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Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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1

Chauhan, Madhu, Meena Balakrishnan, Alex Vidaeff, Uma Yallampalli, Fernando Lugo, Karin Fox, Michael Belfort, and Chandra Yallampalli. "Adrenomedullin2 (ADM2)/Intermedin (IMD): A Potential Role in the Pathophysiology of Preeclampsia." Journal of Clinical Endocrinology & Metabolism 101, no. 11 (September 1, 2016): 4478–88. http://dx.doi.org/10.1210/jc.2016-1333.

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Context: It is not known whether decreases in trophoblast invasion promoting the peptide, adrenomedullin2 (ADM2) system is associated with preeclampsia (PreE). Objective: The objective of the study was to assess the changes in ADM2 levels in plasma, placenta, and amniotic fluid (AF) and its receptor components in placenta from PreE pregnancy compared with the age-matched normal and study the effect of ADM2 on the synthesis of nitric oxide (NO), endothelial nitric oxide synthase (eNOS), and matrix-metalloproteinase (MMP)-2 and MMP-9 in trophoblast cells. Results: PreE is associated with a decreased expression of ADM2 in plasma and placenta (P < .05); ADM2 interacts with a seven-transmembrane G protein-coupled receptor, calcitonin receptor-like receptor (CRLR) in HTR-8/SVneo cells; placental expression of ADM2/CRLR complex is lower in PreE; mRNA for CRLR and receptor activity-modifying protein-3 are lower, whereas receptor activity-modifying protein-2 is higher in the PreE placenta (P < .05); ADM2 levels in the second trimester are lower in the AF from pregnant women who develop PreE later in gestation (P < .05); ADM2 is localized to the epithelium of the amnion and the ectoderm and mesoderm of the chorion in term fetal membranes; ADM2 increases NO production, eNOS, and MMP2/9-immunoreactivity, whereas ADM2 knockdown inhibits the expression of eNOS and MMP2/9 mRNA and S-nitrosylation in HTR-8/SVneo cells; and ADM2-induced increases in MMP2/9 activity is inhibited by L-nitro-arginine methyl ester in HTR-8SV/neo cells. Conclusion: Decreases in the ADM2 system in PreE at term, in AF from pregnant women during the second trimester who develop PreE later in gestation, and ADM2-induced increases in the NO and MMP-2/9 levels in trophoblast cells suggest a potential role for ADM2 via the NO-MMP system in the pathophysiology of PreE.
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2

Ranjbaran, Ali, Hamid Nejabati, Tohid Ghasemnejad, Zeinab Latifi, Kobra Hamdi, Hamed Hajipour, Nathalie Raffel, et al. "Follicular Fluid Levels of Adrenomedullin 2, Vascular Endothelial Growth Factor and its Soluble Receptors Are Associated with Ovarian Response During ART Cycles." Geburtshilfe und Frauenheilkunde 79, no. 01 (January 2019): 86–93. http://dx.doi.org/10.1055/a-0764-4765.

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Abstract Introduction Adrenomedullin 2 (ADM2) and vascular endothelial growth factor (VEGF) affect ovarian function, especially angiogenesis and follicular development. The actions of VEGF can be antagonized by its soluble receptors, soluble Fms-like tyrosine kinase-1 (sFlt-1) and soluble VEGF receptor 2 (sVEGFR-2), as they decrease its free form. In the present study, we evaluated the relationship between follicular fluid (FF) levels of AMD2, VEGF and its soluble receptors, and ICSI outcomes. Materials and Methods ICSI cycle outcomes were evaluated and FF levels of VEGF, sFlt-1, sVEGFR-2 and ADM2 were determined using ELISA kits. Results FF levels of ADM2, VEGF, and sVEGFR-2 were significantly higher in non-responders compared to other ovarian response groups (p < 0.05). There were significant correlations between ADM2, VEGF and sVEGFR-2 levels as well as VEGF/sFlt-1 and VEGF/sVEGFR-2 ratios (r = 0.586, 0.482, 0.260, and − 0.366, respectively). Based on the ROC curve, the cutoff value for ADM2 as a non-responder predictor was 348.55 (pg/ml) with a sensitivity of 67.7% and a specificity of 94.6%. Conclusions For the first time we measured FF ADM2 levels to determine the relationship to VEGF and its soluble receptors. We suggest that ADM2 could be a potential predictive marker for non-responders. Although the exact function of ADM2 in ovarian angiogenesis is not yet understood, our study may shed light on the possible role of ADM2 in folliculogenesis and ovulation.
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3

Chauhan, Madhu, Ancizar Betancourt, Meena Balakrishnan, Akansha Mishra, Karin Fox, Michael Belfort, and Chandra Yallampalli. "Soluble fms-like tyrosine kinase-1 and angiotensin2 target calcitonin gene-related peptide family peptides in maternal vascular smooth muscle cells in pregnancy†." Biology of Reproduction 104, no. 5 (February 24, 2021): 1071–83. http://dx.doi.org/10.1093/biolre/ioab026.

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ABSTRACT Calcitonin gene-related peptide (CALCB), adrenomedullin (ADM), and adrenomedullin2 (ADM2) are hypotensive peptides that belong to CALCB family of peptides. Goal of this study was to identify the effect of fms-like tyrosine kinase (sFLT-1) and angiotensin2 (Ang2) on the function of these peptides in OA smooth muscle cells (OASMC) and assess the sensitivity of OA for these peptides in preeclampsia (PE) and normotensive pregnancy. Methods: Peptide function was assessed by Cyclic adenosine monophosphate (cAMP) assays and wire myograph; mRNA expression by Polymerase chain reaction (PCR) and protein-protein interaction by proximity ligation assay and co-immunoprecipitation. Findings: All three peptides increased cAMP synthesis in the order of efficacy CALCB &gt; ADM = ADM2 and vascular endothelial growth factor (VEGF) mRNA in OASMC (P &lt; 0.05); sFLT-1 mediated decrease in cAMP synthesis (P &lt; 0.05) is differentially rescued by all three CALCB family peptides in OASMC (P &lt; 0.005); sFLT-1 decreased receptor activity-modifying protein (RAMP)1 and RAMP2 mRNA expression (P &lt; 0.05); Ang2 decreased the expression of calcitonin-receptor-like receptor and RAMP1 mRNA and desensitized CALCB and ADM2 receptors in OASMC (P &lt; 0.05); sFLT-1 increased RAMP1and Ang2 type 1 receptor (AT1R) interaction in OASMC which is inhibited in presence of all three peptides; and all three peptides relax OA in PE with enhanced ADM2 response (P &lt; 0.05). Conclusion: sFLT-1 and Ang2 impair OASMC mediated functional responses of CALCB family peptides which can be inhibited by respective peptide treatment. The sensitivity of OA for CALCB, ADM, and ADM2-mediated relaxation is retained in PE.
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4

Kim, Jimin, Seul Ki Lee, Donguk Kim, Han Choe, Yeon Jin Jang, Hye Soon Park, Jong-Hyeok Kim, Joon Pio Hong, Yeon Ji Lee, and Yoonseok Heo. "Altered Expression of Adrenomedullin 2 and its Receptor in the Adipose Tissue of Obese Patients." Journal of Clinical Endocrinology & Metabolism 105, no. 3 (October 23, 2019): e583-e596. http://dx.doi.org/10.1210/clinem/dgz066.

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Abstract Context Adrenomedullin 2 (AM2) plays protective roles in the renal and cardiovascular systems. Recent studies in experimental animals demonstrated that AM2 is an adipokine with beneficial effects on energy metabolism. However, there is little information regarding AM2 expression in human adipose tissue. Objective To investigate the pattern and regulation of the expression of AM2 and its receptor component in human adipose tissue, in the context of obesity and type 2 diabetes. Methods We measured metabolic parameters, serum AM2, and expression of ADM2 and its receptor component genes in abdominal subcutaneous and visceral adipose tissue in obese (with or without type 2 diabetes) and normal-weight women. Serum AM2 was assessed before and 6 to 9 months after bariatric surgery. Expression/secretion of AM2 and its receptor were assessed in human adipocytes. Results ADM2 mRNA in both fat depots was higher in obese patients, whether diabetic or not. Although serum AM2 was significantly lower in obese patients, it was not changed after bariatric surgery. AM2 and its receptor complex were predominantly expressed by adipocytes, and the expression of CALCRL, encoding a component of the AM2 receptor complex, was lower in both fat depots of obese patients. Incubating adipocytes with substances mimicking the microenvironment of obese adipose tissue increased ADM2 mRNA but reduced both AM2 secretion into culture media and CALCRL mRNA expression. Conclusions Our data indicate that AM2 signaling is suppressed in adipose tissue in obesity, involving lower receptor expression and ligand availability, likely contributing to insulin resistance and other aspects of the pathophysiology associated with obesity.
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5

Yallampalli, Chandra, Uma Yallampalli, Meena Balakrishnan, and Madhu Chauhan. "900: Adrenomedullin2 (ADM2) receptor system in placenta from preeclamptic pregnancy." American Journal of Obstetrics and Gynecology 216, no. 1 (January 2017): S514. http://dx.doi.org/10.1016/j.ajog.2016.11.809.

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6

Chang, Chia Lin, Zheqing Cai, and Sheau Yu Teddy Hsu. "Sustained Activation of CLR/RAMP Receptors by Gel-Forming Agonists." International Journal of Molecular Sciences 23, no. 21 (November 2, 2022): 13408. http://dx.doi.org/10.3390/ijms232113408.

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Adrenomedullin (ADM), adrenomedullin 2 (ADM2), and CGRP family peptides are important regulators of vascular vasotone and integrity, neurotransmission, and fetoplacental development. These peptides signal through CLR/RAMP1, 2, and 3 receptors, and protect against endothelial dysfunction in disease models. As such, CLR/RAMP receptor agonists are considered important therapeutic candidates for various diseases. Methods and Results: Based on the screening of a series of palmitoylated chimeric ADM/ADM2 analogs, we demonstrated a combination of lipidation and accommodating motifs at the hinge region of select peptides is important for gaining an enhanced receptor-activation activity and improved stimulatory effects on the proliferation and survival of human lymphatic endothelial cells when compared to wild-type peptides. In addition, by serendipity, we found that select palmitoylated analogs self-assemble to form liquid gels, and subcutaneous administration of an analog gel led to the sustained presence of the peptide in the circulation for >2 days. Consistently, subcutaneous injection of the analog gel significantly reduced the blood pressure in SHR rats and increased vasodilation in the hindlimbs of adult rats for days. Conclusions: Together, these data suggest gel-forming adrenomedullin analogs may represent promising candidates for the treatment of various life-threatening endothelial dysfunction-associated diseases such as treatment-resistant hypertension and preeclampsia, which are in urgent need of an effective drug.
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Hollander, L. L., X. Guo, R. Salem, and C. Cha. "The Novel Tumor Angiogenic Factor, Adrenomedullin-2 (ADM2) Predicts Survival in Pancreatic Adenocarcinoma." Journal of Surgical Research 186, no. 2 (February 2014): 635–36. http://dx.doi.org/10.1016/j.jss.2013.11.651.

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8

Chauhan, Madhu, Uma Yallampalli, Yuan-Lin Dong, Gary D. V. Hankins, and Chandrasekhar Yallampalli. "Expression of Adrenomedullin 2 (ADM2)/Intermedin (IMD) in Human Placenta: Role in Trophoblast Invasion and Migration1." Biology of Reproduction 81, no. 4 (October 1, 2009): 777–83. http://dx.doi.org/10.1095/biolreprod.108.074419.

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Wahyudi, Joko Tri, Indri Maharani, and Yulius Tiranda. "Hubungan Antara Tingkat Fatique Dengan Self Care Pada Pasien Penyakit Ginjal Kronis (PGK) Yang Menjalani Hemodialisa Di RS Pusri Palembang." Masker Medika 10, no. 2 (December 9, 2022): 756–61. http://dx.doi.org/10.52523/maskermedika.v10i2.501.

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Latar Belakang : Hemodialisis merupakan manajemen terapi yang dapat fiberikan kepada pasien Penyakit Ginjal Kronik (PGK) yang berfungsi sebagai pengganti ginjal, dan dapat berlangsung seumur hidup. Data Indonesian Renal Registry (IRR) tahun 2018 mencatat 66.433 pasien baru dan aktif menjalani hemodialisis. Umumnya terapi hemodialisis berdampak pada berbagai komplikasi fisik, seperti kelelahan. Pasien penyakit ginjal kronis dengan kelelahan, kelemahan, dan kehilangan energi dapat mempengaruhi perawatan diri. Metode : Desain dalam penelitian ini adalah kuantitatif, dengan pendekatan cross sectional menggunakan analisis chi square. Total sampling digunakan untuk mengukur kelelahan, juga indeks CKD perawatan diri. Penelitian ini ditindaklanjuti dengan izin etik No: 0159/KEPK/Adm2/II/2022. Hasil : Nilai P sebesar 0,001 (P Value 0,05) terdapat hubungan yang signifikan antara tingkat kelelahan dengan perawatan diri pada pasien penyakit ginjal kronik selama hemodialisa. Pembahasan : Meningkatnya tingkat urutan kelelahan ke tingkat ketergantungan. Kami menyarankan perlunya lebih mengeksplorasi faktor-faktor yang mempengaruhi tingkat kelelahan dan tingkat ketergantungan.
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10

Yallampalli, Chandrasekhar, Alex Vidaeff, Uma Yallampalli, Susan Ramin, Karin Fox, Michael Belfort, and Madhulata Chauhan. "451: Adrenomedullin2 (ADM2) is expressed in fetal membranes and lower amniotic fluid levels are associated with preeclampsia." American Journal of Obstetrics and Gynecology 212, no. 1 (January 2015): S232. http://dx.doi.org/10.1016/j.ajog.2014.10.497.

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11

Moghaddas, Omid, Behdokht Miremadi, and Ehsan Seyed Jafari. "Effect of two commercial acellular dermal scaffolds on biological behavior of human gingival fibroblasts." Journal of Advanced Periodontology & Implant Dentistry 12, no. 2 (December 10, 2020): 85–90. http://dx.doi.org/10.34172/japid.2020.011.

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Background. Periodontal regeneration is an essential goal of periodontal therapy. Acellular dermal matrix (ADM) has been recommended as an alternative to autogenous grafts. However, since it is devoid of cells and vasculature, there are concerns regarding the biological behavior of cells on ADM. This study aimed to assess the effects of two commonly used ADMs on biological behavior, i.e., attachment and proliferation, of human gingival fibroblasts (HGFs). Methods. This in vitro, experimental study was conducted on explanted and cultured HGFs. ADM types 1 and 2 (n=26; measuring 10×15 mm) were rinsed with saline solution, adapted to the bottom of 52 wells, exposed to HGFs with a cell density of 16,000 cells/mL, and incubated at 37°C for 12, 24, and 84 hours and seven days. Cell attachment was assessed 12 hours after incubation using 4›,6-diamidino-2-phenylindole (DAPI) and methyl-thiazol-diphenyl-tetrazolium (MTT) assay under a fluorescence microscope. Cell viability was assessed at 24 and 84 hours and one week using the MTT assay. Cells were then platinum-coated, and their morphology was evaluated under a scanning electron microscope (SEM). Data were analyzed using ANOVA. Results. HGFs were evaluated in 60 samples in three groups (n=20). Cell attachment was the same in the three groups, as shown by the MTT assay and DAPI test (P=0.6). Cell viability at one week was 3.73±0.02, 2.88±0.29, and 2.13±0.24 in the control, ADM 1, and ADM 2 groups, respectively. The difference was statistically significant (P=0.01). Conclusion. Both scaffolds were the same in terms of attachment of HGFs. However, ADM 1 was superior to ADM2 in terms of cell viability and morphology at one week. It was concluded that the quality of acellular dermal scaffolds could significantly influence cellular behaviors and tissue maturation.
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Zhang, Qiang, Fengjun Jiao, and Chongjun Hua. "Perioperative application of salvianolate on oxidative stress and plasma IMD/ADM2 in patients with acute myocardial infarction undergoing PCI." Experimental and Therapeutic Medicine 13, no. 4 (February 10, 2017): 1475–79. http://dx.doi.org/10.3892/etm.2017.4114.

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Morales-Morales, Oscar Omar, Blanca Sánchez-Ramírez, Beatriz Castro-Valenzuela, Maria del Rocío Infante-Ramírez, and M. Eduviges Burrola-Barraza. "IMD/ADM2 operates as a secretory factor that controls cumulus-oocyte complexes (COCs) conformation for oocytes in vitro maturation." In Vitro Cellular & Developmental Biology - Animal 58, no. 2 (January 31, 2022): 149–68. http://dx.doi.org/10.1007/s11626-022-00647-0.

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Chauhan, Madhu, Meena Balakrishnan, and Chandra Yallampalli. "Placental intermedin (IMD)/adrenomedullin2(ADM2) expression is lower in preeclampsia and it regulates expression of angiopoietin-2 in placenta." Placenta 35, no. 9 (September 2014): A88—A89. http://dx.doi.org/10.1016/j.placenta.2014.06.286.

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Lima, Fernando Vitor, Daniela Guimarães Pereira, Rodrigo César Ribeiro Diniz, Daniella Caroline Guilherme Santiago, Betânia de Paula Alves, and Mauro Heleno Chagas. "Efeito da amplitude de movimento no número máximo de repetições no exercício supino livre." Revista Brasileira de Educação Física e Esporte 26, no. 4 (December 2012): 571–79. http://dx.doi.org/10.1590/s1807-55092012000400004.

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Pesquisas mostram resultados divergentes no aumento da força utilizando diferentes amplitudes de movimento (ADM). O objetivo deste estudo foi comparar o número máximo de repetições (NMR) no exercício supino com duas ADM. Quatorze voluntários realizaram a familiarização e o teste de uma repetição máxima (1 RM) nas sessões 1 e 2. Nas sessões 3 e 4 realizaram o NMR em quatro séries a 50% de 1 RM, com um minuto de pausa, com ADM parcial (ADMP) e completa (ADMC). Na ADMP utilizou-se metade do deslocamento vertical da barra comparada a condição ADMC. Foi realizada ANOVA "two-way" com medidas repetidas, seguida pelo "Post hoc" Scheffé. Houve diminuição significante do NMR entre as séries, exceto da terceira para a quarta em ambas ADM. Um maior NMR foi verificado para ADMP. A redução da ADM permite a realização de um maior número de repetições para uma mesma intensidade relativa.
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Groth, Dawid, Izabela Poplawska, Marlena Tynecka, Kamil Grubczak, Jordan Holl, Aleksandra Starosz, Adrian Janucik, et al. "Abdominoplasty Skin-Based Dressing for Deep Wound Treatment—Evaluation of Different Methods of Preparation on Therapeutic Potential." Pharmaceutics 13, no. 12 (December 8, 2021): 2118. http://dx.doi.org/10.3390/pharmaceutics13122118.

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The management of hard-to-heal wounds is a significant clinical challenge. Acellular dermal matrices (ADMs) have been successfully introduced to enhance the healing process. Here, we aimed to develop protocol for the preparation of novel ADMs from abdominoplasty skin. We used three different decellularization protocols for skin processing, namely, 1M NaCl and sodium dodecyl sulfate (SDS, in ADM1); 2M NaCl and sodium dodecyl sulfate (SDS, in ADM1); and a combination of recombinant trypsin and Triton X-100 (in hADM 3). We assessed the effectiveness of decellularization and ADM’s structure by using histochemical and immunochemical staining. In addition, we evaluated the therapeutic potential of novel ADMs in a murine model of wound healing. Furthermore, targeted transcriptomic profiling of genes associated with wound healing was performed. First, we found that all three proposed methods of decellularization effectively removed cellular components from abdominoplasty skin. We showed, however, significant differences in the presence of class I human leukocyte antigen (HLA class I ABC), Talin 1/2, and chondroitin sulfate proteoglycan (NG2). In addition, we found that protocols, when utilized differentially, influenced the preservation of types I, III, IV, and VII collagens. Finally, we showed that abdominoplasty skin-derived ADMs might serve as an effective and safe option for deep wound treatment. More importantly, our novel dressing (ADM1) improves the kinetics of wound closure and scar maturation in the proliferative and remodeling phases of wound healing. In conclusion, we developed a protocol for abdominoplasty skin decellularization suitable for the preparation of biological dressings. We showed that different decellularization methods affect the purity, structure, and therapeutic properties of ADMs.
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Reale, Antonia, Tiffany T. Khong, Sridurga Mithraprabhu, Ioanna Savvidou, Malarmathy Ramachandran, and Andrew Spencer. "TOP2A Knockdown Resensitizes Carfilzomib-Resistant Hmcls to Carfilzomib." Blood 126, no. 23 (December 3, 2015): 4215. http://dx.doi.org/10.1182/blood.v126.23.4215.4215.

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Abstract Introduction/background: Multiple myeloma (MM) remains incurable despite the introduction of novel therapeutic agents. Microarray-based technologies were adopted in our study to determine if a genetic signature associated with resistance to carfilzomib, a second-generation proteasome inhibitor already in use in clinical settings, could be identified. Materials and Methods: 18 genetically heterogeneous human myeloma cell lines (HMCLs) were treated with carfilzomib and a cell viability profile was assessed categorizing the HMCLs as sensitive, intermediate or resistant to carfilzomib. Following categorization gene expression profiling was performed and validated with q-RT-PCR and knockdown assays. Results: 29 genes were differentially regulated between the sensitive and resistant cell lines. Top genes based on intensity values and biological significance were: LOC731314, TSPAN13, APH1B, TSPYL5, COX7B2, PCSK1N, LRRC38, TCIRG1, TOP2A, ADM2, ITM2A, TSPAN13, STOM, UBE2C, SNHG8. Gene ontology (GO) enrichment analysis identified two pathways that were significantly different between the resistant and sensitive HMCLs; pathogenic escherichia coli infection (p=0.002) and lysosome (p=0.006). Eight GO terms were enriched: 4 related to biological processes and 4 related to cellular components. TOP2A, an enzyme that controls and alters the topologic states of DNA during transcription and is involved in cell cycle and proliferation, was identified to be overexpressed in resistant HMCLs. It functions as the target for several anticancer agents and a variety of mutations in this gene have been associated with the development of drug resistance. TOP2A may be used as a predictive factor for patient selection for specific protocols or as independent prognostic marker in solid tumors. TOP2A was also overexpressed in the 'proliferation cluster' associated with greater proliferation rate and poor outcome in newly diagnosed MM patients. Suppression of TOP2A by siRNA in carfilzomib-resistant HMCLs significantly resensitised the cell lines to carfilzomib. Conclusion: Our results suggest that TOP2A is overexpressed in carfilzomib-resistant HMCLs indicating a possible role as a predictive marker of response to carfilzomib in MM. Disclosures No relevant conflicts of interest to declare.
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Reimer, Janice, and T. Schmeing. "Characterization of transglutaminase homologues found in andrimid biosynthesis." Acta Crystallographica Section A Foundations and Advances 70, a1 (August 5, 2014): C476. http://dx.doi.org/10.1107/s2053273314095230.

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Nonribosomal peptide synthetases (NRPSs) are multimodular enzymes that synthesize products with diverse structures and activities ranging from antibiotics to industrial solvents. They are arranged into an assembly line of modules where each module is responsible for incorporating a specific monomer into the final nonribosomal peptide (NRP). Diversity in NRPs stems from the fact that NRPSs utilize not only the 20 proteinogenic amino acids, but also include nonproteinogenic amino acids, fatty acids, and alpha-hydroxy acids as building block substrates. Andrimid is a NRP antibiotic that inhibits membrane biosynthesis by blocking bacterial acetyl coenzyme A carboxylases. It is synthesized in a hybrid NRPS-polyketide synthase (NRPS-PKS) using a fatty acid, phenylalanine, valine, and glycine. A remarkable feature of this synthetic system is that instead of a normal condensation domain, it uses two atypical free-standing proteins with homology to transglutaminases to catalyze the formation of the first and second amide bonds. We are characterizing the action of transglutaminase homologues (TGH) in andrimid synthesis using biochemical assays and X-ray crystallography. Initial investigations of the andrimid biosynthetic cluster found in Panteao agglomerans focused on the TGH, AdmF, which catalyzes the formation of the first amide bond. Crystallization trials have been initiated on AdmF in its apo form and in complex with its interacting binding partner, the peptide carrier protein domain AdmI. To date, only a few andrimid producing bacteria have been discovered. Using genome mining, a biosynthetic cluster homologous to the andrimid biosynthetic cluster found in Panteao agglomerans was identified in Vibrio coralliilyticus. The two TGHs, CoraF and CoraS, were cloned, expressed and purified, and crystallization trials are underway. Our progress in biochemical and biophysical characterization of AdmF, CoraF, and CoraS will be presented.
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Kielstein, J. T. "ADMA." Der Nephrologe 2, no. 4 (June 27, 2007): 285–86. http://dx.doi.org/10.1007/s11560-007-0094-y.

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Klopman, Gilles, Liliana R. Stefan, and Roustem D. Saiakhov. "ADME evaluation." European Journal of Pharmaceutical Sciences 17, no. 4-5 (December 2002): 253–63. http://dx.doi.org/10.1016/s0928-0987(02)00219-1.

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Sun, L. Z., Z. L. Ji, X. Chen, J. F. Wang, and Y. Z. Chen. "ADME-AP: a database of ADME associated proteins." Bioinformatics 18, no. 12 (December 1, 2002): 1699–700. http://dx.doi.org/10.1093/bioinformatics/18.12.1699.

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22

Ghosh, Angsula, and Sadhan K. Adhikari. "Phase transition from adx2−y2to adx2−y2+dxysuperconductor." Physical Review B 60, no. 14 (October 1, 1999): 10401–4. http://dx.doi.org/10.1103/physrevb.60.10401.

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23

Hösel, Marianna, Dennis Webb, Jörg Schröer, Birgit Schmitz, and Walter Doerfler. "Overexpression of the Adenovirus Type 12 (Ad12) pTP or E1A Gene Facilitates Ad12 DNA Replication in Nonpermissive BHK21 Hamster Cells." Journal of Virology 75, no. 21 (November 1, 2001): 10041–53. http://dx.doi.org/10.1128/jvi.75.21.10041-10053.2001.

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ABSTRACT In the adenovirus type 12 (Ad12) hamster cell system, abortive virus infection is one of the factors associated with the highly efficient oncogenesis in newborn Syrian hamsters. We have shown earlier that the replication and efficient late transcription of the Ad12 genome are blocked in Syrian hamster cells. Some of the early Ad12 functions are transcribed in these cells, although at a minimal rate. In the present study, we demonstrate that low expression levels of the E1A and precursor to terminal protein (pTP) genes of Ad12 seem to be responsible for the lack of Ad12 DNA replication in hamster cells. The Ad12 genes for the E1A functions or for pTP were tethered to the strong early promoter of the human cytomegalovirus and transfected into BHK21 cells. Subsequently, these cells were infected with Ad12 virions. In Ad12-infected BHK21 cells, which overexpressed pTP or E1A, full-length Ad12 DNA was de novo synthesized, as documented by metabolic labeling with [3H]thymidine and by zone velocity sedimentation in alkaline sucrose gradients followed by gel electrophoresis of the3H-labeled DNA and Southern blot hybridization to32P-labeled Ad12 DNA. Transfection of the cloned E1A region of Ad2 yielded similar results. The newly synthesized Ad12 DNA was covalently linked to pTP. The Ad12 DNA binding protein (DBP) and DNA polymerase (pol) genes were transcribed at levels similar to those in merely Ad12-infected cells. In pTP or E1A gene-transfected and Ad12-infected BHK21 cells, marginal levels of late Ad12 mRNA were detectable. Late Ad12 proteins were, however, not synthesized. Apparently, Ad12 DNA replication in hamster cells is rendered impossible due to insufficient threshold levels of the viral E1A and/or pTP.
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Wu Fung, Samy, Sanna Tyrväinen, Lars Ruthotto, and Eldad Haber. "ADMM-Softmax: an ADMM approach for multinomial logistic regression." ETNA - Electronic Transactions on Numerical Analysis 52 (2020): 214–29. http://dx.doi.org/10.1553/etna_vol52s214.

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Huang, Zonghao, Rui Hu, Yuanxiong Guo, Eric Chan-Tin, and Yanmin Gong. "DP-ADMM: ADMM-Based Distributed Learning With Differential Privacy." IEEE Transactions on Information Forensics and Security 15 (2020): 1002–12. http://dx.doi.org/10.1109/tifs.2019.2931068.

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Davids, Mariska, Albert J. van Hell, Marlieke Visser, Robert J. Nijveldt, Paul A. M. van Leeuwen, and Tom Teerlink. "Role of the human erythrocyte in generation and storage of asymmetric dimethylarginine." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 8 (April 15, 2012): H1762—H1770. http://dx.doi.org/10.1152/ajpheart.01205.2011.

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Proteolytic activity in whole blood may lead to release of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA). We investigated the role of the human erythrocyte in storage and generation of ADMA in healthy controls ( n = 36) and critically ill patients ( n = 38). Both free and total (sum of free and protein-incorporated) ADMA were measured. Upon incubation of intact erythrocytes with extracellular ADMA (0 to 40 μmol/l), equilibrium between intra- and extracellular ADMA was reached within 3 h. Compared with controls, patients had significantly higher basal concentrations of ADMA in plasma (0.88 ± 0.75 vs. 0.41 ± 0.07 μmol/l) and erythrocytes (1.28 ± 0.55 vs. 0.57 ± 0.14 μmol/l). Intracellular and plasma ADMA were significantly correlated in the patient group only ( r = 0.834). Upon lysis, followed by incubation at 37°C for 2 h, free ADMA increased sevenfold (to 8.60 ± 3.61 μmol/l in patients and 3.90 ± 0.78 μmol/l in controls). In lysates of controls, free ADMA increased further to 9.85 ± 1.35 μmol/l after 18 h. Total ADMA was 15.43 ± 2.44 μmol/l and did not change during incubation. The increase of free ADMA during incubation corresponded to substantial release of ADMA from the erythrocytic protein-incorporated pool (21.9 ± 4.6% at 2 h and 60.8 ± 7.6% at 18 h). ADMA was released from proteins other than hemoglobin, which only occurred after complete lysis and was blocked by combined inhibition of proteasomal and protease activity. Neither intact nor lysed erythrocytes mediated degradation of free ADMA. We conclude that intact erythrocytes play an important role in storage of ADMA, whereas upon erythrocyte lysis large amounts of free ADMA are generated by proteolysis of methylated proteins, which may affect plasma levels in hemolysis-associated diseases.
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Hendrawati, Tetty, Syakib Bakri, and Mansyur Arif. "The Analysis of Asymetric Dimethylarginine and Homocysteine in Patients with Chronic Kidney Disease." Indonesian Biomedical Journal 1, no. 2 (August 1, 2009): 64. http://dx.doi.org/10.18585/inabj.v1i2.96.

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BACKGROUND: Asymmetric dimethylarginine (ADMA) is a competitive inhibitor of nitric oxide synthase (NOS). ADMA reduces NO synthesis when its concentration elevates. ADMA is a novel risk factor for cardiovascular disease. Plasma ADMA accumulates in patients with endstage renal disease, due to reduced renal clearance. Hyperhomocysteinemia is often found in patients with chronic kidney disease (CKD). Homocysteine may cause ADMA to accumulate; however, the mechanism by which ADMA level elevates in hyperhomocysteinemia is still unclear. Objective of this study was to analyze the concentrations of homocysteine and ADMA and to assess the correlation between homocysteine and ADMA concentrations with the severity of chronic kidney disease.METHODS: This was a cross-sectional study on 75 patients with CKD, comprising men and women aged 40-70 years. Assessments were done on the concentrations of creatinine, homocysteine, ADMA, fasting blood glucose, cholesterol HDL and triglyceride.RESULTS: In later stage of CKD there was significantly higher tHcy concentration as compared with the earlier stage of CKD (p=0.0000). In CKD stage 2 to 4 there was a tendency for ADMA concentration to increase to a significant average (p=0.210), but ADMA concentration was lower at stage 5. There was increased ADMA along with increased tHcy concentration of around 20μ mol/L, and this then decreased. The inverse correlation between tHcy and ADMA concentrations started to appear in CKD stage 4, but this correlation was statistically insignificant (r2 =0.19; p=0.499).CONCLUSIONS: This study showed there was a correlation between homocysteine and ADMA concentrations in patients with CKD stage 2 to 5, although statistically not significant.KEYWORDS: Asymetric Dimethylarginine, Homocysteine, Chronic Kidney Disease
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Bode-Böger, Stefanie M., Fortunato Scalera, and Jens Martens-Lobenhoffer. "Asymmetric dimethylarginine (ADMA) accelerates cell senescence." Vascular Medicine 10, no. 2_suppl (May 2005): S65—S71. http://dx.doi.org/10.1191/1358863x05vm606oa.

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Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase and its accumulation has been associated with cardiovascular disease. We aimed to investigate the role of ADMA in endothelial cell senescence. Endothelial cells were cultured until the tenth passage. ADMA was replaced every 48 hours starting at the fourth passage. ADMA significantly accelerated senescence-associated β-galactosidase activity. Additionally, the shortening of telomere length was significantly speeded up and telomerase activity was significantly reduced. This effect was associated with an increase of oxidative stress: both allantoin, a marker of oxygen free radical generation, and intracellular reactive oxygen species increased significantly after ADMA treatment compared with control, whereas nitric oxide synthesis decreased. Furthermore, ADMA-increased oxidative stress was accompanied by a decrease in the activity of dimethylarginine dimethylaminohydrolase, the enzyme that degrades ADMA, which could be prevented by the antioxidant pyrroli-dine dithiocarbamate. Exogenous ADMA also stimulated secretion of monocyte chemotactic protein-1 and interleukin-8. Co-incubation with the methyltransferase inhibitor S-adenosylhomocysteine abolished the effects of ADMA. These data suggest that ADMA accelerates senescence, probably via increased oxygen radical formation by inhibiting nitric oxide elaboration. This study provides evidence that modest changes of intracellular ADMA levels are associated with significant effects on slowing down endothelial senescence.
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Bode-Böger, Stefanie M., Fortunato Scalera, and Jens Martens-Lobenhoffer. "Asymmetric dimethylarginine (ADMA) accelerates cell senescence." Vascular Medicine 10, no. 1_suppl (July 2005): S65—S71. http://dx.doi.org/10.1177/1358836x0501000110.

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Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase and its accumulation has been associated with cardiovascular disease. We aimed to investigate the role of ADMA in endothelial cell senescence. Endothelial cells were cultured until the tenth passage. ADMA was replaced every 48 hours starting at the fourth passage. ADMA significantly accelerated senescence- associated β-galactosidase activity. Additionally, the shortening of telomere length was significantly speeded up and telomerase activity was significantly reduced. This effect was associated with an increase of oxidative stress: both allantoin, a marker of oxygen free radical generation, and intracellular reactive oxygen species increased significantly after ADMA treatment compared with control, whereas nitric oxide syn thesis decreased. Furthermore, ADMA-increased oxidative stress was accompanied by a decrease in the activity of dimethylarginine dimethylaminohydrolase, the enzyme that degrades ADMA, which could be prevented by the antioxidant pyrroli dine dithiocarbamate. Exogenous ADMA also stimulated secretion of monocyte chemotactic protein-1 and interleukin-8. Co-incubation with the methyltransferase inhibitor S-adenosylhomocysteine abolished the effects of ADMA. These data suggest that ADMA accelerates senescence, probably via increased oxygen radical formation by inhibiting nitric oxide elaboration. This study provides evidence that modest changes of intracellular ADMA levels are associated with significant effects on slowing down endothelial senescence.
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Jawalekar, Seema L., Aarti Karnik, and Anil Bhutey. "Risk of Cardiovascular Diseases in Diabetes Mellitus and Serum Concentration of Asymmetrical Dimethylarginine." Biochemistry Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/189430.

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Introduction. Asymmetric dimethylarginine (ADMA) is a nonselective nitric oxide (NO) synthase inhibitor associated with cardiovascular and metabolic disorders. ADMA plays an important role in the regulation of vascular tone by acting as an endogenous inhibitor of NO synthesis.Objectives. This study aimed to investigate ADMA with respect to diabetes and its clinical relevance as an independent predictor of CAD (Coronary Artery Disease).Methodology. The present case control study includes two hundred and forty patients selected randomly. Serum ADMA was analyzed by using enzyme immunoassay for the quantitative determination of endogenous ADMA, and serum nitric oxide was estimated by the method of Cortes.Results. Elevated NO level levels was a strong predictor and significantly (t: 9.86,P<0.001) associated with occurrence of CAD. Increased ADMA level was found to be another strong predictor and associated significantly (t: 8.02,P<0.001) with CAD. On intra group analysis, the relationship between ADMA and NO in diseased group, is significant negative correlation (r=-0.743).P(0.001) was found between ADMA and NO.Conclusion. ADMA level was found to be one of the strong predictors for CAD. ADMA is an emerging independent risk marker for future CVD (cardiovascular disease) events.
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Hochstein, Norbert, Indrikis Muiznieks, Laurence Mangel, Holger Brondke, and Walter Doerfler. "Epigenetic Status of an Adenovirus Type 12 Transgenome upon Long-Term Cultivation in Hamster Cells." Journal of Virology 81, no. 10 (March 7, 2007): 5349–61. http://dx.doi.org/10.1128/jvi.02624-06.

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ABSTRACT The epigenetic status of integrated adenovirus type 12 (Ad12) DNA in hamster cells cultivated for about 4 decades has been investigated. Cell line TR12, a fibroblastic revertant of the Ad12-transformed epitheloid hamster cell line T637 with 15 copies of integrated Ad12 DNA, carries one Ad12 DNA copy plus a 3.9-kbp fragment from a second copy. The cellular insertion site for the Ad12 integrate, identical in both cell lines, is a >5.2-kbp inverted DNA repeat. The Ad12 transgenome is packaged around nucleosomes. The cellular junction is more sensitive to micrococcal nuclease at Ad12-occupied sites than at unoccupied sites. Bisulfite sequencing reveals complete de novo methylation in most of the 1,634 CpGs of the integrated viral DNA, except for its termini. Isolated unmethylated CpGs extend over the entire Ad12 integrate. The fully methylated transgenome segments are characterized by promoter silencing and histone H3 and H4 hypoacetylation. Nevertheless, there is minimal transcriptional activity of the late viral genes controlled by the fully methylated major late promoter of Ad12 DNA.
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Dayal, Sanjana, and Steven R. Lentz. "ADMA and hyperhomocysteinemia." Vascular Medicine 10, no. 2_suppl (May 2005): S27—S33. http://dx.doi.org/10.1191/1358863x05vm599oa.

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Hyperhomocysteinemia is a risk factor for cardiovascular disease and stroke. Like many other cardiovascular risk factors, hyperhomocysteinemia produces endothelial dysfunction due to impaired bioavailability of endothelium-derived nitric oxide (NO). The molecular mechanisms responsible for decreased NO bioavailability in hyperhomocysteinemia are incompletely understood, but emerging evidence suggests that asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, may be a key mediator. Homocysteine is produced during the synthesis of ADMA and can alter ADMA metabolism by inhibiting dimethylarginine dimethylaminohydrolase (DDAH). Several animal and clinical studies have demonstrated a strong association between plasma total homocysteine, plasma ADMA, and endothelial dysfunction. These observations suggest a model in which elevation of ADMA may be a unifying mechanism for endothelial dysfunction during hyper-homocysteinemia. The recent development of transgenic mice with altered ADMA metabolism should provide further mechanistic insights into the role of ADMA in hyperhomocysteinemia.
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33

Chasseaud, L. F. "Accelerating ADME studies." Human & Experimental Toxicology 14, no. 12 (December 1995): 991–92. http://dx.doi.org/10.1177/096032719501401207.

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A novel method is described for quantitative whole- body autoradioluminography using [14C]-radioactive standards prepared from rat red blood cells. MicroComputer Imaging Device model 2 (MCID) and ImageQuant (IQ) imaging systems were evaluat ed for imaging performance and autoradioluminog raphy quantitation. Weighted linear regression analysis resulted in linearity over five orders of magnitude with a lower limit of quantitation of 2.7 nCi g-1. Using IQ, 16 days were necessary for image analysis and data processing of 30 whole-body cryosections and 1080 standards. MCID reduced the image and data processing of the same cryosections and standards to only 4 days. Embedding a series of radioactive standards with each specimen in the same carboxymethyl cellulose block provided an effective method of assessing intrasection and inter section variations in thickness of whole-body cryosections. These results demonstrated that autoradioluminography provided a sensitive, accu rate, precise and reproducible method for the quan titative measurement of the tissue distribution of [14C]-radiolabelled xenobiotics in whole-body cryosections. Evaluating the biodistribution of [14C]- xenobiotics by autoradioluminography, not only provides pharmacokinetic data required for predict ing the potential tissue deposition of an absorbed dose of radioactivity in man, but also allows for visual and quantitative evaluation of radioactivity in small anatomical structures that otherwise could not be detected or measured by conventional tissue combustion technology.
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34

Welch, Thomas R. "ADMA and diabetes." Journal of Pediatrics 158, no. 4 (April 2011): A3. http://dx.doi.org/10.1016/j.jpeds.2011.02.025.

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35

Tarcsa, Edit. "ADME of biologics." Drug Metabolism and Pharmacokinetics 32, no. 1 (January 2017): S1. http://dx.doi.org/10.1016/j.dmpk.2016.10.005.

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36

Fostel, Jennifer. "Predictive ADME-Tox." Expert Opinion on Drug Metabolism & Toxicology 1, no. 3 (September 29, 2005): 565–70. http://dx.doi.org/10.1517/17425255.1.3.565.

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37

Dayal, Sanjana, and Steven R. Lentz. "ADMA and hyperhomocysteinemia." Vascular Medicine 10, no. 1_suppl (July 2005): S27—S33. http://dx.doi.org/10.1177/1358836x0501000105.

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Hyperhomocysteinemia is a risk factor for cardiovascular disease and stroke. Like many other cardiovascular risk factors, hyperhomocysteinemia produces endothelial dysfunction due to impaired bioavailability of endothelium-derived nitric oxide (NO). The molecular mechanisms responsible for decreased NO bioavailabil ity in hyperhomocysteinemia are incompletely understood, but emerging evidence suggests that asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, may be a key mediator. Homocysteine is produced during the synthesis of ADMA and can alter ADMA metabolism by inhibiting dimethylarginine dimethy laminohydrolase (DDAH). Several animal and clinical studies have demonstrated a strong association between plasma total homocysteine, plasma ADMA, and endothelial dysfunction. These observations suggest a model in which elevation of ADMA may be a unifying mechanism for endothelial dysfunction during hyper homocysteinemia. The recent development of transgenic mice with altered ADMA metabolism should provide further mechanistic insights into the role of ADMA in hyperhomocysteinemia.
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Hansch, Corwin, Albert Leo, Suresh Babu Mekapati, and Alka Kurup. "QSAR and ADME." Bioorganic & Medicinal Chemistry 12, no. 12 (June 2004): 3391–400. http://dx.doi.org/10.1016/j.bmc.2003.11.037.

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39

Özen, Seza, Ezgi Deniz Batu, Ekim Z. Taşkıran, Hatice Asuman Özkara, Şule Ünal, Naz Güleray, Abdulsamet Erden, et al. "A Monogenic Disease with a Variety of Phenotypes: Deficiency of Adenosine Deaminase 2." Journal of Rheumatology 47, no. 1 (May 1, 2019): 117–25. http://dx.doi.org/10.3899/jrheum.181384.

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Objective.Deficiency of adenosine deaminase 2 (DADA2) is an autosomal recessive autoinflammatory disorder associated with ADA2 mutations. We aimed to investigate the characteristics and ADA2 enzyme activities of patients with DADA2 compared to non-DADA2 patients.Methods.This is a descriptive study of 24 patients with DADA2 who were admitted to the Adult and Pediatric Rheumatology, Pediatric Haematology, and Pediatric Immunology Departments of Hacettepe University. All ADA2 exons were screened by Sanger sequencing. Serum ADA2 enzyme activity was measured by modified spectrophotometric method.Results.Twenty-four patients with DADA2 were included: 14 with polyarteritis nodosa (PAN)-like phenotype (Group 1); 9 with Diamond-Blackfan anemia (DBA)-like features, and 1 with immunodeficiency (Group 2). Fourteen PAN-like DADA2 patients did not have the typical thrombocytosis seen in classic PAN. Inflammatory attacks were evident only in Group 1 patients. Serum ADA2 activity was low in all patients with DADA2 except one, who was tested after hematopoietic stem cell transplantation. There was no significant difference in ADA2 activities between PAN-like and DBA-like patients. In DADA2 patients with one ADA2 mutation, serum ADA2 activities were as low as those of patients with homozygote DADA2. ADA2 activities were normal in non-DADA2 patients. ADA2 mutations were affecting the dimerization domain in Group 1 patients and the catalytic domain in Group 2 patients.Conclusion.We suggest assessing ADA2 activity along with genetic analysis because there are patients with one ADA2 mutation and absent enzyme activity. Our data suggest a possible genotype–phenotype correlation in which dimerization domain mutations are associated with PAN-like phenotype, and catalytic domain mutations are associated with hematological manifestations.
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40

Woo, Soo Jin, Jeong Hyun Ha, and Ung Sik Jin. "Comparison of irradiated and non-irradiated acellular dermal matrices in breast reconstruction under radiotherapy." Archives of Plastic Surgery 48, no. 1 (January 15, 2021): 33–43. http://dx.doi.org/10.5999/aps.2020.01522.

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Background Acellular dermal matrices (ADMs) have become an essential material for implant-based breast reconstruction. No previous studies have evaluated the effects of sterility of ADM under conditions of radiation. This study compared sterile (irradiated) and aseptic (non-irradiated) ADMs to determine which would better endure radiotherapy.Methods Eighteen male Balb/C mice were assigned to the control group with no irradiation (group 1) or one of two other groups with a radiation intensity of 10 Gy (group 2) or 20 Gy (group 3). Both sterile and aseptic ADMs were inserted into the back of each mouse. The residual volume of the ADM (measured using three-dimensional photography), cell incorporation, α-smooth muscle actin expression, and connective tissue growth factor expression were evaluated. The thickness and CD3 expression of the skin were measured 4 and 8 weeks after radiation.Results In groups 2 and 3, irradiated ADMs had a significantly larger residual volume than the non-irradiated ADMs after 8 weeks (P<0.05). No significant differences were found in cell incorporation and the amount of fibrosis between irradiated and non-irradiated ADMs. The skin was significantly thicker in the non-irradiated ADMs than in the irradiated ADMs in group 3 (P<0.05). CD3 staining showed significantly fewer inflammatory cells in the skin of irradiated ADMs than in non-irradiated ADMs in all three groups after 4 and 8 weeks (P<0.05).Conclusions Under radiation exposure, irradiated ADMs were more durable, with less volume decrease and less deposition of collagen fibers and inflammatory reactions in the skin than in non-irradiated ADMs.
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Billecke, Scott S., Laura A. Kitzmiller, Joseph J. Northrup, Steven E. Whitesall, Masumi Kimoto, Alia V. Hinz, and Louis G. D'Alecy. "Contribution of whole blood to the control of plasma asymmetrical dimethylarginine." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 4 (October 2006): H1788—H1796. http://dx.doi.org/10.1152/ajpheart.00066.2006.

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The endogenous nitric oxide (NO) synthase (NOS) inhibitor asymmetrical dimethylarginine (ADMA) is elevated in many patients and may contribute to the initiation and progression of their disease. While some mechanistic pathways have been identified, tissue-specific contributions to ADMA control remain unclear. We sought to determine if whole blood (WB) could participate in ADMA control ex vivo. Anesthetized male Sprague-Dawley rats underwent exsanguinations, and WB preparations were incubated at 37°C for 5 h. ADMA and symmetrical dimethylarginine were analyzed by high-pressure liquid chromatography. Incubation of lysed red blood cell (RBC) supernatant yielded a significant decrease in ADMA that was blocked by 4124W, a synthetic inhibitor of dimethylarginine dimethylaminohydrolase, the only reported enzyme to hydrolyze ADMA. Hydrolysis of ADMA was diminished by addition of physiologically relevant concentrations of zinc (i.e., 20 μM). Conversely, when rat WB or WB supernatant was incubated at 37°C, it liberated quantities of free ADMA (1–2 μM) that in vivo would likely have pathological consequences. Addition of arginine methyltransferase inhibitors to these incubations did not reduce ADMA release, indicating no dominant role for active protein methylation during these incubations. This ADMA liberation was significantly reduced by addition of protease inhibitors, indicating a dependence on peptide bond hydrolysis. Total ADMA (protein incorporated plus free) was determined by acid hydrolysis and found to be 43.18 ± 4.79 μM in WB with ∼95% of this in RBCs. These ex vivo data demonstrate the potential of blood to control the NO-NOS system by modulating free ADMA.
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Ronden, Rianne A., Alfons J. H. M. Houben, Tom Teerlink, Jaap A. Bakker, Jörgen Bierau, Coen D. A. Stehouwer, Peter W. De Leeuw, and Abraham A. Kroon. "Reduced renal plasma clearance does not explain increased plasma asymmetric dimethylarginine in hypertensive subjects with mild to moderate renal insufficiency." American Journal of Physiology-Renal Physiology 303, no. 1 (July 1, 2012): F149—F156. http://dx.doi.org/10.1152/ajprenal.00045.2012.

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Plasma concentrations of the nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) increase already in the early stages of renal insufficiency. There is no agreement as to whether reduced renal plasma clearance (RPCL) contributes to this increase. Therefore, we investigated the relationship between estimated glomerular filtration rate (eGFR), RPCL, and plasma ADMA and SDMA in essential hypertensive patients with mild to moderate renal insufficiency. In 171 patients who underwent renal angiography, we drew blood samples from the aorta and both renal veins and measured mean renal blood flow (MRBF) using the 133Xe washout technique. RPCL was calculated using arteriovenous concentration differences and MRBF. After correction for potential confounders, reduced eGFR was associated with higher plasma ADMA and SDMA [standardized regression coefficient (β) = −0.22 (95% confidence intervals: −0.41, −0.04) and β = −0.66 (95% confidence intervals: −0.83, −0.49), respectively]. However, eGFR was not independently associated with RPCL of ADMA. Moreover, reduced RPCL of ADMA was not associated with higher plasma ADMA. Contrary to ADMA, reduced eGFR was indeed associated with lower RPCL of SDMA [β = 0.21 (95% confidence intervals: 0.02, 0.40)] . In conclusion, our findings indicate that RPCL of ADMA is independent of renal function in hypertensive patients with mild to moderate renal insufficiency. Unlike the case for SDMA, reduced RPCL of ADMA is of minor importance for the increase in plasma ADMA in these patients, which indicates that increased plasma ADMA in this population is not a direct consequence of the kidneys failing as a plasma ADMA-regulating organ.
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Zoccolillo, Matteo, Immacolata Brigida, Federica Barzaghi, Serena Scala, Raisa Jofra Hernández, Luca Basso-Ricci, Mariasilvia Colantuoni, et al. "Lentiviral correction of enzymatic activity restrains macrophage inflammation in adenosine deaminase 2 deficiency." Blood Advances 5, no. 16 (August 20, 2021): 3174–87. http://dx.doi.org/10.1182/bloodadvances.2020003811.

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Abstract Adenosine deaminase 2 deficiency (DADA2) is a rare inherited disorder that is caused by autosomal recessive mutations in the ADA2 gene. Clinical manifestations include early-onset lacunar strokes, vasculitis/vasculopathy, systemic inflammation, immunodeficiency, and hematologic defects. Anti–tumor necrosis factor therapy reduces strokes and systemic inflammation. Allogeneic hematopoietic stem/progenitor cell (HSPC) transplantation can ameliorate most disease manifestations, but patients are at risk for complications. Autologous HSPC gene therapy may be an alternative curative option for patients with DADA2. We designed a lentiviral vector encoding ADA2 (LV-ADA2) to genetically correct HSPCs. Lentiviral transduction allowed efficient delivery of the functional ADA2 enzyme into HSPCs from healthy donors. Supranormal ADA2 expression in human and mouse HSPCs did not affect their multipotency and engraftment potential in vivo. The LV-ADA2 induced stable ADA2 expression and corrected the enzymatic defect in HSPCs derived from DADA2 patients. Patients’ HSPCs re-expressing ADA2 retained their potential to differentiate into erythroid and myeloid cells. Delivery of ADA2 enzymatic activity in patients’ macrophages led to a complete rescue of the exaggerated inflammatory cytokine production. Our data indicate that HSPCs ectopically expressing ADA2 retain their multipotent differentiation ability, leading to functional correction of macrophage defects. Altogether, these findings support the implementation of HSPC gene therapy for DADA2.
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Zhou, Yi-ming, Xi Lan, Han-bin Guo, Yan Zhang, Li Ma, and Jian-biao Cao. "Rho/ROCK Signal Cascade Mediates Asymmetric Dimethylarginine-Induced Vascular Smooth Muscle Cells Migration and Phenotype Change." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/683707.

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Asymmetric dimethylarginine (ADMA) induces vascular smooth muscle cells (VSMCs) migration. VSMC phenotype change is a prerequisite of migration. RhoA and Rho-kinase (ROCK) mediate migration of VSMCs. We hypothesize that ADMA induces VSMC migration via the activation of Rho/ROCK signal pathway and due to VSMCs phenotype change. ADMA activates Rho/ROCK signal pathway that interpreted by the elevation of RhoA activity and phosphorylation level of a ROCK substrate. Pretreatment with ROCK inhibitor, Y27632 completely reverses the induction of ADMA on ROCK and in turn inhibits ADMA-induced VSMCs migration. When the Rho/ROCK signal pathway has been blocked by pretreatment with Y27632, the induction of ERK signal pathway by ADMA is completely abrogated. Elimination of ADMA via overexpression of dimethylarginine dimethylaminohydrolase 2 (DDAH2) and L-arginine both blocks the effects of ADMA on the activation of Rho/ROCK and extra cellular signal-regulated kinase (ERK) in VSMCs. The expression of differentiated phenotype relative proteins was reduced and the actin cytoskeleton was disassembled by ADMA, which were blocked by Y27632, further interpreting that ADMA inducing VSMCs migration via Rho/ROCK signal pathway is due to its effect on the VSMCs phenotype change. Our present study may help to provide novel insights into the therapy and prevention of atherosclerosis.
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Zhou, Qiu Gen, Min Zhou, Fan Fan Hou, and Xin Peng. "Asymmetrical dimethylarginine triggers lipolysis and inflammatory response via induction of endoplasmic reticulum stress in cultured adipocytes." American Journal of Physiology-Endocrinology and Metabolism 296, no. 4 (April 2009): E869—E878. http://dx.doi.org/10.1152/ajpendo.91011.2008.

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Protein energy wasting, a state of decreased stores of body protein and fat, is a risk factor for mortality in advanced chronic kidney disease (CKD). Little is known about the mechanism underlying loss of fat in CKD. Accumulation of asymmetric dimethylarginine (ADMA) is prevalent in advanced CKD. Here we assessed the effect of ADMA on cellular perturbation in cultured 3T3-L1 adipocytes. Exposure of adipocytes to ADMA induced lipolysis and decreased perilipin A, with no alteration of lipases expression or activity. ADMA treatment also upregulated the expression of inflammatory adipocytokines via activation of nuclear factor-κB (NF-κB). Blocking the inflammatory responses with NF-κB inhibitor partly inhibited the ADMA-induced lipolysis. Furthermore, ADMA treatment triggered endoplasmic reticulum (ER) stress, revealed by phosphorylation of PKR-like eukaryotic initiation factor 2α kinase, eukaryotic translational initiation factor 2α, c-Jun NH2-terminal kinase, and overexpression of glucose-regulated protein 78. Treatment with ER stress inhibitor completely abolished the ADMA-induced lipolysis and inflammatory responses. Moreover, conditioned medium from the ADMA-treated adipocytes increased protein degradation in cultured C2C12 myotubes, suggesting that the ADMA-induced adipocyte perturbation may promote skeletal muscle proteolysis. These data suggest that elevated ADMA promoted the adipocyte perturbation through induction of ER stress, which might have implication for protein energy wasting in CKD.
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46

Irani, M., W. E. Taylor, and E. T. Young. "Transcription of the ADH2 gene in Saccharomyces cerevisiae is limited by positive factors that bind competitively to its intact promoter region on multicopy plasmids." Molecular and Cellular Biology 7, no. 3 (March 1987): 1233–41. http://dx.doi.org/10.1128/mcb.7.3.1233-1241.1987.

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Transcription of the ADH2 gene in the yeast Saccharomyces cerevisiae was inhibited by excess copies of its own promoter region. This competition effect was promoter specific and required the upstream activation sequence of ADH2 as well as sequences 3' to the TATA box. Introducing excess copies of ADR1, an ADH2-specific regulatory gene, did not alleviate the competition that was observed in these circumstances during both constitutive and derepressed ADH2 expression. Excess copies of the upstream region did not release ADH2 from glucose repression, consistent with the view that ADH2 is regulated by positive trans-acting factors.
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47

Iwaki-Egawa, Sachiko, Takaya Yamamoto, and Yasuhiro Watanabe. "Human plasma adenosine deaminase 2 is secreted by activated monocytes." Biological Chemistry 387, no. 3 (March 1, 2006): 319–21. http://dx.doi.org/10.1515/bc.2006.042.

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AbstractAdenosine deaminase (ADA) plays an important role in the immune system, and its activity is composed of two kinetically distinct isozymes, ADA1 and ADA2. ADA2 is a major component of human plasma total ADA activity and ADA2 activity is significantly elevated in patients with various diseases such as HIV infection and chronic hepatitis. However, relatively little is known about ADA2 because of difficulties in purifying this enzyme. In this study we succeeded in purifying human plasma ADA2 and demonstrate the extracellular secretion of ADA2 from human peripheral blood monocytes stimulated with phorbol 12-myristate 13-acetate and calcium ionophore.
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Irani, M., W. E. Taylor, and E. T. Young. "Transcription of the ADH2 gene in Saccharomyces cerevisiae is limited by positive factors that bind competitively to its intact promoter region on multicopy plasmids." Molecular and Cellular Biology 7, no. 3 (March 1987): 1233–41. http://dx.doi.org/10.1128/mcb.7.3.1233.

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Transcription of the ADH2 gene in the yeast Saccharomyces cerevisiae was inhibited by excess copies of its own promoter region. This competition effect was promoter specific and required the upstream activation sequence of ADH2 as well as sequences 3' to the TATA box. Introducing excess copies of ADR1, an ADH2-specific regulatory gene, did not alleviate the competition that was observed in these circumstances during both constitutive and derepressed ADH2 expression. Excess copies of the upstream region did not release ADH2 from glucose repression, consistent with the view that ADH2 is regulated by positive trans-acting factors.
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49

Wang, Sukai, Xuan Li, and Ping Chen. "ADMM-SVNet: An ADMM-Based Sparse-View CT Reconstruction Network." Photonics 9, no. 3 (March 14, 2022): 186. http://dx.doi.org/10.3390/photonics9030186.

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In clinical medical applications, sparse-view computed tomography (CT) imaging is an effective method for reducing radiation doses. The iterative reconstruction method is usually adopted for sparse-view CT. In the process of optimizing the iterative model, the approach of directly solving the quadratic penalty function of the objective function can be expected to perform poorly. Compared with the direct solution method, the alternating direction method of multipliers (ADMM) algorithm can avoid the ill-posed problem associated with the quadratic penalty function. However, the regularization items, sparsity transform, and parameters in the traditional ADMM iterative model need to be manually adjusted. In this paper, we propose a data-driven ADMM reconstruction method that can automatically optimize the above terms that are difficult to choose within an iterative framework. The main contribution of this paper is that a modified U-net represents the sparse transformation, and the prior information and related parameters are automatically trained by the network. Based on a comparison with other state-of-the-art reconstruction algorithms, the qualitative and quantitative results show the effectiveness of our method for sparse-view CT image reconstruction. The experimental results show that the proposed method performs well in streak artifact elimination and detail structure preservation. The proposed network can deal with a wide range of noise levels and has exceptional performance in low-dose reconstruction tasks.
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50

Franz, M., and Z. Tešanović. "Self-Consistent Electronic Structure of adx2−y2and adx2−y2+idxyVortex." Physical Review Letters 80, no. 21 (May 25, 1998): 4763–66. http://dx.doi.org/10.1103/physrevlett.80.4763.

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