes, are key elements of the interaction between copper and iron metabolisms. Crosslinks between these metals have been known for many years, but metabolic effects of one on the other have not been elucidated to date. Neonatal iron deficiency anemia in piglets provides an interesting model for studying this interplay. In duodenal enterocytes of young anemic piglets, we identified iron deposits and demonstrated increased expression of ferritin with a concomitant decline in both Fpn and Heph expression. We postulated that the underlying mechanism involves changes in copper distribution within enterocytes as a result of decreased expression of the copper transporter—Atp7b. Obtained results strongly suggest that regulation of iron absorption within enterocytes is based on the interaction between proteins of copper and iron metabolisms and outcompetes systemic regulation.
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Brady, Kristen, Hsiao-Ching Liu, Julie A. Hicks, Julie A. Long, and Tom E. Porter. "Transcriptome analysis of the hypothalamus and pituitary of turkey hens with low and high egg production." BMC Genomics 21, no. 1 (September 21, 2020). http://dx.doi.org/10.1186/s12864-020-07075-y.
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Abstract Background High egg producing hens (HEPH) show increased hypothalamic and pituitary gene expression related to hypothalamo-pituitary-gonadal (HPG) axis stimulation as well as increased in vitro responsiveness to gonadotropin releasing hormone (GnRH) stimulation in the pituitary when compared to low egg producing hens (LEPH). Transcriptome analysis was performed on hypothalamus and pituitary samples from LEPH and HEPH to identify novel regulators of HPG axis function. Results In the hypothalamus and pituitary, 4644 differentially expressed genes (DEGs) were identified between LEPH and HEPH, with 2021 genes up-regulated in LEPH and 2623 genes up-regulated in HEPH. In LEPH, up-regulated genes showed enrichment of the hypothalamo-pituitary-thyroid (HPT) axis. Beta-estradiol was identified as an upstream regulator regardless of tissue. When LEPH and HEPH samples were compared, beta-estradiol was activated in HEPH in 3 of the 4 comparisons, which correlated to the number of beta-estradiol target genes up-regulated in HEPH. In in vitro pituitary cell cultures from LEPH and HEPH, thyroid hormone pretreatment negatively impacted gonadotropin subunit mRNA levels in cells from both LEPH and HEPH, with the effect being more prominent in HEPH cells. Additionally, the effect of estradiol pretreatment on gonadotropin subunit mRNA levels in HEPH cells was negative, whereas estradiol pretreatment increased gonadotropin subunit mRNA levels in LEPH cells. Conclusions Up-regulation of the HPT axis in LEPH and upstream beta-estradiol activation in HEPH may play a role in regulating HPG axis function, and ultimately ovulation rates. Thyroid hormone and estradiol pretreatment impacted gonadotropin mRNA levels following GnRH stimulation, with the inhibitory effects of thyroid hormone more detrimental in HEPH and estradiol stimulatory effects more prominent in LEPH. Responsiveness to thyroid hormone and estradiol may be due to desensitization to thyroid hormone and estradiol in LEPH and HEPH, respectively, due to up-regulation of the HPT axis in LEPH and of the HPG axis in HEPH. Further studies will be necessary to identify possible target gene desensitization mechanisms and elicit the regulatory role of the HPT axis and beta-estradiol on ovulation rates in turkey hens.
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Zacchi, Paola, Beatrice Belmonte, Alessandro Mangogna, Gaia Morello, Letizia Scola, Anna Martorana, and Violetta Borelli. "The Ferroxidase Hephaestin in Lung Cancer: Pathological Significance and Prognostic Value." Frontiers in Oncology 11 (May 19, 2021). http://dx.doi.org/10.3389/fonc.2021.638856.
Full textAbstract:
Hephaestin (HEPH) belongs to a group of exocytoplasmic ferroxidases which contribute to cellular iron homeostasis by favouring its export. Down-regulation of HEPH expression, possibly by stimulating cell proliferation due to an increase in iron availability, has shown to correlate with poor survival in breast cancer. The lung is particularly sensitive to iron-induced oxidative stress, given the high oxygen tension present, however, HEPH distribution in lung cancer and its influence on prognosis have not been investigated yet. In this study we explored the prognostic value of HEPH and its expression pattern in the most prevalent histotypes of lung cancers, namely lung adenocarcinoma and lung squamous cell carcinoma. In silico analyses, based on UALCAN, Gene Expression Profiling Interactive Analysis (GEPIA) and Kaplan–Meier plotter bioinformatics, revealed a significant correlation between higher levels of HEPH expression and favorable prognosis, in both cancer histotypes. Moreover, TIMER web platform showed a statistically significant association between HEPH expression and cell elements belonging to the tumor microenvironment identified as endothelial cells and a subpopulation of cancer-associated fibroblasts, further confirmed by double immunohistochemical labeling with cell type specific markers. Taken together, these data shed a light on the complex mechanisms of local iron handling lung cancer can exploit to support tumorigenesis.
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"An analysis to improve regional information accessibility to promote the “health for a care-focused mature society”." Health Education and Public Health 1, no. 1 (August 30, 2018). http://dx.doi.org/10.31488/heph.101.
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"Utility of Component-resolved diagnosis in allergic disease in children and adults." Health Education and Public Health 1, no. 1 (August 30, 2018). http://dx.doi.org/10.31488/heph.102.
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"How to Improve Population Mental Health on the Community and Country Level." Health Education and Public Health 1, no. 1 (August 30, 2018). http://dx.doi.org/10.31488/heph.103.
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"Social support among Disabled Palestinian Children in the Gaza Strip." Health Education and Public Health 1, no. 1 (August 30, 2018). http://dx.doi.org/10.31488/heph.104.
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"Replication study : Distracted walking at four dangerous intersections in Manhattan." Health Education and Public Health 1, no. 1 (August 30, 2018). http://dx.doi.org/10.31488/heph.105.
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"Anxiety about ageing and related factors in Japan." Health Education and Public Health 1, no. 2 (December 30, 2018). http://dx.doi.org/10.31488/heph.106.
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"Care Preferences of Elderly People Living Alone in Japan." Health Education and Public Health 1, no. 2 (December 30, 2018). http://dx.doi.org/10.31488/heph.107.
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"Future LTC needs of the elderly in Japan with some reference to Germany." Health Education and Public Health 1, no. 2 (December 30, 2018). http://dx.doi.org/10.31488/heph.108.
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"Improvement prediction process prevent chronic diseases from environmental threat: Integration omics to decision process in quality of health." Health Education and Public Health 1, no. 2 (December 30, 2018). http://dx.doi.org/10.31488/heph.109.
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"Electromagnetic properties of the human blood circulation." Health Education and Public Health 1, no. 2 (December 30, 2018). http://dx.doi.org/10.31488/heph.110.
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