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Literatura académica sobre el tema "Synthèse HP"

Autor: Grafiati

Publicado: 25 de mayo de 2024

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Artículos de revistas sobre el tema "Synthèse HP"

Pelaprat, N., C. Brondino, G. Rigal y B. Boutevin. "Synthèse d'alkylphosphonates à longues chaines hydrocarbonées, modifications chimiques et applications—II. Addition de HP(O)(OEt)2 sur les alcènes et phosphonation directe d'halogénures d'alkyles". European Polymer Journal 32, n.º 6 (junio de 1996): 761–66. http://dx.doi.org/10.1016/0014-3057(95)00189-1.

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Zhu, Hongming, Aijun Sun, Yunzeng Zou y Junbo Ge. "Inducible Metabolic Adaptation Promotes Mesenchymal Stem Cell Therapy for Ischemia". Arteriosclerosis, Thrombosis, and Vascular Biology 34, n.º 4 (abril de 2014): 870–76. http://dx.doi.org/10.1161/atvbaha.114.303194.

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Objective— Ischemic tissue is an environment with limited oxygen and nutrition availability. The poor retention of mesenchymal stem cells (MSC) in ischemic tissues greatly limits their therapeutic potential. The aim of this study was to determine whether and how inducible metabolic adaptation enhances MSC survival and therapy under ischemia. Approach and Results— MSC were subjected to glycogen synthase 1–specific small interfering RNA or vehicle treatment, and then sublethal hypoxic preconditioning (HP) was applied to induce glycogenesis. The treated cells were subjected to ischemic challenge. The results exhibited that HP of MSC induced glycogen storage and stimulated glycogen catabolism and cellular ATP production, thereby preserving cell viability in long-term ischemia. In vivo study using the mouse limb ischemia model transplanted with HP or control MSC into the ischemic thigh muscles revealed a significant increased retention of MSC with glycogen storage associated with improved limb salvage, perfusion recovery and angiogenesis in the ischemic muscles. In contrast, glycogen synthesis inhibition significantly abolished these improvements. Further molecular analysis indicated that phosphoinositide 3-kinase/AKT, hypoxia-inducible factor-1, and glycogen synthase kinase-3β regulated expression of glycogenesis genes, including glucose transporter 1, hexokinase, phosphoglucomutase 1, glycogen synthase 1, and glycogen phosphorylase, thereby regulating glycogen metabolism of stem cell during HP. Conclusions— HP-induced glycogen storage improves MSC survival and therapy in ischemic tissues. Thus, inducible metabolic adaptation in stem cells may be considered as a novel strategy for potentiating stem cell therapy for ischemia.

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Wang, Li, Yuan Zhou, Jun Peng, Zhe Zhang, De-Jian Jiang y Yuan-Jian Li. "Role of endogenous nitric oxide synthase inhibitor in gastric mucosal injury". Canadian Journal of Physiology and Pharmacology 86, n.º 3 (marzo de 2008): 97–104. http://dx.doi.org/10.1139/y08-003.

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To explore the role of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA) in gastric mucosal injury, 3 models of gastric mucosal injury induced by ethanol, indomethacin, or cold stress were used in rats. The cultured human gastric mucosal epithelial cell line GES-1 infected by Helicobacter pylori (Hp) was selected to mimic human gastric mucosal injury. Gastric mucosal ulcer index (UI), levels of ADMA and NO, and activity of dimethylarginine dimethylaminohydrolase (DDAH) were determined in the mucosal injury models; in Hp-infected or ADMA-treated GES-1 cells, levels of ADMA, NO, and TNF-α and activity of DDAH were measured. The results showed that UI and levels of ADMA were markedly increased and accompanied by significantly decreased DDAH activity in the mucosal injury models. Incubation of GES-1 cells with Hp increased levels of TNF-α and ADMA and decreased activity of DDAH. Administration of ADMA also increased levels of TNF-α. The results suggest that ADMA plays an important role in facilitating gastric mucosal injury, an effect which is associated with inhibiting NO synthesis and inducing inflammatory reaction.

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Hoque, Sanzana, Yuki Kondo, Nodoka Sakata, Yusei Yamada, Madoka Fukaura, Taishi Higashi, Keiichi Motoyama et al. "Differential Effects of 2-Hydroxypropyl-Cyclodextrins on Lipid Accumulation in Npc1-Null Cells". International Journal of Molecular Sciences 21, n.º 3 (30 de enero de 2020): 898. http://dx.doi.org/10.3390/ijms21030898.

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Niemann–Pick disease type C (NPC) is an autosomal recessive disorder characterized by abnormal accumulation of free cholesterol and sphingolipids in lysosomes. The iminosugar miglustat, which inhibits hexosylceramide synthesis, is used for NPC treatment, and 2-hydroxypropyl-β-cyclodextrin (HP-β-CD), a cyclic oligosaccharide derivative, is being developed to treat NPC. Moreover, therapeutic potential of 2-hydroxypropyl-γ-cyclodextrin (HP-γ-CD) was shown in NPC models, although its mechanism of action remains unclear. Here, we investigated the effects of HP-β-CD, HP-γ-CD, and their homolog 2-hydroxypropyl-α-cyclodextrin (HP-α-CD) on lipid accumulation in Npc1-null Chinese hamster ovary (CHO) cells compared with those of miglustat. HP-β-CD and HP-γ-CD, unlike HP-α-CD, reduced intracellular free cholesterol levels and normalized the lysosome changes in Npc1-null cells but not in wild-type CHO cells. In contrast, miglustat did not normalize intracellular free cholesterol accumulation or lysosome changes in Npc1-null cells. However, miglustat decreased the levels of hexosylceramide and tended to increase those of sphingomyelins in line with its action as a glucosylceramide synthase inhibitor in both Npc1-null and wild-type CHO cells. Interestingly, HP-β-CD and HP-γ-CD, unlike HP-α-CD, reduced sphingomyelins in Npc1-null, but not wild-type, cells. In conclusion, HP-β-CD and HP-γ-CD reduce the accumulation of sphingolipids, mainly sphingomyelins, and free cholesterol as well as lysosome changes in Npc1-null, but not in wild-type, CHO cells.

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Doherty, Neil C., Feifei Shen, Nigel M. Halliday, David A. Barrett, Kim R. Hardie, Klaus Winzer y John C. Atherton. "In Helicobacter pylori, LuxS Is a Key Enzyme in Cysteine Provision through a Reverse Transsulfuration Pathway". Journal of Bacteriology 192, n.º 5 (8 de enero de 2010): 1184–92. http://dx.doi.org/10.1128/jb.01372-09.

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ABSTRACT In many bacteria, LuxS functions as a quorum-sensing molecule synthase. However, it also has a second, more central metabolic function in the activated methyl cycle (AMC), which generates the S-adenosylmethionine required by methyltransferases and recycles the product via methionine. Helicobacter pylori lacks an enzyme catalyzing homocysteine-to-methionine conversion, rendering the AMC incomplete and thus making any metabolic role of H. pylori LuxS (LuxSHp) unclear. Interestingly, luxS Hp is located next to genes annotated as cysK Hp and metB Hp, involved in other bacteria in cysteine and methionine metabolism. We showed that isogenic strains carrying mutations in luxS Hp, cysK Hp, and metB Hp could not grow without added cysteine (whereas the wild type could), suggesting roles in cysteine synthesis. Growth of the ΔluxS Hp mutant was restored by homocysteine or cystathionine and growth of the ΔcysK Hp mutant by cystathionine only. The ΔmetB Hp mutant had an absolute requirement for cysteine. Metabolite analyses showed that S-ribosylhomocysteine accumulated in the ΔluxS Hp mutant, homocysteine in the ΔcysK Hp mutant, and cystathionine in the ΔmetB Hp mutant. This suggests that S-ribosylhomocysteine is converted by LuxSHp to homocysteine (as in the classic AMC) and thence by CysKHp to cystathionine and by MetBHp to cysteine. In silico analysis suggested that cysK-metB-luxS were acquired by H. pylori from a Gram-positive source. We conclude that cysK-metB-luxS encode the capacity to generate cysteine from products of the incomplete AMC of H. pylori in a process of reverse transsulfuration. We recommend that the misnamed genes cysK Hp and metB Hp be renamed mccA (methionine-to-cysteine-conversion gene A) and mccB, respectively.

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Shih, Jui-Hu, Yow-Fu Tsai, I.-Hsun Li, Ming-Hua Chen y Yuahn-Sieh Huang. "Hp-s1 Ganglioside Suppresses Proinflammatory Responses by Inhibiting MyD88-Dependent NF-κB and JNK/p38 MAPK Pathways in Lipopolysaccharide-Stimulated Microglial Cells". Marine Drugs 18, n.º 10 (29 de septiembre de 2020): 496. http://dx.doi.org/10.3390/md18100496.

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Hp-s1 ganglioside is isolated from the sperm of sea urchin (Hemicentrotus pulcherrimus). In addition to neuritogenic activity, the biological function of Hp-s1 in neuroinflammation is unknown. In this study, we investigated the anti-neuroinflammatory effect of Hp-s1 on lipopolysaccharide (LPS)-stimulated microglial cells. MG6 microglial cells were stimulated with LPS in the presence or absence of different Hp-s1 concentrations. The anti-inflammatory effect and underlying mechanism of Hp-s1 in LPS-activated microglia cells were assessed through a Cell Counting kit-8 assay, Western blot analysis, and immunofluorescence. We found that Hp-s1 suppressed not only the expression of inducible nitric oxide synthase and cyclooxygenase-2 but also the expression of proinflammatory cytokines, such as TNF-α, IL-1β, and IL-6. Hp-s1 inhibited the LPS-induced NF-κB signaling pathway by attenuating the phosphorylation and translocation of NF-κB p65 and by disrupting the degradation and phosphorylation of inhibitor κB-α (IκBα). Moreover, Hp-s1 inhibited the LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Hp-s1 also reduced the expression of myeloid differentiation factor 88 (MyD88) and TNF receptor-associated factors 6 (TRAF6), which are prerequisites for NF-κB and MAPKs activation. These findings indicated that Hp-s1 alleviated LPS-induced proinflammatory responses in microglial cells by downregulating MyD88-mediated NF-κB and JNK/p38 MAPK signaling pathways, suggesting further evaluation as a new anti-neuroinflammatory drug.

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Liu, Jie, Irene Ginis, Maria Spatz y John M. Hallenbeck. "Hypoxic preconditioning protects cultured neurons against hypoxic stress via TNF-α and ceramide". American Journal of Physiology-Cell Physiology 278, n.º 1 (1 de enero de 2000): C144—C153. http://dx.doi.org/10.1152/ajpcell.2000.278.1.c144.

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Brief “preconditioning” ischemia induces ischemic tolerance (IT) and protects the animal brain from subsequent otherwise lethal ischemia. Identification of the signaling steps most proximal to the development of the IT will allow induction of the resistance to ischemia shortly after the onset of stroke. Animal studies demonstrate a key role of tumor necrosis factor-α (TNF-α) in induction of IT. The sphingolipid ceramide is known as a second messenger in many of the multiple effects of TNF-α. We hypothesized that ceramide could mediate IT. We demonstrate that preconditioning of rat cortical neurons with mild hypoxia protects them from hypoxia and O2-glucose deprivation injury 24 h later (50% protection). TNF-α pretreatment could be substituted for hypoxic preconditioning (HP). HP was attenuated by TNF-α-neutralizing antibody. HP and TNF-α pretreatment cause a two- to threefold increase of intracellular ceramide levels, which coincides with the state of tolerance. Fumonisin B1, an inhibitor of ceramide synthase, attenuated ceramide upregulation and HP. C-2 ceramide added to the cultures right before the hypoxic insult mimicked the effect of HP. Ceramide did not induce apoptosis. These results suggest that HP is mediated via ceramide synthesis triggered by TNF-α.

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Niepolski, Leszek y Kamila Malinowska-Loba. "Association of Circulating Endothelial Nitric Oxide Synthase Levels with Phosphataemia in Patients on Haemodialysis". Biomedicines 12, n.º 3 (19 de marzo de 2024): 687. http://dx.doi.org/10.3390/biomedicines12030687.

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The amount of evidence indicates that hyperphosphataemia (HP) can induce endothelial damage and significantly impair endothelial nitric oxide synthase (eNOS) expression. There are no clinical studies that have assessed HP and its correlation with circulating eNOS concentration in patients with end-stage renal disease (ESRD). Our preliminary study aimed to evaluate the relationship between plasma inorganic phosphorus (P) levels and circulating plasma eNOS concentration in patients on haemodialysis (HD). A total of 50 patients on HD were enrolled to the study. They were divided into groups according to the tertiles of P. The examined HD group was also analysed and compared with controls as a whole group; then, the group was divided into patients with and without dyslipidaemia (D) as well as into those with and without type 2 diabetes mellitus (type 2 DM). A total of 26 age-matched healthy volunteers were included in the study as the control group. The plasma levels of eNOS in HD patients are reduced in comparison to those in healthy subjects. There was no difference in plasma eNOS concentrations between HD patients with type 2 DM and those without DM as well as between those with D and without D. In the entire group of HD patients, there were positive correlations between circulating levels of eNOS and plasma P concentrations. In HD patients with D, higher systolic and diastolic blood pressure were accompanied by decreased plasma eNOS concentrations. In conclusion, HP and high blood pressure appear to decrease the circulating eNOS levels. These findings demonstrate an additional negative impact of HP on eNOS activity.

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Huang, Ho-Shiang, Ming-Chieh Ma y Jun Chen. "Chronic l-arginine administration increases oxidative and nitrosative stress in rat hyperoxaluric kidneys and excessive crystal deposition". American Journal of Physiology-Renal Physiology 295, n.º 2 (agosto de 2008): F388—F396. http://dx.doi.org/10.1152/ajprenal.00405.2007.

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Hyperoxaluric kidneys show an impaired diuretic response to acute infusion of l-arginine. In this study, we examined the chronic effect of l-arginine supplementation on CaOx crystal formation in hyperoxaluric rat kidneys. Eight groups were tested: control (received drinking water), L group (received l-arginine, 0.6%), LN group [received NG-nitro-l-arginine methyl ester (l-NAME, 10 mg/kg)], L + LN group (received l-arginine + l-NAME), HP group [received hydroxyl-l-proline (HP, 5%) mixed with chow to induce hyperoxaluria], L + HP group (received HP + l-arginine), HP + LN group, and L + HP + LN group. The duration was 42 days, and each group had eight animals. Urinary biochemistry and renal CaOx amounts were measured, as well as renal expressions of nitric oxide synthase (NOS) isoforms and NAD(P)H oxidase. The distribution of inducible NOS (iNOS), NAD(P)H oxidase, ED1-positive cells, and nitrotyrosine was examined by immunohistochemical and immunofluorescence studies, whereas superoxide production from the kidneys was examined by fluorescence spectrometric assay. Compared with the HP group, the L + HP group had excessive CaOx crystal accumulation and enhanced endothelial NOS (eNOS), iNOS, and NAD(P)H oxidase protein expression in the kidney. Urinary excretion of nitrotyrosine was markedly increased. Increased superoxide formation in the L + HP kidney was derived from NAD(P)H oxidase and uncoupled eNOS, and increased nitrotyrosine formation might derive from iNOS and ED1-positive cells that gathered around the CaOx crystals. l-NAME cotreatment (L + HP + LN group) reduced renal oxidative nitrosative stress and tubular damage, which were induced by L + HP. The results showed that chronic l-arginine treatment to the hyperoxaluric kidney with massive CaOx crystal deposition may have a toxic effect by enhancing intrarenal oxidative and nitrosative stress.

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Duin, Stam, Uitterdijk, Bartelds, Danser, Reiss, Duncker y Merkus. "Intervening with the Nitric Oxide Pathway to Alleviate Pulmonary Hypertension in Pulmonary Vein Stenosis". Journal of Clinical Medicine 8, n.º 8 (12 de agosto de 2019): 1204. http://dx.doi.org/10.3390/jcm8081204.

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Pulmonary hypertension (PH) as a result of pulmonary vein stenosis (PVS) is extremely difficult to treat. The ideal therapy should not target the high-pressure/low-flow (HP/LF) vasculature that drains into stenotic veins, but only the high-pressure/high-flow (HP/HF) vasculature draining into unaffected pulmonary veins, reducing vascular resistance and pressure without risk of pulmonary oedema. We aimed to assess the activity of the nitric oxide (NO) pathway in PVS during the development of PH, and investigate whether interventions in the NO pathway differentially affect vasodilation in the HP/HF vs. HP/LF territories. Swine underwent pulmonary vein banding (PVB; n = 7) or sham surgery (n = 6) and were chronically instrumented to assess progression of PH. Pulmonary sensitivity to exogenous NO (sodium nitroprusside, SNP) and the contribution of endogenous NO were assessed bi-weekly. The pulmonary vasodilator response to phosphodiesterase-5 (PDE5) inhibition was assessed 12 weeks after PVB or sham surgery. After sacrifice, 12 weeks post-surgery, interventions in the NO pathway on pulmonary small arteries isolated from HP/LF and HP/HF territories were further investigated. There were no differences in the in vivo pulmonary vasodilator response to SNP and the pulmonary vasoconstrictor response to endothelial nitric oxide synthase (eNOS) inhibition up to 8 weeks after PVB as compared to the sham group. However, at 10 and 12 weeks post-PVB, the in vivo pulmonary vasodilation in response to SNP was larger in the PVB group. Similarly, the vasoconstriction to eNOS inhibition was larger in the PVB group, particularly during exercise, while pulmonary vasodilation in response to PDE5 inhibition was larger in the PVB group both at rest and during exercise. In isolated pulmonary small arteries, sensitivity to NO donor SNP was similar in PVB vs. sham groups irrespective of HP/LF and HP/HF, while sensitivity to the PDE5 inhibitor sildenafil was lower in PVB HP/HF and sensitivity to bradykinin was lower in PVB HP/LF. In conclusion, both NO availability and sensitivity were increased in the PVB group. The increased nitric oxide sensitivity was not the result of a decreased PDE5 activity, as PDE5 activity was even increased. Some vasodilators differentially effect HP/HF vs. HP/LF vasculature.

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Capítulos de libros sobre el tema "Synthèse HP"

Prakasam, M., F. Balima, S. Cygan, P. Klimczyk, L. Jaworska y A. Largeteau. "Ultrahigh pressure SPS (HP-SPS) as new syntheses and exploration tool in materials science". En Spark Plasma Sintering, 201–18. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-817744-0.00009-x.

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