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| 1 | T_3-induced liver AMP-activated protein kinase signaling:Redox dependency and upregulation of downstream targets显示文摘AIM:To investigate the redox dependency and promotion of downstream targets in thyroid hormone(T3)-induced AMP-activated protein kinase(AMPK)signaling as cellular energy sensor to limit metabolic stresses in the liver.METHODS:Fed male Sprague-Dawley rats were given a single ip dose of 0.1 mg T3/kg or T3 vehicle(Na OH0.1 N;controls)and studied at 8 or 24 h after treatment.Separate groups of animals received 500 mg N-acetylcysteine(NAC)/kg or saline ip 30 min prior T3.Measurements included plasma and liver 8-isoprostane and serumβ-hydroxybutyrate levels(ELISA),hepaticlevels of m RNAs(q PCR),proteins(Western blot),and phosphorylated AMPK(ELISA).RESULTS:T3 upregulates AMPK signaling,including the upstream kinases Ca2+-calmodulin-dependent protein kinase kinase-βand transforming growth factor-β-activated kinase-1,with T3-induced reactive oxygen species having a causal role due to its suppression by pretreatment with the antioxidant NAC.Accordingly,AMPK targets acetyl-Co A carboxylase and cyclic AMP response element binding protein are phosphorylated,with the concomitant carnitine palmitoyltransferase-1α(CPT-1α)activation and higher expression of peroxisome proliferator-activated receptor-γco-activator-1αand that of the fatty acid oxidation(FAO)-related enzymes CPT-1α,acyl-Co A oxidase 1,and acylCo A thioesterase 2.Under these conditions,T3 induced a significant increase in the serum levels ofβ-hydroxybutyrate,a surrogate marker for hepatic FAO.CONCLUSION:T3 administration activates liver AMPK signaling in a redox-dependent manner,leading to FAO enhancement as evidenced by the consequent ketogenic response,which may constitute a key molecular mechanism regulating energy dynamics to support T3preconditioning against ischemia-reperfusion injury. | Luis A Videla Virginia Fernández Pamela Cornejo Romina Vargas Paula Morales Juan Ceballo Alvaro Fischer Nicolás Escudero Oscar Escobar | 2014 | World Journal of Gastroenterology2014，20，46： | 3 |
| 2 | Neuromuscular electrical stimulation and testosterone did not influence heterotopic ossification size after spinal cor injury: A case series显示文摘Neuromuscular electrical stimulation(NMES) and testosterone replacement therapy(TRT) are effective rehabilitation strategies to attenuate muscle atrophy and evoke hypertrophy in persons with spinal cord injury(SCI). However both interventions might increase heterotopic ossification(HO) size in SCI patients. We present the results of two men with chronic traumatic motor complete SCI who also had pre-existing HO and participated in a study investigating the effects of TRT or TRT plus NMES resistance training(RT) on body composition. The 49-year-old male, Subject A, has unilateral HO in his right thigh. The 31-year-old male, Subject B, has bilateral HO in both thighs. Both participants wore transdermal testosterone patches(4-6 mg/d) daily for 16 wk. Subject A also underwent progressive NMES-RT twice weekly for 16 wk. Magnetic resonance imaging scans were acquired prior to and post intervention. Cross-sectional areas(CSA) of thewhole thigh and knee extensor skeletal muscles, femoral bone, and HO were measured. In Subject A(NMES-RT + TRT), the whole thigh skeletal muscle CSA increased by 10%, the knee extensor CSA increased by 17%, and the HO + femoral bone CSA did not change. In Subject B(TRT), the whole thigh skeletal muscle CSA increased by 13% in the right thigh and 6% in the left thigh. The knee extensor CSA increased by 7% in the right thigh and did not change in the left thigh. The femoral bone and HO CSAs in both thighs did not change. Both the TRT and NMES-RT + TRT protocols evoked muscle hypertrophy without stimulating the growth of preexisting HO. | Pamela D Moore Ashraf S Gorgey Rodney C Wade Refka E Khalil Timothy D Lavis Rehan Khan Robert A Adler | 2016 | World Journal of Clinical Cases2016，4，7： | 3 |
| 3 | Meeting report:a hard look at the state of enamel research显示文摘The Encouraging Novel Amelogenesis Models and Ex vivo cell Lines(ENAMEL) Development workshop was held on 23 June 2017 at the Bethesda headquarters of the National Institute of Dental and Craniofacial Research(NIDCR). Discussion topics included model organisms, stem cells/cell lines, and tissues/3 D cell culture/organoids. Scientists from a number of disciplines,representing institutions from across the United States, gathered to discuss advances in our understanding of enamel, as well as future directions for the field. | ophir d klein olivier duverger wendy shaw rodrigo s lacruz derk joester janet moradian-oldak megan k pugach j timothy wright sarah e millar ashok b kulkarni john d bartlett thomas gh diekwisch pamela den besten james p simmer | 2017 | International Journal of Oral Science2017，9，4： | 3 |
| 4 | Expression of genes that control core fucosylation in hepatocellular carcinoma: Systematic review显示文摘BACKGROUND Changes in N-linked glycosylation have been observed in the circulation of individuals with hepatocellular carcinoma. In particular, an elevation in the level of core fucosylation has been observed. However, the mechanisms through which core fucose is increased are not well understood. We hypothesized that a review of the literature and related bioinformatic review regarding six genes known to be involved in the attachment of core fucosylation, the synthesis of the fucosylation substrate guanosine diphosphate(GDP)-fucose, or the transport of the substrate into the Golgi might offer mechanistic insight into the regulation of core fucose levels.AIM To survey the literature to capture the involvement of genes regulating core Nlinked fucosylation in hepatocellular carcinoma METHODS The PubMed biomedical literature database was searched for the association of hepatocellular carcinoma and each of the core fucose-related genes and their protein products. We also queried The Cancer Genome Atlas Liver hepatocellular carcinoma(LIHC) dataset for genetic, epigenetic and gene expression changes for the set of six genes using the tools at cBioportal.RESULTS A total of 27 citations involving one or more of the core fucosylation-related genes(FPGT, FUK, FUT8, GMDS, SLC35 C1, TSTA3) and hepatocellular carcinoma were identified. The same set of gene symbols was used to query the371 patients with liver cancer in the LIHC dataset to identify the frequency of m RNA over or under expression, as well as non-synonymous mutations, copy number variation and methylation level. Although all six genes trended to moresamples displaying over expression relative to under-expression, it was noted that a number of tumor samples had undergone amplification of the genes of the de novo synthesis pathway, GMDS(27 samples) and TSTA3(78 samples). In contrast, the other four genes had undergone amplification in 2 or fewer samples.CONCLUSION Amplification of genes involved in the de novo pathway for generation of GDPfucose, GMDS and TSTA3, likely contributes to the elevated core fucose observed in hepatocellular carcinoma. | Pamela A Norton Anand S Mehta | 2019 | World Journal of Gastroenterology2019，25，23： | 3 |
| 5 | Stereotactic body radiation therapy for management of spinal metastases in patients without spinal cord compression: a phase 1–2 trial显示文摘 | Xin Shelley Wang Laurence D Rhines Almon S Shiu James N Yang Ugur Selek Ibrahima Gning Ping Liu Pamela K Allen Syed S Azeem Paul D Brown Hadley J Sharp David C Weksberg Charles S Cleeland Eric L Chang | 2012 | Lancet Oncology2012，，4： | 2 |
| 6 | Focus determination for the James Webb Telescope Instruments: a survey of methods 显示文摘 | PAMELA S D MATTEW R B | 2003 | SPIE2003，265，62： | 1 |
| 7 | Azepinone as a conformational constraint in the design of κ opioid receptor agonists显示文摘 | Paul A T Pamela R S William B | 2004 | Bioorg Med Chem Lett2004，14，22： | 1 |
| 8 | Somatostatin stimulates ductal bile absorption and inhibits ductal bile secretion in mice via SSTR2 on cholangiocytes显示文摘 | Gong A Y Pamela S T Melissa A M | 2003 | Am J Cell Physiol2003，25，6： | 1 |
| 9 | Employee creativity in taiwan : an application of role identity theory 显示文摘 | Farmer S M Pamela T Kate K - M | 2003 | The Academy of Management Journal2003，46，5： | 1 |
| 10 | Creative self - efficacy: its potential antecedents and relationship to creative performance显示文摘 | Pamela T Farmer S M | 2002 | The Academy of Management Journal2002，45，6： | 1 |
| 11 | A computerized method of visual acuity testing显示文摘 | Roy W Beck Pamela S Moke Andrew H Turpin Frederick L Ferris John Paul SanGiovanni Chris A Johnson Eileen E Birch Danielle L Chandler Terry A Cox R.Clifford Blair Raymond T Kraker | 2003 | American Journal of Ophthalmology2003，，2： | 1 |
| 12 | Margaret Drabble' s The Radiant Way: Feminist Metafiction 显示文摘 | Bromberg Pamela S | 1990 | A Forum on Fiction1990，，24： | 1 |
| 13 | Long-term rectal administration of high-dose Sus- tained-release morphine tablets 显示文摘 | Declan W Pamela S | 2002 | Supportive Care in Cancer2002，10，8： | 1 |
| 14 | The Role of Phylogenetics in Comparative Genetics显示文摘 | Douglas E S Pamela S S | 2003 | Plant Physiology2003，132，： | 1 |
| 15 | Hyperion, a space-based imaging spectrometer显示文摘 | Jay S Pearlman Pamela S Barry Carol C Segal | 2003 | IEEE2003，41，6： | 1 |
| 16 | Comparison ofPre-and postsurgical concentrations of blood HER-2mRNA and HER-2extracellular domain reflects HER-2status in early breast cancer显示文摘 | Benedetta S Pamela P Vito D | 2005 | Clinical Chemistry2005，，： | 1 |
| 17 | Comparative immunogenicity of a PreS/S hepatitis B vaccine in non-and low responders to conventional vaccine 显示文摘 | Pamela RW Daniel S Blaise G | 2006 | Vaccine2006，24，15： | 1 |
| 18 | Primary Non-Hodgkin Lymphoma of the Small Bowel显示文摘 | Moon-June Cho Pamela K Allen | 1999 | Radiology1999，211，1： | 1 |
| 19 | Moving to Maintain Function in Knee Osteoarthritis:Evidenee From the Osteoarthritis Initiative显示文摘 | Dorothy DD Pamela S Jing S | 2010 | Ar- chives of Physical Medicine and Rehabilitation2010，91，5： | 1 |
| 20 | The role of social support in the stressor-strain relationship: an examination of work-family conflict显示文摘 | Dawn S Carlson Pamela L Perrewé | 1999 | Journal of Management1999，，4： | 1 |
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