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[PMID]: 29524401
[Au] Autor:Shao S; Yao Z; Lu J; Song Y; He Z; Yu C; Zhou X; Zhao L; Zhao J; Gao L
[Ad] Address:Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, PR China; Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, PR China; Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, PR China.
[Ti] Title:Ablation of prolactin receptor increases hepatic triglyceride accumulation.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Increasing prevalence of non-alcoholic fatty liver disease (NAFLD) worldwide has necessitated a more thorough understanding of it and expanded the scope of research in this field. Women are more resistant to NAFLD than men despite equal exposure to major risk factors, such as obesity or hyperlipidemia. Female resistance is hormone-dependent, as evidenced by the sharp increase in NAFLD incidence in post-menopausal women who do not take hormone replacement therapy. Here, we found that the estrogen-responsive pituitary hormone prolactin (PRL), through specific PRL receptor (PRLR), down-regulates hepatic triglyceride (TG) accumulation. PRL was demonstrated to significantly down-regulate hepatic TG accumulation in female mice and protect male mice from liver steatosis induced by high-fat diet. Interestingly, Ad-shPRLR injected mice, whose hepatic PRLR abundance was effectively decreased at the protein levels, exhibited significantly aggravated liver steatosis. PRL could decrease the expression of stearoyl-coenzyme A desaturase 1 (SCD1), the rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids, in animal models and multiple hepatic cell lines. Following knockdown of PRLR, the changes to PRL-triggered SCD1 expression disappeared. Thus, PRL acted as a previously unrecognized master regulator of liver TG metabolism, indicating that modification of PRL via PRLR might serve as a potential therapeutic target for NAFLD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 186066 MEDLINE  
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[PMID]: 29515749
[Au] Autor:Mirambo MM; Senyaeli N; Mshana SE
[Ad] Address:Department of Microbiology and Immunology, Weill Bugando School of Medicine, P.O. Box 1464, Mwanza, Tanzania.
[Ti] Title:Low humoral responses to human cytomegalovirus is associated with immunological treatment failure among HIV infected patients on highly active antiretroviral therapy.
[So] Source:Pan Afr Med J;28:131, 2017.
[Is] ISSN:1937-8688
[Cp] Country of publication:Uganda
[La] Language:eng
[Ab] Abstract:Human cytomegalovirus (HCMV) is one of the opportunistic infections associated with significant morbidity and mortality among HIV/AIDS patients especially before introduction of antiretroviral therapy (ART). Little is known regarding the humoral immune response against HCMV in relation to CD4 counts among HIV infected individuals. A total of 90 achieved sera from HIV infected patients attending Bugando Medical centre care and treatment centre (CTC) aged 18 years and above were retrieved and analyzed. Sociodemographic data were collected using structured data collection tool. Detection of specific HCMV antibodies was done using Indirect Enzyme Linked Immunosorbent Assay (ELISA). Data were analyzed by using STATA version 11. A total of 90 HIV infected patients were enrolled in the study whereby 36(40%) had immunological treatment failure. The mean age of the study participants was 39±12.3 years. The Prevalence of specific HCMV IgG antibodies was 84(93.3%, 95% CI: 88-98.5) while the prevalence of specific HCMV IgM antibodies was 2(2.3% 95% CI: 0.8-5.4). The median CD4 counts at 6 months and 12 months on HAART were significantly high in treatment success group. At 12 months of HAART as CD4 counts increases the HCMV IgG index value was also found to increase significantly, p=0.04. Significant proportion of HIV infected individuals was infected with HCMV. Higher median HCMV IgG titers were observed among patients with immunological treatment success. There is a need to investigate humoral immune responses in HIV infected individuals in relation to CD4 counts against various infectious diseases in developing countries where most of these infections are endemic.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.11604/pamj.2017.28.131.10480

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[PMID]: 29515119
[Au] Autor:Ricciardiello F; Votta G; Palorini R; Raccagni I; Brunelli L; Paiotta A; Tinelli F; D'Orazio G; Valtorta S; De Gioia L; Pastorelli R; Moresco RM; La Ferla B; Chiaradonna F
[Ad] Address:Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, 20126, Italy.
[Ti] Title:Inhibition of the Hexosamine Biosynthetic Pathway by targeting PGM3 causes breast cancer growth arrest and apoptosis.
[So] Source:Cell Death Dis;9(3):377, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cancer aberrant N- and O-linked protein glycosylation, frequently resulting from an augmented flux through the Hexosamine Biosynthetic Pathway (HBP), play different roles in tumor progression. However, the low specificity and toxicity of the existing HBP inhibitors prevented their use for cancer treatment. Here we report the preclinical evaluation of FR054, a novel inhibitor of the HBP enzyme PGM3, with a remarkable anti-breast cancer effect. In fact, FR054 induces in different breast cancer cells a dramatic decrease in cell proliferation and survival. In particular, in a model of Triple Negative Breast Cancer (TNBC) cells, MDA-MB-231, we show that these effects are correlated to FR054-dependent reduction of both N- and O-glycosylation level that cause also a strong reduction of cancer cell adhesion and migration. Moreover we show that impaired survival of cancer cells upon FR054 treatment is associated with the activation of the Unfolded Protein Response (UPR) and accumulation of intracellular ROS. Finally, we show that FR054 suppresses cancer growth in MDA-MB-231 xenograft mice, supporting the advantage of targeting HBP for therapeutic purpose and encouraging further investigation about the use of this small molecule as a promising compound for breast cancer therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0405-4

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[PMID]: 29514461
[Au] Autor:Moore IMK; Koerner KM; Gundy PM; Montgomery DW; Insel KC; Harris LL; Taylor OA; Hockenberry MJ
[Ad] Address:1 College of Nursing, The University of Arizona, Tucson, AZ, USA.
[Ti] Title:Changes in Oxidant Defense, Apoptosis, and Cognitive Abilities During Treatment for Childhood Leukemia.
[So] Source:Biol Res Nurs;:1099800418763124, 2018 Jan 01.
[Is] ISSN:1552-4175
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aggressive central nervous system (CNS)-directed treatment for acute lymphoblastic leukemia (ALL), the most prevalent cancer among children and adolescents, prevents metastasis of leukemia cells into the brain. Up to 60% of survivors experience cognitive problems, but knowledge about risk factors for and mechanisms of neurologic injury is lacking. Objectives of the present study were to (1) quantify changes in oxidant defense and apoptosis over the course of ALL therapy and (2) elucidate risk factors for long-term cognitive problems. The sample included 71 children with ALL. Cerebrospinal fluid (CSF) samples were collected at diagnosis and during intrathecal chemotherapy administration. Oxidant defense was measured by reduced glutathione (GSH), oxidized glutathione (GSSG), and the ratio of GSH:GSSG. Apoptosis was measured by activity of several cysteine-dependent aspartate-specific protease (abbreviated as caspase) enzymes that initiate (caspases 8 and 9) or execute (caspases 3/7) apoptosis. Cognitive abilities were assessed by standardized measures of short-term memory, visual-motor integration, and attention 3 years after ALL diagnosis. GSH and GSSG concentration increased significantly during ALL therapy, and a low GSH:GSSG ratio was indicative of an oxidized extracellular environment. Caspase enzyme activity increased significantly, and caspases 3/7 activity was significantly and negatively associated with performance on measures of cognitive abilities. Younger age at time of ALL diagnosis was associated with some measures of attention. Efflux of glutathione into CSF maintains oxidant defense by scavenging free radicals and other reactive oxygen species and is an early event in apoptosis. These mechanisms may be involved in neurologic injury associated with CNS-directed treatment and subsequent cognitive problems.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1177/1099800418763124

  5 / 186066 MEDLINE  
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[PMID]: 29470952
[Au] Autor:Bai M; Feng J; Liang G
[Ad] Address:Clinical Laboratory Department of Aerospace Central Hospital, Yuquan Road 15, Haidian District, Beijing 100049, China.
[Ti] Title:Urinary myeloperoxidase to creatinine ratio as a new marker for monitoring treatment effects of urinary tract infection.
[So] Source:Clin Chim Acta;481:9-11, 2018 Feb 19.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:OBJECTIVE: We want to determine whether urinary myeloperoxidase to creatinine ratio could be served as a new marker for monitoring treatment effects of urinary tract infection or not. METHODS: A total of 328 patients suspected of UTI were enrolled in present study. Patients been received antibiotic therapy within two weeks were excluded (n = 26). Patients with urine contaminated specimens (n = 49) and negative urine culture results (n = 96) were also excluded, the remaining culture positive subjects (n = 157) were followed up for 7 to 14 days, finally, a total of 49 subjects were followed up and further divided into cure (n = 35) and none-cure (n = 14) subgroups according to urine culture results. MPO concentration was determined by immunoturbidimetric method and creatinine level was measured by creatinine enzyme method. Two sided P values < 0.05 were considered statistically significant. RESULTS: Urinary MCR level between before and after antibiotic treatment of cure group were (1437.1 ±â€¯1777.9 vs.48.3 ±â€¯59.3, t = 4.608, P = 0.001), respectively. Urinary MCR level between before and after antibiotic treatment of none-cure group were (1633.1 ±â€¯2168.7 vs. 999.4 ±â€¯1708.0, t = 1.809, P = 0.094), respectively. CONCLUSIONS: Urinary MCR could be served as a promising marker for monitoring treatment effects of urinary tract infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 186066 MEDLINE  
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[PMID]: 29460030
[Au] Autor:Vogel KR; Ainslie GR; Walters DC; McConnell A; Dhamne SC; Rotenberg A; Roullet JB; Gibson KM
[Ad] Address:Department of Neuroscience, University of Wisconsin, Madison, WI, USA.
[Ti] Title:Succinic semialdehyde dehydrogenase deficiency, a disorder of GABA metabolism: an update on pharmacological and enzyme-replacement therapeutic strategies.
[So] Source:J Inherit Metab Dis;, 2018 Feb 19.
[Is] ISSN:1573-2665
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:We present an update to the status of research on succinic semialdehyde dehydrogenase (SSADH) deficiency (SSADHD), a rare disorder of GABA metabolism. This is an unusual disorder featuring the accumulation of both GABA and its neuromodulatory analog, gamma-hydroxybutyric acid (GHB), and recent studies have advanced the potential clinical application of NCS-382, a putative GHB receptor antagonist. Animal studies have provided proof-of-concept that enzyme replacement therapy could represent a long-term therapeutic option. The characterization of neuronal stem cells (NSCs) derived from aldehyde dehydrogenase 5a1 (aldh5a1 ) mice, the murine model of SSADHD, has highlighted NSC utility as an in vitro system in which to study therapeutics and associated toxicological properties. Gene expression analyses have revealed that transcripts encoding GABA receptors are down-regulated and may remain largely immature in aldh5a1 brain, characterized by excitatory as opposed to inhibitory outputs, the latter being the expected action in the mature central nervous system. This indicates that agents altering chloride channel activity may be therapeutically relevant in SSADHD. The most recent therapeutic prospects include mTOR (mechanistic target of rapamycin) inhibitors, drugs that have received attention with the elucidation of the effects of elevated GABA on autophagy. The outlook for novel therapeutic trials in SSADHD continues to improve.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1007/s10545-018-0153-8

  7 / 186066 MEDLINE  
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[PMID]: 29454978
[Au] Autor:Mohanty PS; Bansal AK; Naaz F; Gupta UD; Dwivedi VD; Yadava U
[Ad] Address:Department of Epidemiology, National JALMA Institute for Leprosy and Other Mycobacterial Diseases, M. Miyazaki Marg, Tajganj, Agra, India. Electronic address: m.sarathipartha@gmail.com.
[Ti] Title:Ribonucleotide reductase as a drug target against drug resistance Mycobacterium leprae: A molecular docking study.
[So] Source:Infect Genet Evol;60:58-65, 2018 Feb 15.
[Is] ISSN:1567-7257
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Leprosy is a chronic infection of skin and nerve caused by Mycobacterium leprae. The treatment is based on standard multi drug therapy consisting of dapsone, rifampicin and clofazamine. The use of rifampicin alone or with dapsone led to the emergence of rifampicin-resistant Mycobacterium leprae strains. The emergence of drug-resistant leprosy put a hurdle in the leprosy eradication programme. The present study aimed to predict the molecular model of ribonucleotide reductase (RNR), the enzyme responsible for biosynthesis of nucleotides, to screen new drugs for treatment of drug-resistant leprosy. The study was conducted by retrieving RNR of M. leprae from GenBank. A molecular 3D model of M. leprae was predicted using homology modelling and validated. A total of 325 characters were included in the analysis. The predicted 3D model of RNR showed that the Ï• and φ angles of 251 (96.9%) residues were positioned in the most favoured regions. It was also conferred that 18 α-helices, 6 ß turns, 2 γ turns and 48 helix-helix interactions contributed to the predicted 3D structure. Virtual screening of Food and Drug Administration approved drug molecules recovered 1829 drugs of which three molecules, viz., lincomycin, novobiocin and telithromycin, were taken for the docking study. It was observed that the selected drug molecules had a strong affinity towards the modelled protein RNR. This was evident from the binding energy of the drug molecules towards the modelled protein RNR (-6.10, -6.25 and -7.10). Three FDA-approved drugs, viz., lincomycin, novobiocin and telithromycin, could be taken for further clinical studies to find their efficacy against drug resistant leprosy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29454073
[Au] Autor:Geffroy G; Benyahia R; Frey S; Desquiret-Dumas V; Gueguen N; Bris C; Belal S; Inisan A; Renaud A; Chevrollier A; Henrion D; Bonneau D; Letournel F; Lenaers G; Reynier P; Procaccio V
[Ad] Address:UMR CNRS 6015-INSERM U1083, MitoVasc Institute, Angers University, Angers, France.
[Ti] Title:The accumulation of assembly intermediates of the mitochondrial complex I matrix arm is reduced by limiting glucose uptake in a neuronal-like model of MELAS syndrome.
[So] Source:Biochim Biophys Acta;1864(5 Pt A):1596-1608, 2018 Feb 14.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Ketogenic diet (KD) which combined carbohydrate restriction and the addition of ketone bodies has emerged as an alternative metabolic intervention used as an anticonvulsant therapy or to treat different types of neurological or mitochondrial disorders including MELAS syndrome. MELAS syndrome is a severe mitochondrial disease mainly due to the m.3243A > G mitochondrial DNA mutation. The broad success of KD is due to multiple beneficial mechanisms with distinct effects of very low carbohydrates and ketones. To evaluate the metabolic part of carbohydrate restriction, transmitochondrial neuronal-like cybrid cells carrying the m.3243A > G mutation, shown to be associated with a severe complex I deficiency was exposed during 3 weeks to glucose restriction. Mitochondrial enzyme defects were combined with an accumulation of complex I (CI) matrix intermediates in the untreated mutant cells, leading to a drastic reduction in CI driven respiration. The severe reduction of CI was also paralleled in post-mortem brain tissue of a MELAS patient carrying high mutant load. Importantly, lowering significantly glucose concentration in cell culture improved CI assembly with a significant reduction of matrix assembly intermediates and respiration capacities were restored in a sequential manner. In addition, OXPHOS protein expression and mitochondrial DNA copy number were significantly increased in mutant cells exposed to glucose restriction. The accumulation of CI matrix intermediates appeared as a hallmark of MELAS pathophysiology highlighting a critical pathophysiological mechanism involving CI disassembly, which can be alleviated by lowering glucose fuelling and the induction of mitochondrial biogenesis, emphasizing the usefulness of metabolic interventions in MELAS syndrome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 186066 MEDLINE  
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Clinical Trials Registry
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[PMID]: 28741050
[Au] Autor:Schulman G; Berl T; Beck GJ; Remuzzi G; Ritz E; Shimizu M; Kikuchi M; Shobu Y
[Ad] Address:Vanderbilt University School of Medicine, Nashville, TN, USA.
[Ti] Title:Risk factors for progression of chronic kidney disease in the EPPIC trials and the effect of AST-120.
[So] Source:Clin Exp Nephrol;22(2):299-308, 2018 Apr.
[Is] ISSN:1437-7799
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:BACKGROUND: Two randomized, double-blind, placebo-controlled trials (EPPIC-1 and EPPIC-2) investigated the efficacy and safety of AST-120, an oral spherical carbon adsorbent, in adults with chronic kidney disease (CKD). While the benefit of adding AST-120 to standard therapy was not supported by these trials, we performed a post hoc analysis to focus on CKD progression and to determine the risk factors for the primary endpoint in the EPPIC trial population. METHODS: In the EPPIC trials, patients were randomly assigned 1:1 to treatment with AST-120 or placebo. The primary endpoint was a composite of dialysis initiation, kidney transplantation, or doubling of serum creatinine. The EPPIC trial pooled population was evaluated with the same statistical methods used for analysis of the primary and secondary efficacy endpoints. The trials were registered on ClinicalTrials.gov (NCT00500682 [EPPIC-1] and NCT00501046 [EPPIC-2]). RESULTS: An analysis of the placebo population suggested baseline urinary protein to urinary creatinine ratio (UP/UCr) ≥1.0 and hematuria were independent risk factors for event occurrence and eGFR lowering. Analysis of the high risk patients revealed a difference in the primary endpoint occurrence between treatment groups, if angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers were administered (hazard ratio 0.74, 95% confidence interval 0.56-0.96). Also, the eGFR changes from baseline in the AST-120 group were smaller than that in the placebo group (P = 0.035). CONCLUSIONS: CKD progression may have an association with baseline UP/UCr and hematuria. Treatment with AST-120 may delay the time to the primary endpoint in patients with progressive CKD receiving standard therapy, thus warranting further investigation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1707
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Process
[do] DOI:10.1007/s10157-017-1447-0

  10 / 186066 MEDLINE  
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[PMID]: 29524288
[Au] Autor:Ibrahim H; El Taieb M; El Gamel Z; El Saied AR
[Ad] Address:Department of Dermatology, Venereology and Andrology, Qena Faculty of Medicine, South Valley University, Qena, Egypt.
[Ti] Title:Effect of narrow-band ultraviolet B on the serum of 25-hydroxyvitamin D in vitiligo patients.
[So] Source:J Cosmet Dermatol;, 2018 Mar 10.
[Is] ISSN:1473-2165
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Narrow-band ultraviolet B (NB-UVB) is the gold standard in the treatment of vitiligo. 25-hydroxyvitamin D (25-OH- vitamin D) might play a physiological role in photo-induced melanogenesis in human skin so the association between vitamin D levels and vitiligo still needs to be investigated more thoroughly. OBJECTIVE: we aim to investigate the influence of cumulative doses of NB-UVB phototherapy on vitamin D in patients with vitiligo and their correlation with NB-UVB-induced pigmentation. METHODS: Eighty patients of vitiligo and twenty number of age and sex matched controls were recruited in a case-control study. Patients with vitiligo were treated with NB-UVB twice weekly for 24 weeks. 25-hydroxy vitamin D levels were measured at 0, 12, and 24 weeks in the cases and at 0 only in control by enzyme-linked immunosorbent assay (ELISA) and Vitiligo Area Severity Index (VASI) were calculated at 0 (baseline) and 24 weeks. RESULTS: The mean baseline level of 25-hydroxyvitamin D (at 0 week) was significantly lower in patients than the control group. Levels of 25(OH) vitamin D at 12 and 24 weeks showed significant improvement and Patients show significant reduction in VASI score after 24 weeks of therapy. CONCLUSIONS: Cumulative doses of NB-UVB therapy improve low vitamin D levels in patients with vitiligo, which might have a significant role in NB-UVB-induced repigmentation and may contribute to its therapeutic efficacy but further studies with larger sample size are needed to prove the complete mechanisms of NB-UVB-induced pigmentations and vitamin D in vitiligo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/jocd.12515


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