Journal articles: 'MtArgH'

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Das, Kishore, Tima Thomas, Omar Garnica, and Subramanian Dhandayuthapani. "Recombinant spore delivered M. tuberculosis antigens elicit immune response in mice." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 145.4. http://dx.doi.org/10.4049/jimmunol.196.supp.145.4.

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Abstract BCG, the vaccine against tuberculosis (TB), is one of the mandatory vaccines administered to infants in several parts of the world. However, BCG conferred immunity wanes when children reach adulthood. To develop booster vaccines, we engineered recombinant Bacillus subtilis spores to deliver Mycobacterium tuberculosis (Mtb) antigens. MTAG1 recombinant strain was designed to express a fusion protein of CotC-Ag85B-CFP10 on the spore coat, while MTAG2 and MTAG3 strains were designed to express Ag85B-CFP10 fusion protein in vegetative cells. The difference between MTAG2 and MTAG3 strains is that the latter expresses secreted listeriolysin (LLO) in addition to Ag85B-CFP10. Immunoblot analysis revealed that MTAG1 strain showed positive signals for Ag85B and CFP10 in the spore-coat and other strains in the vegetative cell extracts, indicating that antigens are expressed in these strains as expected. Splenocytes of mice immunized with recombinant spores, through intranasal route, displayed significantly higher antigen specific proliferation of IFN-γ producing cells compared to the splenocytes of control mice. Also, the culture fluids of splenocytes from recombinant spores immunized mice exhibited higher antigen specific release of Th1 cytokines than the culture fluids of splenocytes from control mice. These results indicate that antigens delivered via recombinant spores can be processed and presented to the immune cells. Additional in vivo studies may reveal whether these recombinant spores can be used to boost immunity in BCG vaccinated individuals.

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Liu, Rui, Zhenfei Guo, and Shaoyun Lu. "Genome-Wide Identification and Expression Analysis of the Aux/IAA and Auxin Response Factor Gene Family in Medicago truncatula." International Journal of Molecular Sciences 22, no. 19 (September 28, 2021): 10494. http://dx.doi.org/10.3390/ijms221910494.

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Aux/IAA and auxin response transcription factor (ARF) genes are key regulators of auxin responses in plants. A total of 25 MtIAA and 40 MtARF genes were identified based on the latest updated Medicago truncatula reference genome sequence. They were clustered into 10 and 8 major groups, respectively. The homologs among M. truncatula, soybean, and Arabidopsis thaliana shared close relationships based on phylogenetic analysis. Gene structure analysis revealed that MtIAA and MtARF genes contained one to four concern motifs and they are localized to eight chromosomes, except chromosome 6 without MtARFs. In addition, some MtIAA and MtARF genes were expressed in all tissues, while others were specifically expressed in specific tissues. Analysis of cis-acting elements in promoter region and expression profiles revealed the potential response of MtIAA and MtARF genes to hormones and abiotic stresses. The prediction protein–protein interaction network showed that some ARF proteins could interact with multiple Aux/IAA proteins, and the reverse is also true. The investigation provides valuable, basic information for further studies on the biological functions of MtIAA and MtARF genes in the regulation of auxin-related pathways in M. truncatula.

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Hristov, Danail G. Georgiev, Petya Vassileva Racheva, Galya Konstantinova Toncheva, and Kiril Blazhev Gavazov. "Extraction-Chromogenic System for Cobalt Based on 5-Methyl-4-(2-thiazolylazo) Resorcinol and Benzalkonium Chloride." Acta Chimica Slovenica 68, no. 1 (March 20, 2021): 37–43. http://dx.doi.org/10.17344/acsi.2020.6035.

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The interaction between CoII and 5-methyl-4-(2-thiazolylazo)-resorcinol (MTAR) was studied in a water-chloroform system, in the presence or absence of benzalkonium chloride (BZC) as a cationic ion-association reagent. The optimum pH, concentration of the reagents and extraction time for the extraction of Co were found. In the presence of BZC, the extracted ion-associate could be represented by the formula (BZ+)[CoIII(MTAR2–)2], where MTAR is in its deprotonated form. The following extraction-spectrophotometric characteristics were determined: absorption maximum, molar absorptivity, Sandell’s sensitivity, limit of detection, limit of quantification, constant of extraction, distribution ratio and fraction extracted. In the absence of BZC, the extraction is incomplete and occurs in a narrow pH range. The extracted chelate contains one deprotonated and one monoprotonated ligand: [CoIII(MTAR2–)(HMTAR–)].

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Xu, Dong, Jill R. Guthrie, Sherry Mabry, Thomas M. Sack, and William E. Truog. "Mitochondrial aldehyde dehydrogenase attenuates hyperoxia-induced cell death through activation of ERK/MAPK and PI3K-Akt pathways in lung epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 5 (November 2006): L966—L975. http://dx.doi.org/10.1152/ajplung.00045.2006.

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Oxygen toxicity is one of the major risk factors in the development of the chronic lung disease or bronchopulmonary dysplasia in premature infants. Using proteomic analysis, we discovered that mitochondrial aldehyde dehydrogenase (mtALDH or ALDH2) was downregulated in neonatal rat lung after hyperoxic exposure. To study the role of mtALDH in hyperoxic lung injury, we overexpressed mtALDH in human lung epithelial cells (A549) and found that mtALDH significantly reduced hyperoxia-induced cell death. Compared with control cells (Neo-A549), the necrotic cell death in mtALDH-overexpressing cells (mtALDH-A549) decreased from 25.3 to 6.5%, 50.5 to 9.1%, and 52.4 to 15.1% after 24-, 48-, and 72-h hyperoxic exposure, respectively. The levels of intracellular and mitochondria-derived reactive oxygen species (ROS) in mtALDH-A549 cells after hyperoxic exposure were significantly lowered compared with Neo-A549 cells. mtALDH overexpression significantly stimulated extracellular signal-regulated kinase (ERK) phosphorylation under normoxic and hyperoxic conditions. Inhibition of ERK phosphorylation partially eliminated the protective effect of mtALDH in hyperoxia-induced cell death, suggesting ERK activation by mtALDH conferred cellular resistance to hyperoxia. mtALDH overexpression augmented Akt phosphorylation and maintained the total Akt level in mtALDH-A549 cells under normoxic and hyperoxic conditions. Inhibition of phosphatidylinositol 3-kinase (PI3K) activation by LY294002 in mtALDH-A549 cells significantly increased necrotic cell death after hyperoxic exposure, indicating that PI3K-Akt activation by mtALDH played an important role in cell survival after hyperoxia. Taken together, these data demonstrate that mtALDH overexpression attenuates hyperoxia-induced cell death in lung epithelial cells through reduction of ROS, activation of ERK/MAPK, and PI3K-Akt cell survival signaling pathways.

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de Oliveira, Augusto Born, Ahmad Saif Ur Rehman, and Sebastian Fischmeister. "mTags." ACM SIGOPS Operating Systems Review 46, no. 2 (July 16, 2012): 67–79. http://dx.doi.org/10.1145/2331576.2331587.

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Calçada, Dario Brito, Cantídio de Moura Campos Neto, Vivian Lerner Amato, Roberta Akemi Sinoara, and Solange Oliveira Rezende. "Identification of factors related to complications in myocardial revascularization surgery: an approach with multi-target association rules networks." Research, Society and Development 11, no. 15 (November 24, 2022): e506111537638. http://dx.doi.org/10.33448/rsd-v11i15.37638.

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Myocardial revascularization surgery is one of the recommended approaches for the treatment of chronic coronary disease. Several complications related to mortality, sequelae, length of stay, and hospital costs are also associated with this procedure. Death rates and complications depend on the characteristics of each patient. Knowing the factors related to hospital mortality and complications is paramount to improving outcomes. Association Rules Mining may support the discovery of those factors. In this work we propose a new approach, called Multi-target Association Rules Network (MTARN), to analyze association rules based on networks with a simultaneous focus on two parameters. The use of association rules networks aids the analysis of a high number of association rules and the multi-target strategy allows a complete exploration, explaining which factors directly influence the analyzed set. We evaluated our approach in conjunction with domain experts and compared it to two other approaches: Decision Trees and Filtered-ARNs, a single target approach based on networks for pattern visualization. The results indicates that MTARNs optimize the discovery of knowledge directly linked to complication and death factors in patients undergoing coronary artery bypass grafting. These parameters may be used in the construction of an intelligent monitoring system to aid myocardial revascularization patients.

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Lerman, Jerrold, Lucinda Everett, and Charles J. Cote. "Response to Mtaweh et al." Journal of Child Neurology 29, no. 11 (November 25, 2013): 1580. http://dx.doi.org/10.1177/0883073813510604.

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Drugge, E. D., M. A. Carroll, and J. C. McGiff. "Cells in culture from rabbit medullary thick ascending limb of Henle's loop." American Journal of Physiology-Cell Physiology 256, no. 5 (May 1, 1989): C1070—C1081. http://dx.doi.org/10.1152/ajpcell.1989.256.5.c1070.

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Freshly isolated cells obtained from the medullary segment of the rabbit thick ascending limb of Henle's loop (mTALH) metabolize arachidonic acid (AA) primarily by the cytochrome P-450 monooxygenase pathway forming several products; a vasorelaxant and an inhibitor of Na+-K+-ATPase have been identified. These studies have been extended to mTALH cells in culture. The ability of cells isolated from 1-mo-old rabbits to grow in culture far surpassed that of cells isolated from adult rabbits, whereas similar cytochrome P-450-dependent AA metabolites were produced by freshly isolated cells from rabbits of both ages. Three-week-old mTALH cultures formed ouabain-sensitive "domes" when grown on plastic surfaces and developed transepithelial voltages (4.7 + 1.2 mV, n = 6) when grown on gas-permeable surfaces. Electron microscopy of the cells showed typical mTALH cell characteristics. The presence of Tamm-Horsfall protein, a surface membrane protein of mTALH cells, in 90-95% of the cells confirmed the homogeneity of the cultures. Although several environmental manipulations were tested, mTALH cells in culture did not produce the same cytochrome P-450-dependent AA metabolites as those produced by mTALH cells before culture. However, a cytochrome P-450-dependent AA metabolite that differs from the AA metabolites formed by freshly isolated mTALH cells was produced by hemin-treated mTALH and heterogenous cell cultures.

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Wang, Zhiqiang, Xiaoling Shi, Yujingyun Zhou, Fang Tang, Xiwu Gao, and Pei Liang. "Cap ‘n’ Collar C and Aryl Hydrocarbon Receptor Nuclear Translocator Facilitate the Expression of Glutathione S-Transferases Conferring Adaptation to Tannic Acid and Quercetin in Micromelalopha troglodyta (Graeser) (Lepidoptera: Notodontidae)." International Journal of Molecular Sciences 24, no. 3 (January 22, 2023): 2190. http://dx.doi.org/10.3390/ijms24032190.

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Micromelalopha troglodyta (Graeser) (Lepidoptera: Notodontidae) is a notorious pest of poplar. Coevolution with poplars rich in plant secondary metabolites prompts M. troglodyta to expand effective detoxification mechanisms against toxic plant secondary metabolites. Although glutathione S-transferases (GSTs) play an important role in xenobiotic detoxification in M. troglodyta, it is unclear how GSTs act in response to toxic secondary metabolites in poplar. In this study, five GST gene core promoters were accurately identified by a 5’ loss luciferase reporter assay, and the core promoters were significantly induced by two plant secondary metabolites in vitro. Two transcription factors, cap ‘n’ collar C (CncC) and aryl hydrocarbon receptor nuclear translocator (ARNT), were cloned in M. troglodyta. MtCncC and MtARNT clustered well with other insect CncCs and ARNTs, respectively. In addition, MtCncC and MtARNT could bind the MtGSTt1 promoter and strongly improve transcriptional activity, respectively. However, MtCncC and MtARNT had no regulatory function on the MtGSTz1 promoter. Our findings revealed the molecular mechanisms of the transcription factors MtCncC and MtARNT in regulating the GST genes of M. troglodyta. These results provide useful information for the control of M. troglodyta.

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Hebert, S. C. "Hypertonic cell volume regulation in mouse thick limbs. I. ADH dependency and nephron heterogeneity." American Journal of Physiology-Cell Physiology 250, no. 6 (June 1, 1986): C907—C919. http://dx.doi.org/10.1152/ajpcell.1986.250.6.c907.

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Differential interference contrast microscopy was used in combination with standard electrophysiological techniques in the in vitro perfused mouse medullary (mTALH) and cortical (cTALH) thick ascending limbs of Henle to evaluate the cell volume responses of these nephron segments to sudden increases in peritubular osmolality and to assess the role of antidiuretic hormone (ADH) and net NaCl absorption on hypertonic volume regulation. In the absence of CO2/HCO3- in external media, the cells of the mTALH behaved in a simple osmometric fashion, with an osmotic space equivalent to 70-80% of the total cell volume. However, in CO2/HCO3- -containing media, the cells of the mTALH, but not the cTALH, were able to increase their cell volume to the original volume after shrinkage in peritubular media made hypertonic with either NaCl or mannitol. This volume-regulatory increase response (VRI) in the mTALH was mediated by an increase in intracellular osmoles, and required peritubular ADH, at concentrations that stimulate maximally the rate of net NaCl absorption. This ADH effect on VRI could be mimicked by addition of dibutyryladenosine 3',5'-cyclic monophosphate to the bath in the absence of hormone. However, 10(-4) M luminal furosemide, a concentration that abolishes ADH-dependent NaCl absorption in the mTALH, had no effect on the VRI response. These results indicate that the cells of the mTALH, but not the cTALH, are capable of hypertonic volume regulation, that ADH (via adenosine 3',5'-cyclic monophosphate) is required for expression of the VRI response in the mTALH, and that the effects of ADH on net NaCl absorption and the VRI response in the mTALH are completely dissociable. Thus these results are consistent with a role for ADH in hypertonic VRI in the mammalian mTALH, which may operate to maintain constant cell volume in this nephron segment during antidiuresis.

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Figuccia, Sonia, Andrea Degiorgi, Camilla Ceccatelli Berti, Enrico Baruffini, Cristina Dallabona, and Paola Goffrini. "Mitochondrial Aminoacyl-tRNA Synthetase and Disease: The Yeast Contribution for Functional Analysis of Novel Variants." International Journal of Molecular Sciences 22, no. 9 (April 26, 2021): 4524. http://dx.doi.org/10.3390/ijms22094524.

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In most eukaryotes, mitochondrial protein synthesis is essential for oxidative phosphorylation (OXPHOS) as some subunits of the respiratory chain complexes are encoded by the mitochondrial DNA (mtDNA). Mutations affecting the mitochondrial translation apparatus have been identified as a major cause of mitochondrial diseases. These mutations include either heteroplasmic mtDNA mutations in genes encoding for the mitochondrial rRNA (mtrRNA) and tRNAs (mttRNAs) or mutations in nuclear genes encoding ribosomal proteins, initiation, elongation and termination factors, tRNA-modifying enzymes, and aminoacyl-tRNA synthetases (mtARSs). Aminoacyl-tRNA synthetases (ARSs) catalyze the attachment of specific amino acids to their cognate tRNAs. Differently from most mttRNAs, which are encoded by mitochondrial genome, mtARSs are encoded by nuclear genes and then imported into the mitochondria after translation in the cytosol. Due to the extensive use of next-generation sequencing (NGS), an increasing number of mtARSs variants associated with large clinical heterogeneity have been identified in recent years. Being most of these variants private or sporadic, it is crucial to assess their causative role in the disease by functional analysis in model systems. This review will focus on the contributions of the yeast Saccharomyces cerevisiae in the functional validation of mutations found in mtARSs genes associated with human disorders.

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Yu, Ming, Bernardo Lopez, Elisabete A. Dos Santos, John R. Falck, and Richard J. Roman. "Effects of 20-HETE on Na+ transport and Na+-K+-ATPase activity in the thick ascending loop of Henle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 6 (June 2007): R2400—R2405. http://dx.doi.org/10.1152/ajpregu.00791.2006.

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Previous studies have indicated that 20-hydroxyeicosatetraenoic acid (20-HETE) inhibits Na+ transport in the medullary thick ascending loop of Henle (mTALH), but the mechanisms involved remain uncertain. The present study compared the effects of 20-HETE with those of ouabain and furosemide on intracellular Na+ concentration ([Na+]i), Na+-K+-ATPase activity, and 86Rb+ uptake, an index of Na+ transport, in mTALH isolated from rats. Ouabain (2 mM) increased, whereas furosemide (100 μM) decreased, [Na+]i in the mTALH of rats. Ouabain and furosemide inhibited 86Rb+ uptake by 91 and 30%, respectively. 20-HETE (1 μM) had a similar effect as ouabain and increased [Na+]i from 19 ± 1 to 30 ± 1 mM. 20-HETE reduced Na+-K+-ATPase activity by 30% and 86Rb+ uptake by 37%, but it had no effect on 86Rb+ uptake or [Na+]i in the mTALH of rats pretreated with ouabain. 20-HETE inhibited 86Rb+ uptake by 12% and increased [Na+]i by 19 mM in mTALH pretreated with furosemide. These findings indicate that 20-HETE secondarily inhibits Na+ transport in the mTALH of the rat, at least, in part by inhibiting the Na+-K+-ATPase activity and raising [Na+]i.

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Escalante, B. A., N. R. Ferreri, C. E. Dunn, and J. C. McGiff. "Cytokines affect ion transport in primary cultured thick ascending limb of Henle's loop cells." American Journal of Physiology-Cell Physiology 266, no. 6 (June 1, 1994): C1568—C1576. http://dx.doi.org/10.1152/ajpcell.1994.266.6.c1568.

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Tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) affect epithelial cell ion transport. However, the site of action along the nephron has not been elucidated fully for these cytokines. Thus, the effect of TNF and IL-1 on the ion transport function of primary cultured medullary thick ascending limb of Henle's loop (mTALH) cells was determined by measuring rubidium (86Rb) uptake. TNF, IL-1, and lipopolysaccharide (LPS), a known activator of cytokine production, inhibited 86Rb uptake by cultured mTALH cells after a 24-h incubation period but had no effect when incubated with the cells for 1 or 4 h. Furthermore, mTALH cells produced biologically active TNF after stimulation with LPS for 24 h, and the LPS-induced inhibition of 86Rb uptake was abolished in the presence of an anti-TNF antibody, suggesting that TNF produced by the mTALH cells acted in an autocrine manner to inhibit 86Rb uptake. The effects of LPS on 86Rb uptake also were inhibited by the cyclooxygenase inhibitor, indomethacin. As TNF increased prostaglandin E2 synthesis by cultured mTALH cells and as prostaglandin E2 also inhibited 86Rb uptake, LPS presumably inhibited 86Rb uptake by inducing a TNF-mediated increase in prostaglandin synthesis. These data demonstrate that a prostanoid produced by mTALH cells mediates the inhibitory effect of LPS and TNF on 86Rb uptake and imply that endogenous TNF inhibits ion fluxes in the mTALH via a prostaglandin-dependent mechanism.

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Kalinowski, Piotr, Wiktor Smyk, Małgorzata Nowosad, Rafał Paluszkiewicz, Łukasz Michałowski, Bogna Ziarkiewicz-Wróblewska, Susanne N. Weber, et al. "MTARC1 and HSD17B13 Variants Have Protective Effects on Non-Alcoholic Fatty Liver Disease in Patients Undergoing Bariatric Surgery." International Journal of Molecular Sciences 23, no. 24 (December 13, 2022): 15825. http://dx.doi.org/10.3390/ijms232415825.

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The severity of hepatic steatosis is modulated by genetic variants, such as patatin-like phospholipase domain containing 3 (PNPLA3) rs738409, transmembrane 6 superfamily member 2 (TM6SF2) rs58542926, and membrane-bound O-acyltransferase domain containing 7 (MBOAT7) rs641738. Recently, mitochondrial amidoxime reducing component 1 (MTARC1) rs2642438 and hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13) rs72613567 polymorphisms were shown to have protective effects on liver diseases. Here, we evaluate these variants in patients undergoing bariatric surgery. A total of 165 patients who underwent laparoscopic sleeve gastrectomy and intraoperative liver biopsies and 314 controls were prospectively recruited. Genotyping was performed using TaqMan assays. Overall, 70.3% of operated patients presented with hepatic steatosis. NASH (non-alcoholic steatohepatitis) was detected in 28.5% of patients; none had cirrhosis. The increment of liver fibrosis stage was associated with decreasing frequency of the MTARC1 minor allele (p = 0.03). In multivariate analysis MTARC1 was an independent protective factor against fibrosis ≥ 1b (OR = 0.52, p = 0.03) and ≥ 1c (OR = 0.51, p = 0.04). The PNPLA3 risk allele was associated with increased hepatic steatosis, fibrosis, and NASH (OR = 2.22, p = 0.04). The HSD17B13 polymorphism was protective against liver injury as reflected by lower AST (p = 0.04) and ALT (p = 0.03) activities. The TM6SF2 polymorphism was associated with increased ALT (p = 0.04). In conclusion, hepatic steatosis is common among patients scheduled for bariatric surgery, but the MTARC1 and HSD17B13 polymorphisms lower liver injury in these individuals.

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Mann, Jake P., Maik Pietzner, Laura B. Wittemans, Emmanuela De Lucia Rolfe, Nicola D. Kerrison, Fumiaki Imamura, Nita G. Forouhi, et al. "Insights into genetic variants associated with NASH-fibrosis from metabolite profiling." Human Molecular Genetics 29, no. 20 (July 28, 2020): 3451–63. http://dx.doi.org/10.1093/hmg/ddaa162.

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Abstract Several genetic discoveries robustly implicate five single-nucleotide variants in the progression of non-alcoholic fatty liver disease to non-alcoholic steatohepatitis and fibrosis (NASH-fibrosis), including a recently identified variant in MTARC1. To better understand these variants as potential therapeutic targets, we aimed to characterize their impact on metabolism using comprehensive metabolomics data from two population-based studies. A total of 9135 participants from the Fenland study and 9902 participants from the EPIC-Norfolk cohort were included in the study. We identified individuals with risk alleles associated with NASH-fibrosis: rs738409C>G in PNPLA3, rs58542926C>T in TM6SF2, rs641738C>T near MBOAT7, rs72613567TA>T in HSD17B13 and rs2642438A>G in MTARC1. Circulating levels of 1449 metabolites were measured using targeted and untargeted metabolomics. Associations between NASH-fibrosis variants and metabolites were assessed using linear regression. The specificity of variant-metabolite associations were compared to metabolite associations with ultrasound-defined steatosis, gene variants linked to liver fat (in GCKR, PPP1R3B and LYPLAL1) and gene variants linked to cirrhosis (in HFE and SERPINA1). Each NASH-fibrosis variant demonstrated a specific metabolite profile with little overlap (8/97 metabolites) comprising diverse aspects of lipid metabolism. Risk alleles in PNPLA3 and HSD17B13 were both associated with higher 3-methylglutarylcarnitine and three variants were associated with lower lysophosphatidylcholine C14:0. The risk allele in MTARC1 was associated with higher levels of sphingomyelins. There was no overlap with metabolites that associated with HFE or SERPINA1 variants. Our results suggest a link between the NASH-protective variant in MTARC1 to the metabolism of sphingomyelins and identify distinct molecular patterns associated with each of the NASH-fibrosis variants under investigation.

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Sartor, Klaus. "Fortbildung - auch für unsere MTARs?!" Radiologie up2date 3, no. 1 (March 2003): 1. http://dx.doi.org/10.1055/s-2003-37873.

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Kelsen, Silvia, Bijal J. Patel, Lawson B. Parker, Trinity Vera, John M. Rimoldi, Rama S. V. Gadepalli, Heather A. Drummond, and David E. Stec. "Heme oxygenase attenuates angiotensin II-mediated superoxide production in cultured mouse thick ascending loop of Henle cells." American Journal of Physiology-Renal Physiology 295, no. 4 (October 2008): F1158—F1165. http://dx.doi.org/10.1152/ajprenal.00057.2008.

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Heme oxygenase (HO)-1 induction can attenuate the development of angiotensin II (ANG II)-dependent hypertension. However, the mechanism by which HO-1 lowers blood pressure is not clear. The goal of this study was to test the hypothesis that induction of HO-1 can reduce the ANG II-mediated increase in superoxide production in cultured thick ascending loop of Henle (TALH) cells. Studies were performed on an immortalized cell line of mouse TALH (mTALH) cells. HO-1 was induced in cultured mTALH cells by treatment with cobalt protoporphyrin (CoPP, 10 μM) or hemin (50 μM) or by transfection with a plasmid containing the human HO-1 isoform. Treatment of mTALH cells with 10−9 M ANG II increased dihydroethidium (DHE) fluorescence (an index of superoxide levels) from 35.5 ± 5 to 136 ± 18 relative fluorescence units (RFU)/μm2. Induction of HO-1 via CoPP, hemin, or overexpression of the human HO-1 isoform significantly reduced ANG II-induced DHE fluorescence to 64 ± 5, 64 ± 8, and 41 ± 4 RFU/μm2, respectively. To determine which metabolite of HO-1 is responsible for reducing ANG II-mediated increases in superoxide production in mTALH cells, cells were preincubated with bilirubin or carbon monoxide (CO)-releasing molecule (CORM)-A1 (each at 100 μM) before exposure to ANG II. DHE fluorescence averaged 80 ± 7 RFU/μm2 after incubation with ANG II and was significantly decreased to 55 ± 7 and 53 ± 4 RFU/μm2 after pretreatment with bilirubin and CORM-A1. These results demonstrate that induction of HO-1 in mTALH cells reduces the levels of ANG II-mediated superoxide production through the production of both bilirubin and CO.

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Lerolle, Nicolas, Soline Bourgeois, Françoise Leviel, Gaëtan Lebrun, Michel Paillard, and Pascal Houillier. "Angiotensin II inhibits NaCl absorption in the rat medullary thick ascending limb." American Journal of Physiology-Renal Physiology 287, no. 3 (September 2004): F404—F410. http://dx.doi.org/10.1152/ajprenal.00265.2003.

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NaCl reabsorption in the medullary thick ascending limb of Henle (MTALH) contributes to NaCl balance and is also responsible for the creation of medullary interstitial hypertonicity. Despite the presence of angiotensin II subtype 1 (AT1) receptors in both the luminal and the basolateral plasma membranes of MTALH cells, no information is available on the effect of angiotensin II on NaCl reabsorption in MTALH and, furthermore, on angiotensin II-dependent medullary interstitial osmolality. MTALHs from male Sprague-Dawley rats were isolated and microperfused in vitro; transepithelial net chloride absorption ( JCl) as well as transepithelial voltage ( Vte) were measured. Luminal or peritubular 10−11 and 10−10 M angiotensin II had no effect on JCl or Vte. However, 10−8 M luminal or peritubular angiotensin II reversibly decreased both JCl and Vte. The effect of both luminal and peritubular angiotensin II was prevented by the presence of losartan (10−6 M). By contrast, PD-23319, an AT2-receptor antagonist, did not alter the inhibitory effect of 10−8 M angiotensin II. Finally, no additive effect of luminal and peritubular angiotensin II was observed. We conclude that both luminal and peritubular angiotensin II inhibit NaCl absorption in the MTALH via AT1 receptors. Because of intrarenal angiotensin II synthesis, angiotensin II concentration in medullary tubular and interstitial fluids may be similar in vivo to the concentration that displays an inhibitory effect on NaCl reabsorption under the present experimental conditions.

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Alvo, M., J. Calamia, and J. Eveloff. "Lack of potassium effect on Na-Cl cotransport in the medullary thick ascending limb." American Journal of Physiology-Renal Physiology 249, no. 1 (July 1, 1985): F34—F39. http://dx.doi.org/10.1152/ajprenal.1985.249.1.f34.

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The effect of potassium on sodium chloride uptake into rabbit renal medullary thick ascending limb of Henle's loop (mTALH) cells was studied to assess whether K participates in the Na-Cl cotransport system. Na uptake into the mTALH cells was inhibited 70% at 3 min by 1 mM furosemide. The total and furosemide-sensitive Na uptake was stimulated by Cl. Additionally, Cl uptake into the mTALH cells was stimulated by Na gradients and inhibited 42% at 3 min by 1 mM furosemide. Na uptake was studied in the presence of 0,5, or 140 mM external K gradients. Na uptake was similar in the absence and presence of K. Additionally, furosemide inhibited Na uptake as effectively in the absence or presence of K. Similar studies were conducted to study the effects of Na on 86Rb uptake. Na did not stimulate 86Rb uptake. The uptake of 86Rb was similar in the presence of 0,5, or 140 mM Na gradients. Furosemide had no significant inhibitory effect on 86Rb uptake. Barium (5 mM), an inhibitor of K conductance pathways, inhibited total 86Rb uptake by 19%. In the presence of 5 mM BaCl2, Na still did not have a stimulatory effect on 86Rb uptake. The results confirm the existence of a Na-Cl cotransport system in mTALH cells, but a direct effect of K on the NaCl cotransport system could not be demonstrated under the experimental conditions we used.

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Allen, M. L., A. Nakao, W. K. Sonnenburg, M. Burnatowska-Hledin, W. S. Spielman, and W. L. Smith. "Immunodissection of cortical and medullary thick ascending limb cells from rabbit kidney." American Journal of Physiology-Renal Physiology 255, no. 4 (October 1, 1988): F704—F710. http://dx.doi.org/10.1152/ajprenal.1988.255.4.f704.

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A procedure was developed for isolating thick ascending limb cells from either the outer medulla or the inner cortex from rabbit kidneys. Dispersed cells derived from the medulla or cortex were incubated with goat anti-human uromucoid (Tamm-Horsfall glycoprotein) serum, washed, and applied to culture dishes coated with affinity-purified anti-goat immunoglobulin G. Nonadherent cells were removed by washing. Routinely, 10(6) or 7 X 10(4) adherent cells were obtained per gram of rabbit outer medulla or inner cortex, respectively. Greater than 97% of the adherent cells stained for Tamm-Horsfall antigen, and examination of freshly isolated cells by transmission electron microscopy established that they had morphological properties expected for thick limb cells. Freshly isolated medullary thick limb (MTALH) cells consistently accumulated cAMP in response to arginine vasopressin (AVP), thyrocalcitonin, prostaglandin E2 (PGE2), and glucagon. PGE2, thyrocalcitonin, parathyroid hormone, and AVP, but not isoproterenol or glucagon, reproducibly stimulated cAMP accumulation in freshly isolated cortical thick limb (CTALH) cells. MTALH cells produced immunoreactive PGE2 when incubated with 10 microM arachidonic acid. In summary, large numbers of highly purified and hormonally responsive rabbit MTALH and CTALH cells can be obtained by immunodissection using commercially available antibody preparations. Because the Tamm-Horsfall antigen is present as an extracellular determinant on thick ascending limb epithelia from many species, this general approach likely can be used to isolate CTALH and MTALH cells from most mammalian kidneys.

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Cartwright, C. A., M. A. Hutchinson, and W. Eckhart. "Structural and functional modification of pp60c-src associated with polyoma middle tumor antigen from infected or transformed cells." Molecular and Cellular Biology 5, no. 10 (October 1985): 2647–52. http://dx.doi.org/10.1128/mcb.5.10.2647-2652.1985.

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The polyoma middle tumor antigen (MTAg) associates with the src proto-oncogene product pp60c-src in infected or transformed rodent cells. The tyrosine protein kinase activity of pp60c-src, as measured by in vitro phosphorylation of pp60c-src itself or the exogenous substrate enolase, was increased 10- to 20-fold in cells transformed or infected with transformation-competent polyoma virus compared with controls. pp60c-src associated with MTAg and precipitated with polyoma antitumor serum had a novel site(s) of in vitro tyrosine phosphorylation within its amino-terminal domain. These observations suggest that association of MTAg with pp60c-src alters the accessibility of pp60c-src tyrosine residues for phosphorylation in vitro and increases pp60c-src protein kinase activity. Several transformation-defective mutants of MTAg did not cause amino-terminal tyrosine phosphorylation of pp60c-src in vitro or enhance its protein kinase activity, suggesting that these properties correlate with the transforming ability of MTAg. However, one transformation-defective MTAg mutant, dl1015, did cause amino-terminal tyrosine phosphorylation of pp60c-src in vitro and did enhance its protein kinase activity. This suggests that properties of MTAg, in addition to modifying the structure and function of pp60c-src, may be important for transformation.

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Cartwright, C. A., M. A. Hutchinson, and W. Eckhart. "Structural and functional modification of pp60c-src associated with polyoma middle tumor antigen from infected or transformed cells." Molecular and Cellular Biology 5, no. 10 (October 1985): 2647–52. http://dx.doi.org/10.1128/mcb.5.10.2647.

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The polyoma middle tumor antigen (MTAg) associates with the src proto-oncogene product pp60c-src in infected or transformed rodent cells. The tyrosine protein kinase activity of pp60c-src, as measured by in vitro phosphorylation of pp60c-src itself or the exogenous substrate enolase, was increased 10- to 20-fold in cells transformed or infected with transformation-competent polyoma virus compared with controls. pp60c-src associated with MTAg and precipitated with polyoma antitumor serum had a novel site(s) of in vitro tyrosine phosphorylation within its amino-terminal domain. These observations suggest that association of MTAg with pp60c-src alters the accessibility of pp60c-src tyrosine residues for phosphorylation in vitro and increases pp60c-src protein kinase activity. Several transformation-defective mutants of MTAg did not cause amino-terminal tyrosine phosphorylation of pp60c-src in vitro or enhance its protein kinase activity, suggesting that these properties correlate with the transforming ability of MTAg. However, one transformation-defective MTAg mutant, dl1015, did cause amino-terminal tyrosine phosphorylation of pp60c-src in vitro and did enhance its protein kinase activity. This suggests that properties of MTAg, in addition to modifying the structure and function of pp60c-src, may be important for transformation.

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EL RUBÉ, IBRAHIM, NAIF ALAJLAN, MOHAMED S. KAMEL, MAHER AHMED, and GEORGE H. FREEMAN. "MTAR: A ROBUST 2D SHAPE REPRESENTATION." International Journal of Image and Graphics 06, no. 03 (July 2006): 421–43. http://dx.doi.org/10.1142/s021946780600232x.

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In this paper, a new 2D shape Multiscale Triangle-Area Representation (MTAR) method is proposed. This representation utilizes a simple geometric principle, that is, the area of the triangles formed by the shape boundary points. The wavelet transform is used for smoothing and decomposing the shape boundaries into multiscale levels. At each scale level, a TAR image and the corresponding Maxima-Minima lines are obtained. The resulting MTAR is more robust to noise, less complex, and more selective than similar methods such as the curvature scale-space (CSS). Furthermore, the MTAR is invariant to the general affine transformations. The proposed MTAR is tested and compared to the CSS method using MPEG-7 CE-shape-1 part B and Columbia Object Image Library (COIL-20) datasets. The results show that the proposed MTAR outperforms the CSS method for the conducted tests.

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CASTELLANI, LEONARDO, RICCARDO D’ AURIA, and DAVIDE FRANCO. "ON TYPE II SUPERSTRINGS: THE σ MODEL AND COMPACTIFICATION TO D=4." International Journal of Modern Physics A 06, no. 22 (September 20, 1991): 4009–39. http://dx.doi.org/10.1142/s0217751x91001969.

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We present a geometric construction of the σ model describing type II superstrings propagating on an arbitrary Mtarget. Specializing the covering space of the internal target manifold to be the nine-dimensional group manifold SU(2)3, we discuss the massless vertices both in the (4+9)-dimensional a model and in the D=4 superconformal theory, and show how they are related via dimensional reduction.

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Shelver, Daniel, Lakshmi Rajagopal, Theresa O. Harris, and Craig E. Rubens. "MtaR, a Regulator of Methionine Transport, Is Critical for Survival of Group B Streptococcus In Vivo." Journal of Bacteriology 185, no. 22 (November 15, 2003): 6592–99. http://dx.doi.org/10.1128/jb.185.22.6592-6599.2003.

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ABSTRACT The group B streptococcus (GBS) is an important human pathogen that infects newborns as well as adults. GBS also provides a model system for studying adaptation to different host environments due to its ability to survive in a variety of sites within the host. In this study, we have characterized a transcription factor, MtaR, that is essential for the ability of GBS to survive in vivo. An isogenic strain bearing a kanamycin insertion in mtaR was attenuated for survival in a neonatal-rat model of sepsis. The mtaR mutant grew poorly in human plasma, suggesting that its utilization of plasma-derived nutrients was inefficient. When an excess of exogenous methionine (200 μg/ml) was provided to the mtaR mutant, its growth rate in plasma was restored to that of the wild-type strain. The mtaR mutant grew poorly in chemically defined medium (CDM) prepared with methionine at a concentration similar to that of plasma (4 μg/ml) but was able to grow normally in CDM prepared with a high concentration of methionine (400 μg/ml). Both the wild-type strain and the mtaR mutant were incapable of growth in CDM lacking methionine, indicating that GBS cannot synthesize methionine de novo. When the abilities of the strains to incorporate radiolabeled methionine were compared, the mtaR mutant incorporated fivefold less methionine than the wild-type strain during a 10-min period. Collectively, the results from this study suggest that the ability to regulate expression of a methionine transport system is critical for GBS survival in vivo.

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Fujino, Takayuki, Sharifi Muhib, Nobuyuki Sato, and Naoyuki Hasebe. "Silencing of p53 RNA through transarterial delivery ameliorates renal tubular injury and downregulates GSK-3β expression after ischemia-reperfusion injury." American Journal of Physiology-Renal Physiology 305, no. 11 (December 1, 2013): F1617—F1627. http://dx.doi.org/10.1152/ajprenal.00279.2013.

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p53, a pivotal protein in the apoptotic pathway, has been identified as a mediator of transcriptional responses to ischemia-reperfusion (IR) injury. The characteristics and functional significance of the p53 response in vivo are largely unknown in IR-induced kidney injury. Therapeutic opportunities of delivering small interfering RNA (siRNA) via venous injection have gained recognition; however, systemic adverse effects of siRNA therapy should be considered. To prevent IR-induced kidney injury, we tested the efficacy of transarterial administration of siRNA targeting p53 (p53 siRNA). Female C57BL/6 mice underwent unilateral renal artery ischemia for 30 min, followed by reperfusion. siRNA experiments utilized short hairpin (sh) RNA plasmid-based approaches. Transfection of shRNA was performed using cationic polymer transfection reagent. Injection of synthetic p53 shRNA into the left renal artery just after ischemia improved tubular injury, apoptosis, and the swelling of mitochondria in cells of the thick ascending limb of Henle (mTALH) at the outer medullary regions. Staining of upregulated p53 was colocalized with the inducible expression of glycogen synthase kinase-3β (GSK-3β) at mTALH after IR injury. p53 shRNA inhibited GSK-3β expression and restored β-catenin expression at mTALH. For IR-induced kidney injury, transarterial delivery of p53 siRNA is an effective pharmacological intervention. Targeting siRNA to p53 leads to an attenuation of apoptosis and mitochondrial damage through the downregulation of GSK-3β expression and upregulation of β-catenin. Local delivery of vectors such as p53 siRNA through a transaortic catheter is clinically useful in reducing the adverse effect of siRNA-related therapy.

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Escalante, B., D. Erlij, J. R. Falck, and J. C. McGiff. "Cytochrome P-450 arachidonate metabolites affect ion fluxes in rabbit medullary thick ascending limb." American Journal of Physiology-Cell Physiology 266, no. 6 (June 1, 1994): C1775—C1782. http://dx.doi.org/10.1152/ajpcell.1994.266.6.c1775.

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The medullary thick ascending limb of Henle's loop (mTALH) of the rabbit metabolizes arachidonic acid (AA) via a cytochrome P-450 (P-450) monooxygenase pathway to several products, of which the principal are 20-hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE) and 1,20-eicosatetraenedioic acid (20-COOH-AA). To understand their mechanism of action on alkali cation metabolism in mTALH cells, we have compared their effects with those of ouabain and furosemide. Incubation of rabbit isolated mTALH cells with either 1 mM ouabain or furosemide decreased K+ content from a control of 1,015 +/- 51 peq/micrograms protein to 717 +/- 41 and to 548 +/- 48 peq/micrograms protein, respectively, whereas they had opposite effects on Na+ content; from a control of 138 +/- 22 peq/micrograms protein, ouabain increased Na+ content to 357 +/- 37 peq/micrograms protein, and furosemide decreased it to 64 +/- 23 peq/micrograms protein. Preincubation with either 20-HETE (1 microM) or 20-COOH-AA (1 microM) decreased Na+ and K+, resembling furosemide in their effects on Na+ and K+ content. In other experiments we used monensin-treated cells to determine 86Rb uptake under conditions in which Na+ entry into the cell was not rate limiting. Under these conditions ouabain still inhibited 86Rb uptake, and the effect of AA was blocked. A major action of AA metabolites on Na(+)-K(+)-adenosinetriphosphatase was thereby excluded. Furthermore, AA metabolites did not inhibit Ba(2+)-sensitive 86Rb efflux, indicating that they do not act through K+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

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Ono, M., M. Yakushinji, K. Segawa, and M. Kuwano. "Transformation by viral and cellular oncogenes of a mouse BALB/3T3 cell mutant resistant to transformation by chemical carcinogens." Molecular and Cellular Biology 8, no. 10 (October 1988): 4190–96. http://dx.doi.org/10.1128/mcb.8.10.4190-4196.1988.

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The mouse cell line MO-5 is resistant to transformation by various chemical carcinogens and also by UV irradiation (C. Yasutake, Y. Kuratomi, M. Ono, S. Masumi, and M. Kuwano, Cancer Res. 47:4894-4899, 1987). Northern (RNA) blot analysis showed active expression of ras and myc genes in MO-5 and BALB/3T3 cells. The effect of transfection of various oncogenes on transformation was compared in MO-5 cells and parental BALB/3T3 cells. Activated c-H-ras, c-N-ras, and v-mos gene induced transformation foci of MO-5 and BALB/3T3. Introduction of the polyomavirus middle T-antigen (mTag) or the Rous sarcoma virus-related oncogene v-src, however, efficiently transformed BALB/3T3 but not MO-5 cells. Expression and phosphorylation of mTag and the associated c-src proteins were observed in mTag-transfected clones of MO-5 as in BALB/3T3 and phosphorylation of the src protein was observed in v-src-transfected BALB/3T3 and MO-5 clones. Hybrids between mTag- or v-src-induced transformants of BALB/3T3 and untransformed MO-5 maintained the transformation phenotype, suggesting that no dominant suppressor of transformation exists in MO-5. A hybrid clone between BALB/3T3 and MO-5 induced efficient transformation foci after transfection with the mTag gene, suggesting that the deficient transformation phenotype of MO-5 was recessive. Instead, some other alteration of MO-5, plausibly membrane function, might lead to abortive transformation by chemical carcinogens and also by mTag and the v-src gene product.

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Ono, M., M. Yakushinji, K. Segawa, and M. Kuwano. "Transformation by viral and cellular oncogenes of a mouse BALB/3T3 cell mutant resistant to transformation by chemical carcinogens." Molecular and Cellular Biology 8, no. 10 (October 1988): 4190–96. http://dx.doi.org/10.1128/mcb.8.10.4190.

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The mouse cell line MO-5 is resistant to transformation by various chemical carcinogens and also by UV irradiation (C. Yasutake, Y. Kuratomi, M. Ono, S. Masumi, and M. Kuwano, Cancer Res. 47:4894-4899, 1987). Northern (RNA) blot analysis showed active expression of ras and myc genes in MO-5 and BALB/3T3 cells. The effect of transfection of various oncogenes on transformation was compared in MO-5 cells and parental BALB/3T3 cells. Activated c-H-ras, c-N-ras, and v-mos gene induced transformation foci of MO-5 and BALB/3T3. Introduction of the polyomavirus middle T-antigen (mTag) or the Rous sarcoma virus-related oncogene v-src, however, efficiently transformed BALB/3T3 but not MO-5 cells. Expression and phosphorylation of mTag and the associated c-src proteins were observed in mTag-transfected clones of MO-5 as in BALB/3T3 and phosphorylation of the src protein was observed in v-src-transfected BALB/3T3 and MO-5 clones. Hybrids between mTag- or v-src-induced transformants of BALB/3T3 and untransformed MO-5 maintained the transformation phenotype, suggesting that no dominant suppressor of transformation exists in MO-5. A hybrid clone between BALB/3T3 and MO-5 induced efficient transformation foci after transfection with the mTag gene, suggesting that the deficient transformation phenotype of MO-5 was recessive. Instead, some other alteration of MO-5, plausibly membrane function, might lead to abortive transformation by chemical carcinogens and also by mTag and the v-src gene product.

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Hebert, S. C., and T. E. Andreoli. "Ionic conductance pathways in the mouse medullary thick ascending limb of Henle. The paracellular pathway and electrogenic Cl- absorption." Journal of General Physiology 87, no. 4 (April 1, 1986): 567–90. http://dx.doi.org/10.1085/jgp.87.4.567.

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Net Cl- absorption in the mouse medullary thick ascending limb of Henle (mTALH) involves a furosemide-sensitive Na+:K+:2 Cl- apical membrane symport mechanism for salt entry into cells, which occurs in parallel with a Ba++-sensitive apical K+ conductance. The present studies, using the in vitro microperfused mouse mTALH, assessed the concentration dependence of blockade of this apical membrane K+-conductive pathway by Ba++ to provide estimates of the magnitudes of the transcellular (Gc) and paracellular (Gs) electrical conductances (millisiemens per square centimeter). These studies also evaluated the effects of luminal hypertonicity produced by urea on the paracellular electrical conductance, the electrical Na+/Cl- permselectivity ratio, and the morphology of in vitro mTALH segments exposed to peritubular antidiuretic hormone (ADH). Increasing luminal Ba++ concentrations, in the absence of luminal K+, produced a progressive reduction in the transcellular conductance that was maximal at 20 mM Ba++. The Ba++-sensitive transcellular conductance in the presence of ADH was 61.8 +/- 1.7 mS/cm2, or approximately 65% of the total transepithelial conductance. In phenomenological terms, the luminal Ba++-dependent blockade of the transcellular conductance exhibited negative cooperativity. The transepithelial osmotic gradient produced by luminal urea produced blebs on apical surfaces, a striking increase in shunt conductance, and a decrease in the shunt Na+/Cl- permselectivity (PNa/PCl), which approached that of free solution. The transepithelial conductance obtained with luminal 800 mM urea, 20 mM Ba++, and 0 K+ was 950 +/- 150 mS/cm2 and provided an estimate of the maximal diffusion resistance of intercellular spaces, exclusive of junctional complexes. The calculated range for junctional dilution voltages owing to interspace salt accumulation during ADH-dependent net NaCl absorption was 0.7-1.1 mV. Since the Ve accompanying ADH-dependent net NaCl absorption is 10 mV, lumen positive, virtually all of the spontaneous transepithelial voltage in the mouse mTALH is due to transcellular transport processes. Finally, we developed a series of expressions in which the ratio of net Cl- absorption to paracellular Na+ absorption could be expressed in terms of a series of electrical variables. Specifically, an analysis of paired measurement of PNa/PCl and Gs was in agreement with an electroneutral Na+:K+:2 Cl- apical entry step. Thus, for net NaCl absorption, approximately 50% of Na+ was absorbed via a paracellular route.

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Hill, W. David. "Comment on ‘Large-Scale Cognitive GWAS Meta-Analysis Reveals Tissue-Specific Neural Expression and Potential Nootropic Drug Targets’ by Lam et al." Twin Research and Human Genetics 21, no. 2 (March 19, 2018): 84–88. http://dx.doi.org/10.1017/thg.2018.12.

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Intelligence and educational attainment are strongly genetically correlated. This relationship can be exploited by Multi-Trait Analysis of GWAS (MTAG) to add power to Genome-wide Association Studies (GWAS) of intelligence. MTAG allows the user to meta-analyze GWASs of different phenotypes, based on their genetic correlations, to identify association's specific to the trait of choice. An MTAG analysis using GWAS data sets on intelligence and education was conducted by Lam et al. (2017). Lam et al. (2017) reported 70 loci that they described as ‘trait specific’ to intelligence. This article examines whether the analysis conducted by Lam et al. (2017) has resulted in genetic information about a phenotype that is more similar to education than intelligence.

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Abascal, F., D. Posada, and R. Zardoya. "MtArt: A New Model of Amino Acid Replacement for Arthropoda." Molecular Biology and Evolution 24, no. 1 (October 16, 2006): 1–5. http://dx.doi.org/10.1093/molbev/msl136.

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Rehman, Ahmad Saif Ur, Augusto Born de Oliveira, Mahesh Tripunitara, and Sebastian Fischmeister. "The use of mTags for mandatory security: a case study." Software: Practice and Experience 44, no. 12 (September 19, 2013): 1511–23. http://dx.doi.org/10.1002/spe.2222.

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BEN YOUSSEF, Youssef, Mohamed Merrouchi, Elhassane Abdelmounim, and Taoufiq Gadi. "Classification of Aircraft in Remote Sensing Images Based on Deep Convolutional Neural Networks." Statistics, Optimization & Information Computing 10, no. 1 (February 8, 2022): 4–11. http://dx.doi.org/10.19139/soic-2310-5070-1143.

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Convolutional Neural Network (CNN) is a component of Deep Learning(DL) recently exploited in different fifields. In this work, we improve the performance of multi-label classifification based on CNN for remote sensing images of aircraft types. Intensive preprocessing limits the classifification rate in previous studies. In order to avoid under-fifitting and over-fifitting problems, we optimized the architecture and Network parameters. To validate our method the recent public image dataset called Multi-Type Aircraft Remote Sensing Images (MTARSI) is used. Extensive experiments prove the effectiveness of the proposed method in terms of classifification rate.

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Rössing, Claudia, and Dorothee Berief. "Anpassung der Berufsbezeichnung und noch einiges mehr – das neue Gesetz für Medizin Technologische Berufe (MTBG-bisher MTA-Gesetz)." Klinische Neurophysiologie 53, no. 01 (March 2022): 68–69. http://dx.doi.org/10.1055/a-1734-2481.

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Die Berufsausübung der MTA-Berufe basiert auf dem MTA-Gesetz (MTAG) von 1993. Seitdem gab es vielfältige Veränderungen im Klinik- und Praxisalltag, die eine Novellierung des Gesetzes dringend erforderlich machten. Dafür setzte sich in den vergangenen Jahren der Dachverband für Technologen/-innen und Analytiker/-innen in der Medizin Deutschland e.V. (DVTA) ein. Im Juni 2020 erreichte den Bundesvorstand des DVTA die Information aus dem Bundesministerium für Gesundheit (BMG), dass die Neuordnung des MTAG auf den Weg gebracht wird. Ab 01.01.2023 tritt das neue MT-Berufe-Gesetz in Kraft.

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Augustine, J. A., S. L. Sutor, and R. T. Abraham. "Interleukin 2- and polyomavirus middle T antigen-induced modification of phosphatidylinositol 3-kinase activity in activated T lymphocytes." Molecular and Cellular Biology 11, no. 9 (September 1991): 4431–40. http://dx.doi.org/10.1128/mcb.11.9.4431-4440.1991.

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Stimulation of activated T lymphocytes with interleukin 2 (IL-2) results in rapid increases in intracellular protein tyrosine phosphorylation. Both the identity of the protein tyrosine kinase (PTK) activated by IL-2 receptor ligation and the identities of the critical target proteins for this PTK remain largely undefined. In this article, we demonstrate that stimulation of activated murine or human T cells with IL-2 for 10 to 30 min induces two- to threefold increases in the level of phosphatidylinositol (PtdIns) 3-kinase activity present in antiphosphotyrosine (p-Tyr) antibody immunoprecipitates from these cells. Furthermore, substantial levels of PtdIns 3-kinase activity were coprecipitated from IL-2-deprived T cells by antibodies to the src-related PTK p59fyn. Cellular stimulation with IL-2 induced a two- to threefold increase in the level of p59fyn-associated PtdIns 3-kinase activity. To examine the effect of a constitutive increase in PtdIns 3-kinase activity on the growth factor responsiveness of activated T cells, murine CTLL-2 cells were transfected with a polyomavirus middle T antigen (MTAg) expression vector. Anti-p-Tyr and anti-p59fyn immunoprecipitates from MTAg-transfected CTLL-2 cells contained three- to sixfold higher levels of PtdIns 3-kinase activity than wild-type cells. Immune complex kinase assays revealed that MTAg expression concomitantly induced a constitutive threefold increase in the PTK activity of p59fyn in these cells. However, stable MTAg expression did not abrogate the dependence of CTLL-2 cells on exogenous IL-2 for continued growth and proliferation.

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Augustine, J. A., S. L. Sutor, and R. T. Abraham. "Interleukin 2- and polyomavirus middle T antigen-induced modification of phosphatidylinositol 3-kinase activity in activated T lymphocytes." Molecular and Cellular Biology 11, no. 9 (September 1991): 4431–40. http://dx.doi.org/10.1128/mcb.11.9.4431.

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Stimulation of activated T lymphocytes with interleukin 2 (IL-2) results in rapid increases in intracellular protein tyrosine phosphorylation. Both the identity of the protein tyrosine kinase (PTK) activated by IL-2 receptor ligation and the identities of the critical target proteins for this PTK remain largely undefined. In this article, we demonstrate that stimulation of activated murine or human T cells with IL-2 for 10 to 30 min induces two- to threefold increases in the level of phosphatidylinositol (PtdIns) 3-kinase activity present in antiphosphotyrosine (p-Tyr) antibody immunoprecipitates from these cells. Furthermore, substantial levels of PtdIns 3-kinase activity were coprecipitated from IL-2-deprived T cells by antibodies to the src-related PTK p59fyn. Cellular stimulation with IL-2 induced a two- to threefold increase in the level of p59fyn-associated PtdIns 3-kinase activity. To examine the effect of a constitutive increase in PtdIns 3-kinase activity on the growth factor responsiveness of activated T cells, murine CTLL-2 cells were transfected with a polyomavirus middle T antigen (MTAg) expression vector. Anti-p-Tyr and anti-p59fyn immunoprecipitates from MTAg-transfected CTLL-2 cells contained three- to sixfold higher levels of PtdIns 3-kinase activity than wild-type cells. Immune complex kinase assays revealed that MTAg expression concomitantly induced a constitutive threefold increase in the PTK activity of p59fyn in these cells. However, stable MTAg expression did not abrogate the dependence of CTLL-2 cells on exogenous IL-2 for continued growth and proliferation.

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Muths, Erin. "The Meritorious Teaching Award in Herpetology (MTAH)." Herpetologica 76, no. 1 (March 4, 2020): 94. http://dx.doi.org/10.1655/0018-0831-76.1.94.

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Lee, Oesook, and Dong Wan Shin. "On geometric ergodicity of the MTAR process." Statistics & Probability Letters 48, no. 3 (July 2000): 229–37. http://dx.doi.org/10.1016/s0167-7152(99)00208-4.

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Klimašauskas, Saulius, Gražvydas Lukinavičius, Edita Kriukienė, Giedrė Urbanavičiūtė, Rūta Gerasimaitė, Zdislav Staševskij, Alexandra Plotnikova, and Giedrius Vilkaitis. "MTAG: A new molecular tool for biotechnology." Journal of Biotechnology 136 (October 2008): S100—S101. http://dx.doi.org/10.1016/j.jbiotec.2008.07.229.

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Eveloff, J. L., and J. Calamia. "Effect of osmolarity on cation fluxes in medullary thick ascending limb cells." American Journal of Physiology-Renal Physiology 250, no. 1 (January 1, 1986): F176—F180. http://dx.doi.org/10.1152/ajprenal.1986.250.1.f176.

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The effects of a hypertonic extracellular medium on furosemide-sensitive Na and K fluxes were studied in isolated cells from the rabbit medullary thick ascending limb of Henle's loop (mTALH). In the control incubation medium, the furosemide-sensitive 22Na uptake was 379.1 +/- 24.4 pmol . mg protein-1 . min-1 and the furosemide-sensitive 86Rb uptake was 30.5 +/- 16.9. The furosemide-sensitive 22Na flux was not stimulated by K gradients directed into the cells, and, conversely, the furosemide-sensitive 86Rb flux was not stimulated by Na gradients directed into the cells. These findings are consistent with a Na-Cl cotransport system. In the presence of 200 mM mannitol, the furosemide-sensitive 22Na and 86Rb fluxes were increased dramatically to 919.4 +/- 76.6 and 106.1 +/- 29.2 pmol . mg protein-1 . min-1, respectively. When the osmolarity of the incubation medium was increased, not only were the furosemide-sensitive fluxes increased but these fluxes became inter-dependent, i.e., removing Na or K prevented the increase in the furosemide-sensitive flux of the other cation. This finding is consistent with a Na-K-2Cl cotransport system in the mTALH cells. The data suggest that the Na-Cl and the Na-K-2Cl cotransport systems may be distinct functions of the same furosemide-sensitive cotransport system and that their expression may be regulated by changes in cell volume.

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Zhao, Yang, Rong Liu, Yiteng Xu, Minmin Wang, Jing Zhang, Mingyi Bai, Chao Han, et al. "AGLF provides C-function in floral organ identity through transcriptional regulation of AGAMOUS in Medicago truncatula." Proceedings of the National Academy of Sciences 116, no. 11 (February 19, 2019): 5176–81. http://dx.doi.org/10.1073/pnas.1820468116.

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Floral development is one of the model systems for investigating the mechanisms underlying organogenesis in plants. Floral organ identity is controlled by the well-known ABC model, which has been generalized to many flowering plants. Here, we report a previously uncharacterized MYB-like gene, AGAMOUS-LIKE FLOWER (AGLF), involved in flower development in the model legume Medicago truncatula. Loss-of-function of AGLF results in flowers with stamens and carpel transformed into extra whorls of petals and sepals. Compared with the loss-of-function mutant of the class C gene AGAMOUS (MtAG) in M. truncatula, the defects in floral organ identity are similar between aglf and mtag, but the floral indeterminacy is enhanced in the aglf mutant. Knockout of AGLF in the mutants of the class A gene MtAP1 or the class B gene MtPI leads to an addition of a loss-of-C-function phenotype, reflecting a conventional relationship of AGLF with the canonical A and B genes. Furthermore, we demonstrate that AGLF activates MtAG in transcriptional levels in control of floral organ identity. These data shed light on the conserved and diverged molecular mechanisms that control flower development and morphology among plant species.

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Rixen, Sophia, Patrick M. Indorf, Christian Kubitza, Michel A. Struwe, Cathrin Klopp, Axel J. Scheidig, Thomas Kunze, and Bernd Clement. "Reduction of Hydrogen Peroxide by Human Mitochondrial Amidoxime Reducing Component Enzymes." Molecules 28, no. 17 (August 31, 2023): 6384. http://dx.doi.org/10.3390/molecules28176384.

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The mitochondrial amidoxime reducing component (mARC) is a human molybdoenzyme known to catalyze the reduction of various N-oxygenated substrates. The physiological function of mARC enzymes, however, remains unknown. In this study, we examine the reduction of hydrogen peroxide (H2O2) by the human mARC1 and mARC2 enzymes. Furthermore, we demonstrate an increased sensitivity toward H2O2 for HEK-293T cells with an MTARC1 knockout, which implies a role of mARC enzymes in the cellular response to oxidative stress. H2O2 is a reactive oxygen species (ROS) formed in all living cells involved in many physiological processes. Furthermore, H2O2 constitutes the first mARC substrate without a nitrogen–oxygen bond, implying that mARC enzymes may have a substrate spectrum going beyond the previously examined N-oxygenated compounds.

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44

Cook, Steve. "Simulation Analysis of Threshold Autoregressive Unit Root Tests." ISRN Probability and Statistics 2012 (June 20, 2012): 1–12. http://dx.doi.org/10.5402/2012/649134.

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Using numerical simulation, the finite-sample properties of threshold autoregressive (TAR) and momentum-threshold (MTAR) autoregressive-based unit root tests under both deterministic and consistent methods of threshold estimation are examined in the presence of generalised autoregressive conditional heteroskedasticity (GARCH). Previous research is extended by considering both the impact of alternative robust methods of covariance matrix estimation and the behaviour of the secondary tests of asymmetry associated with the TAR and MTAR models. The results obtained reveal many interesting features, in particular the distortionary effects of consistent-threshold estimation. In summary, the findings presented indicate that caution should be exercised when interpreting the results of these frequently employed threshold-based testing methods.

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45

Kim, J. K., S. N. Summer, and R. W. Schrier. "Cellular action of arginine vasopressin in the isolated renal tubules of hypothyroid rats." American Journal of Physiology-Renal Physiology 253, no. 1 (July 1, 1987): F104—F110. http://dx.doi.org/10.1152/ajprenal.1987.253.1.f104.

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Hypothyroidism has been demonstrated to be associated with an impaired concentrating capacity and specific morphological changes in the thick ascending limbs. This study was performed to evaluate the cellular action of arginine vasopressin (AVP) in the isolated renal tubules from control (C) and hypothyroid (HT) rats. Hypothyroidism was induced by feeding aminotriazole for 4 wk. Urinary volume was higher in HT rats (C 13.5 +/- 0.9, HT 17.7 +/- 0.9 ml/24 h, P less than 0.005) and urinary osmolality was lower in HT rats (C 1,707 +/- 49, HT 1,229 +/- 35 mosmol/kgH2O, P less than 0.001). Plasma AVP levels were significantly higher in HT rats (C 1.93 +/- 0.59, HT 4.12 +2- 0.62 pg/ml, P less than 0.05), thus documenting AVP resistance. The adenylate cyclase response to AVP (10(-6) M) was significantly lower (P less than 0.02) in the medullary thick ascending limb of Henle's loop (mTALH) in HT (14.3 +/- 2.4 to 41.7 +/- 5.8 fm X 30 min-1 X mm-1, P less than 0.001) than in mTALH in C rats (14.4 +/- 2.8 to 110.1 +/- 24.9 fm X 30 min-1 X mm-1, P less than 0.001). In contrast, the adenylate cyclase response to AVP was not significantly different in collecting tubules of cortex, outer medulla, and inner medulla from C and HT rats, although a slight decrease in response to AVP was observed in cortical and outer medullary collecting tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

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46

Faccioli, Lanuza A. P., Zeliha Cetin, Zehra N. Kocas-Kilicarslan, Kimberly Ortiz, Yiyue Sun, Zhiping Hu, Takeshi Kurihara, et al. "Evaluation of Human Hepatocyte Drug Metabolism Carrying High-Risk or Protection-Associated Liver Disease Genetic Variants." International Journal of Molecular Sciences 24, no. 17 (August 29, 2023): 13406. http://dx.doi.org/10.3390/ijms241713406.

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Metabolic-dysfunction-associated steatotic liver disease (MASLD), which affects 30 million people in the US and is anticipated to reach over 100 million by 2030, places a significant financial strain on the healthcare system. There is presently no FDA-approved treatment for MASLD despite its public health significance and financial burden. Understanding the connection between point mutations, liver enzymes, and MASLD is important for comprehending drug toxicity in healthy or diseased individuals. Multiple genetic variations have been linked to MASLD susceptibility through genome-wide association studies (GWAS), either increasing MASLD risk or protecting against it, such as PNPLA3 rs738409, MBOAT7 rs641738, GCKR rs780094, HSD17B13 rs72613567, and MTARC1 rs2642438. As the impact of genetic variants on the levels of drug-metabolizing cytochrome P450 (CYP) enzymes in human hepatocytes has not been thoroughly investigated, this study aims to describe the analysis of metabolic functions for selected phase I and phase II liver enzymes in human hepatocytes. For this purpose, fresh isolated primary hepatocytes were obtained from healthy liver donors (n = 126), and liquid chromatography–mass spectrometry (LC–MS) was performed. For the cohorts, participants were classified into minor homozygotes and nonminor homozygotes (major homozygotes + heterozygotes) for five gene polymorphisms. For phase I liver enzymes, we found a significant difference in the activity of CYP1A2 in human hepatocytes carrying MBOAT7 (p = 0.011) and of CYP2C8 in human hepatocytes carrying PNPLA3 (p = 0.004). It was also observed that the activity of CYP2C9 was significantly lower in human hepatocytes carrying HSD17B13 (p = 0.001) minor homozygous compared to nonminor homozygous. No significant difference in activity of CYP2E1, CYP2C8, CYP2D6, CYP2E1, CYP3A4, ECOD, FMO, MAO, AO, and CES2 and in any of the phase II liver enzymes between human hepatocytes carrying genetic variants for PNPLA3 rs738409, MBOAT7 rs641738, GCKR rs780094, HSD17B13 rs72613567, and MTARC1 rs2642438 were observed. These findings offer a preliminary assessment of the influence of genetic variations on drug-metabolizing cytochrome P450 (CYP) enzymes in healthy human hepatocytes, which may be useful for future drug discovery investigations.

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Schneider, Carolin V., Kai Markus Schneider, Donna M. Conlon, Joseph Park, Marijana Vujkovic, Inuk Zandvakili, Yi-An Ko, et al. "A genome-first approach to mortality and metabolic phenotypes in MTARC1 p.Ala165Thr (rs2642438) heterozygotes and homozygotes." Med 2, no. 7 (July 2021): 851–63. http://dx.doi.org/10.1016/j.medj.2021.04.011.

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Acquah, Henry de-Graft. "Threshold Effects and Asymmetric Price Adjustments within the Ghanaian Maize Market." Journal of Economics and Behavioral Studies 4, no. 9 (September 15, 2012): 497–504. http://dx.doi.org/10.22610/jebs.v4i9.351.

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This study investigated co integration and asymmetric adjustments in the end equilibrium between Ghanaian retail and wholesale maize markets using the Enders and Siklos technique. Two competing models, namely Consistent Threshold Autoregressive (C-TAR) and Consistent Momentum Threshold Autoregressive (C-MTAR) models were estimated. Following the application of a standard model selection technique, CMTAR model is selected as most appropriate. The results of the C-MTAR model confirm that the retail and wholesale prices of maize in Ghana are co integrated with threshold adjustment. Furthermore, it suggests that the process is asymmetric when the retail and wholesale prices of Ghanaian maize adjust to achieve the longterm equilibrium. Additionally, the adjustment is relatively faster when the price differential is increasing than when it is decreasing.

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Yelamanchi, Soujanya D., Sumaithangi Thattai Arun Kumar, Archita Mishra, Thottethodi Subrahmanya Keshava Prasad, and Avadhesha Surolia. "Metabolite Dysregulation by Pranlukast in Mycobacterium tuberculosis." Molecules 27, no. 5 (February 24, 2022): 1520. http://dx.doi.org/10.3390/molecules27051520.

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Mycobacterium tuberculosis has been infecting millions of people worldwide over the years, causing tuberculosis. Drugs targeting distinct cellular mechanisms including synthesis of the cell wall, lipids, proteins, and nucleic acids in Mtb are currently being used for the treatment of TB. Although extensive research is being carried out at the molecular level in the infected host and pathogen, the identification of suitable drug targets and drugs remains under explored. Pranlukast, an allosteric inhibitor of MtArgJ (Mtb ornithine acetyltransferase) has previously been shown to inhibit the survival and virulence of Mtb. The main objective of this study was to identify the altered metabolic pathways and biological processes associated with the differentially expressed metabolites by PRK in Mtb. Here in this study, metabolomics was carried out using an LC-MS/MS-based approach. Collectively, 50 metabolites were identified to be differentially expressed with a significant p-value through a global metabolomic approach using a high-resolution mass spectrometer. Metabolites downstream of argJ were downregulated in the arginine biosynthetic pathway following pranlukast treatment. Predicted human protein interactors of pranlukast-treated Mtb metabolome were identified in association with autophagy, inflammation, DNA repair, and other immune-related processes. Further metabolites including N-acetylglutamate, argininosuccinate, L-arginine, succinate, ergothioneine, and L-phenylalanine were validated by multiple reaction monitoring, a targeted mass spectrometry-based metabolomic approach. This study facilitates the understanding of pranlukast-mediated metabolic changes in Mtb and holds the potential to identify novel therapeutic approaches using metabolic pathways in Mtb.

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Bourgeois, Soline, Sandrine Massé, Michel Paillard, and Pascal Houillier. "Basolateral membrane Cl−-, Na+-, and K+-coupled base transport mechanisms in rat MTALH." American Journal of Physiology-Renal Physiology 282, no. 4 (April 1, 2002): F655—F668. http://dx.doi.org/10.1152/ajprenal.00220.2000.

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Mechanisms involved in basolateral HCO[Formula: see text] transport were examined in the in vitro microperfused rat medullary thick ascending limb of Henle (MTALH) by microfluorometric monitoring of cell pH. Removing peritubular Cl− induced a cellular alkalinization that was inhibited in the presence of peritubular 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) and blunted in the absence of external CO2/HCO[Formula: see text]. The alkalinization elicited by removing peritubular Cl−persisted in the bilateral absence of Na+, together with a voltage clamp. When studied in Cl−-free solutions, lowering peritubular pH induced a base efflux that was inhibited by peritubular DIDS or by the absence of external CO2/HCO[Formula: see text]. Removing peritubular Na+ elicited a cellular acidification that was accounted for by stimulation of a DIDS- and ethylisopropylamiloride (EIPA)-insensitive Na+-HCO[Formula: see text] cotransport and inhibition of a basolateral Na+/H+exchange. Increasing bath K+ induced an intracellular alkalinization that was inhibited in the absence of external CO2/HCO[Formula: see text]. At 2 mM, peritubular Ba2+, which inhibits the K+-Cl−cotransport, did not induce any change in transepithelial voltage but elicited a cellular alkalinization and inhibited K+-induced cellular alkalinization, consistent with the presence of a basolateral, electroneutral Ba2+-sensitive K+-Cl− cotransport that may operate as a K+-HCO[Formula: see text] cotransport. This cotransport was inhibited in the peritubular presence of furosemide, [(dihydroindenyl)oxy]alkanoic acid, 5-nitro-2-(3-phenylpropylamino)benzoate, or DIDS. At least three distinct basolateral HCO[Formula: see text] transport mechanisms are functional under physiological conditions: electroneutral Cl−/HCO[Formula: see text] exchange, DIDS- and EIPA-insensitive Na+-HCO[Formula: see text] cotransport, and Ba2+-sensitive electroneutral K+-Cl−(HCO[Formula: see text]) cotransport.

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Journal articles on the topic 'MtArgH'

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