Journal articles: 'PNGO'

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Guise, Mira, Alistair Knott, and Lubica Benuskova. "A Bayesian Model of Polychronicity." Neural Computation 26, no. 9 (September 2014): 2052–73. http://dx.doi.org/10.1162/neco_a_00620.

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A significant feature of spiking neural networks with varying connection delays, such as those in the brain, is the existence of strongly connected groups of neurons known as polychronous neural groups (PNGs). Polychronous groups are found in large numbers in these networks and are proposed by Izhikevich ( 2006a ) to provide a neural basis for representation and memory. When exposed to a familiar stimulus, spiking neural networks produce consistencies in the spiking output data that are the hallmarks of PNG activation. Previous methods for studying the PNG activation response to stimuli have been limited by the template-based methods used to identify PNG activation. In this letter, we outline a new method that overcomes these difficulties by establishing for the first time a probabilistic interpretation of PNG activation. We then demonstrate the use of this method by investigating the claim that PNGs might provide the foundation of a representational system.

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Vigneron, O., Y. Duchossoy, and P. Moissonnier. "The use of the cutaneous saphenous nerve as a source of nerve graft material in the dog (the use of the CSN as a graft)." Veterinary and Comparative Orthopaedics and Traumatology 14, no. 02 (2001): 84–89. http://dx.doi.org/10.1055/s-0038-1632680.

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This paper analyses the feasibility of using the cutaneous saphenous nerve (CSN) as a source of peripheral nerve graft (PNG). In 34 fresh dog cadavers, the PNG length (PNGL) was measured, pattern of collateralization was studied, fascicles diameter and number were assessed at multiple levels along the length of the CSN (levels of section A, B, C and D) and surgical approach was described. The PNGL was correlated to femoral length. The pattern of CSN collateralization was consistent for all but 2 of the dogs. The average cross section diameter and fascicle number of the CSN was 2.0 to 0.1 mm (1 to 7 fascicles). CSN provides a large-sized, easily accessible nerve graft that could be used to bridge nerve gaps in the dog.

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TSEUNG, Chi-Wah, Laura G. McMAHON, Jorge VÁZQUEZ, Jan POHL, and Jesse F. GREGORY. "Partial amino acid sequence and mRNA analysis of cytosolic pyridoxine-beta-d-glucoside hydrolase from porcine intestinal mucosa: proposed derivation from the lactase-phlorizin hydrolase gene." Biochemical Journal 380, no. 1 (May 15, 2004): 211–18. http://dx.doi.org/10.1042/bj20031416.

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We have previously identified and purified a novel β-glucosidase, designated PNGH (pyridoxine-5´-β-d-glucoside hydrolase), from the cytosolic fraction of pig intestinal mucosal. PNGH catalyses the hydrolysis of PNG (pyridoxine-5´-β-d-glucoside), a plant derivative of vitamin B6 that exhibits partial nutritional bioavailability in humans and animals. Preliminary amino acid sequence analysis indicated regions of close similarity of PNGH to the precursor form of LPH (lactase–phlorizin hydrolase), the β-glucosidase localized to the brush-border membrane. We report in the present study amino acid sequence data for PNGH and results of Northern blot analyses, upon which we propose a common genomic origin of PNGH and LPH. Internal Edman sequencing of the PNGH band isolated by SDS/PAGE yielded data for 16 peptides, averaging 10.8 amino acids in length. These peptides from PNGH (approx. 140 kDa) were highly similar to sequences existing over most of the length of the >200 kDa precursor of rabbit LPH; however, we found no PNGH sequences that corresponded to approx. 350 amino acids between positions 463 and 812 of the LPH precursor, a region encoded by exon 7 of the LPH precursor gene (amino acids 568–784), and no sequences that corresponded to regions near the N-terminus. MS analysis of tryptic peptides yielded 25 peptides, averaging 15 amino acids, with masses that matched segments of the rabbit LPH precursor. Northern blot analysis of pig and human small intestinal polyadenylated mRNA using a non-specific LPH cDNA probe showed an expected approx. 6 kb transcript of the LPH precursor, but also an approx. 4 kb transcript that was consistent with the size predicted from the PNGH protein mass. Using a probe specific to the region encoded by exon 7, hybridization occurred only with the 6 kb transcript. Based on these observations, we propose that both PNGH and LPH enzymes have the same genomic origin, but differ in transcriptional and, possibly, post-translational processing.

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Blay, W. M., S. Gnanakaran, B. Foley, N. A. Doria-Rose, B. T. Korber, and N. L. Haigwood. "Consistent Patterns of Change during the Divergence of Human Immunodeficiency Virus Type 1 Envelope from That of the Inoculated Virus in Simian/Human Immunodeficiency Virus-Infected Macaques." Journal of Virology 80, no. 2 (January 15, 2006): 999–1014. http://dx.doi.org/10.1128/jvi.80.2.999-1014.2006.

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ABSTRACT We have analyzed changes to proviral Env gp120 sequences and the development of neutralizing antibodies (NAbs) during 1 year of simian/human immunodeficiency virus SHIV-89.6P infection in 11 Macaca nemestrina macaques. Seven macaques had significant env divergence from that of the inoculum, and macaques with greater divergence had higher titers of homologous NAbs. Substitutions in sequons encoding potential N-linked glycosylation sites (PNGs) were among the first to be established, although overall the total number of sequons did not increase significantly. The majority (19 of 23) of PNGs present in the inoculum were conserved in the sequences from all macaques. Statistically significant variations in PNGs occurred in multiple macaques within constrained regions we term “hot spots,” resulting in the selection of sequences more similar to the B consensus. These included additions on V1, the N-terminal side of V4, and the outer region of C2. Complex mutational patterns resulted in convergent PNG shifts in V2 and V5. Charge changes in Env V1V2, resulting in a net acidic charge, and a proline addition in V5 occurred in several macaques. Molecular modeling of the 89.6P sequence showed that the conserved glycans lie on the silent face of Env and that many are proximal to disulfide bonds, while PNG additions and shifts are proximal to the CD4 binding site. Nonsynonymous-to-synonymous substitution ratios suggest that these changes result from selective pressure. This longitudinal and cross-sectional study of mutations in human immunodeficiency virus (HIV) env in the SHIV background provides evidence that there are more constraints on the configuration of the glycan shield than were previously appreciated.

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Sachdeva, Rahul, Kaitlin Farrell, Mary-Katharine McMullen, Jeffery L. Twiss, and John D. Houle. "Dynamic Changes in Local Protein Synthetic Machinery in Regenerating Central Nervous System Axons after Spinal Cord Injury." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/4087254.

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Intra-axonal localization of mRNAs and protein synthesis machinery (PSM) endows neurons with the capacity to generate proteins locally, allowing precise spatiotemporal regulation of the axonal response to extracellular stimuli. A number of studies suggest that this local translation is a promising target to enhance the regenerative capacity of damaged axons. Using a model of central nervous system (CNS) axons regenerating into intraspinal peripheral nerve grafts (PNGs) we established that adult regenerating CNS axons contain several different mRNAs and protein synthetic machinery (PSM) components in vivo. After lower thoracic level spinal cord transection, ascending sensory axons regenerate into intraspinal PNGs but axon growth is stalled when they reach the distal end of the PNG (3 versus 7 weeks after grafting, resp.). By immunofluorescence with optical sectioning of axons by confocal microscopy, the total and phosphorylated forms of PSMs are significantly lower in stalled compared with actively regenerating axons. Reinjury of these stalled axons increased axonal localization of the PSM proteins, indicative of possible priming for a subcellular response to axotomy. These results suggest that axons downregulate protein synthetic capacity as they cease growing, yet they retain the ability to upregulate PSM after a second injury.

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Loewith, Robbie, Maria Meijer, Susan P. Lees-Miller, Karl Riabowol, and Dallan Young. "Three Yeast Proteins Related to the Human Candidate Tumor Suppressor p33ING1 Are Associated with Histone Acetyltransferase Activities." Molecular and Cellular Biology 20, no. 11 (June 1, 2000): 3807–16. http://dx.doi.org/10.1128/mcb.20.11.3807-3816.2000.

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ABSTRACT Three Saccharomyces cerevisiae proteins (Yng1/YOR064c, Yng2/YHR090c, and Pho23) and two Schizosaccharomyces pombeproteins (Png1/CAA15917 and Png2/CAA21250) share significant sequence identity with the human candidate tumor suppressor p33ING1in their C-terminal regions. The homologous regions contain PHD finger domains which have been implicated in chromatin-mediated transcriptional regulation. We show that GFP-Yng2, like human Ing1, is localized in the nucleus. Deletion of YNG2 results in several phenotypes, including an abnormal multibudded morphology, an inability to utilize nonfermentable carbon sources, heat shock sensitivity, slow growth, temperature sensitivity, and sensitivity to caffeine. These phenotypes are suppressed by expression of either human Ing1 or S. pombe Png1, suggesting that the yeast and human proteins are functionally conserved. Yng1- and Pho23-deficient cells also share some of these phenotypes. We demonstrated by yeast two-hybrid and coimmunoprecipitation tests that Yng2 interacts with Tra1, a component of histone acetyltransferase (HAT) complexes. We further demonstrated by coimmunoprecipitation that HA-Yng1, HA-Yng2, HA-Pho23, and HA-Ing1 are associated with HAT activities in yeast. Genetic and biochemical evidence indicate that the Yng2-associated HAT is Esa1, suggesting that Yng2 is a component of the NuA4 HAT complex. These studies suggest that the yeast Ing1-related proteins are involved in chromatin remodeling. They further suggest that these functions may be conserved in mammals and provide a possible mechanism for the human Ing1 candidate tumor suppressor.

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Wan, Hong, Liwei Zhang, Stephane Blanchard, Stephanie Bigou, Delphine Bohl, Chuncheng Wang, and Song Liu. "Combination of hypoglossal-facial nerve surgical reconstruction and neurotrophin-3 gene therapy for facial palsy." Journal of Neurosurgery 119, no. 3 (September 2013): 739–50. http://dx.doi.org/10.3171/2013.1.jns121176.

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Object Facial nerve injury results in facial palsy that has great impact on the psychosocial conditions of affected patients. Reconstruction of the facial nerve to restore facial symmetry and expression is still a significant surgical challenge. In this study, the authors assessed a hypoglossal-facial nerve anastomosis method combined with neurotrophic factor gene therapy to treat facial palsy in adult rats after facial nerve injury. Methods Surgery consisted of the interposition of a predegenerated nerve graft (PNG) that was anastomosed with the hypoglossal and facial nerves at each of its extremities. The hypoglossal nerve was cut approximately 50% for this anastomosis to conserve partial hypoglossal function. Before their transplantation, the PNGs were genetically engineered using lentiviral vectors to induce overexpression of the neurotrophic factor neurotrophin-3 (NT-3) to improve axonal regrowth in the reconstructed nerve pathway. Reconstruction was performed after facial nerve injury, either immediately or after a delay of 9 weeks. The rats were followed up for 4 months postoperatively, and treatment outcomes were then assessed. Results Compared with the functional innervation in control rats that underwent facial nerve injury without subsequent treatment, functional innervation of the paralyzed whisker pad by hypoglossal motoneurons in rats treated 4 months after nerve reconstruction was evidenced by the retrograde transport of neuronal tracers, the recording of muscle action potentials conducted by the PNG, and the recovery of facial symmetry. Although a better outcome was observed when reconstruction was performed immediately after facial nerve injury, reconstruction with NT3-treated PNGs significantly improved functional reinnervation of the paralyzed whisker pad even when implantation occurred 9 weeks posttrauma. Conclusions Results demonstrated that hypoglossal-facial nerve anastomosis facilitates innervation of paralyzed facial muscle via hypoglossal motoneurons without sacrificing ipsilateral hemitongue function. Neurotrophin-3 treatment through gene therapy could effectively improve such innervation, even after delayed reconstruction. These findings suggest that the combination of surgical reconstruction and NT-3 gene therapy is promising for its potential application in treating facial palsy in humans.

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NISHIOKA, Yoshiharu, and Juri NAGATSU. "PNG Elevation Tile." Geoinformatics 26, no. 4 (2015): 155–63. http://dx.doi.org/10.6010/geoinformatics.26.4.155.

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Garg, Meena, Manikkavasagar Thamotharan, Shilpa A. Oak, Gerald Pan, Duncan C. MacLaren, Paul W. N. Lee, and Sherin U. Devaskar. "Early exercise regimen improves insulin sensitivity in the intrauterine growth-restricted adult female rat offspring." American Journal of Physiology-Endocrinology and Metabolism 296, no. 2 (February 2009): E272—E281. http://dx.doi.org/10.1152/ajpendo.90473.2008.

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We examined the effect of early exercise training (Ex) on glucose kinetics, basal, and insulin-stimulated skeletal muscle (SKM) plasma membrane (PM) GLUT4 in pre- and/or postnatal nutrient-restricted adult rat offspring compared with sedentary (Sed) state. Pregestational control female (Ex CON vs. Sed CON) and offspring exposed to prenatal (Ex IUGR vs. Sed IUGR), postnatal (Ex PNGR vs. Sed PNGR), or pre- and postnatal (Ex IUGR + PNGR vs. Sed IUGR + PNGR) nutrient restriction were studied. The combined effect of exercise and pre/postnatal nutrition in the Ex IUGR demonstrated positive effects on basal and glucose-stimulated plasma insulin response (GSIR) with suppression of endogenous hepatic glucose production (HGP) compared with sedentary state. Ex PNGR was hyperglycemic after glucose challenge with no change in glucose-stimulated insulin production or HGP compared with sedentary state. Ex IUGR + PNGR remained glucose tolerant with unchanged glucose-stimulated insulin production but increased endogenous HGP compared with sedentary state. Basal SKM PM-associated GLUT4 was unchanged by exercise in all four groups. Whereas Ex PNGR and Ex IUGR + PNGR insulin responsiveness was similar to that of Ex CON, Ex IUGR remained nonresponsive to insulin. Early introduction of regular Ex in the pregestational female offspring had a positive effect on hepatic adaptation to GSIR and HGP in IUGR and IUGR + PNGR, with no effect in PNGR. Change in insulin responsiveness of SKM GLUT4 translocation was observed in exercised IUGR + PNGR and PNGR but not in exercised IUGR.

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Kaloper, Nemanja, and Lorenzo Sorbo. "Of pNGB quiScript Ntessence." Journal of Cosmology and Astroparticle Physics 2006, no. 04 (April 19, 2006): 007. http://dx.doi.org/10.1088/1475-7516/2006/04/007.

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Sun, Haoqi, Olga Sourina, and Guang-Bin Huang. "Learning Polychronous Neuronal Groups Using Joint Weight-Delay Spike-Timing-Dependent Plasticity." Neural Computation 28, no. 10 (October 2016): 2181–212. http://dx.doi.org/10.1162/neco_a_00879.

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Polychronous neuronal group (PNG), a type of cell assembly, is one of the putative mechanisms for neural information representation. According to the reader-centric definition, some readout neurons can become selective to the information represented by polychronous neuronal groups under ongoing activity. Here, in computational models, we show that the frequently activated polychronous neuronal groups can be learned by readout neurons with joint weight-delay spike-timing-dependent plasticity. The identity of neurons in the group and their expected spike timing at millisecond scale can be recovered from the incoming weights and delays of the readout neurons. The detection performance can be further improved by two layers of readout neurons. In this way, the detection of polychronous neuronal groups becomes an intrinsic part of the network, and the readout neurons become differentiated members in the group to indicate whether subsets of the group have been activated according to their spike timing. The readout spikes representing this information can be used to analyze how PNGs interact with each other or propagate to downstream networks for higher-level processing.

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Chi, Wanhao, Atulya S. R. Iyengar, Monique Albersen, Marjolein Bosma, Nanda M. Verhoeven-Duif, Chun-Fang Wu, and Xiaoxi Zhuang. "Pyridox (am) ine 5'-phosphate oxidase deficiency induces seizures in Drosophila melanogaster." Human Molecular Genetics 28, no. 18 (July 2, 2019): 3126–36. http://dx.doi.org/10.1093/hmg/ddz143.

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AbstractPyridox (am) ine 5'-phosphate oxidase (PNPO) is a rate-limiting enzyme in converting dietary vitamin B6 (VB6) to pyridoxal 5'-phosphate (PLP), the biologically active form of VB6 and involved in the synthesis of neurotransmitters including γ-aminobutyric acid (GABA), dopamine, and serotonin. In humans, PNPO mutations have been increasingly identified in neonatal epileptic encephalopathy and more recently also in early-onset epilepsy. Till now, little is known about the neurobiological mechanisms underlying PNPO-deficiency-induced seizures due to the lack of animal models. Previously, we identified a c.95 C>A missense mutation in sugarlethal (sgll)—the Drosophila homolog of human PNPO (hPNPO)—and found mutant (sgll95) flies exhibiting a lethal phenotype on a diet devoid of VB6. Here, we report the establishment of both sgll95 and ubiquitous sgll knockdown (KD) flies as valid animal models of PNPO-deficiency-induced epilepsy. Both sgll95 and sgll KD flies exhibit spontaneous seizures before they die. Electrophysiological recordings reveal that seizures caused by PNPO deficiency have characteristics similar to that in flies treated with the GABA antagonist picrotoxin. Both seizures and lethality are associated with low PLP levels and can be rescued by ubiquitous expression of wild-type sgll or hPNPO, suggesting the functional conservation of the PNPO enzyme between humans and flies. Results from cell type-specific sgll KD further demonstrate that PNPO in the brain is necessary for seizure prevention and survival. Our establishment of the first animal model of PNPO deficiency will lead to better understanding of VB6 biology, the PNPO gene and its mutations discovered in patients, and can be a cost-effective system to test therapeutic strategies.

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Terai, S., I. Ueda-Hayakawa, C. T. H. Nguyen, N. T. M. Ly, F. Yamazaki, N. Kambe, Y. Son, and H. Okamoto. "Palisaded neutrophilic and granulomatous dermatitis associated with systemic lupus erythematosus: possible involvement of CD163+ M2 macrophages in two cases, and a review of published works." Lupus 27, no. 14 (October 30, 2018): 2220–27. http://dx.doi.org/10.1177/0961203318809892.

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Background Palisaded neutrophilic and granulomatous dermatitis (PNGD) is a commonly occurring condition related to systemic autoimmune disease. It is characterized histopathologically by a distinct pattern of granulomatous inflammation in the presence or absence of leukocytoclastic vasculitis. The properties of granulomatous cells in PNGD are still uncertain. Objective We sought further investigation on the phenotype of the infiltrated cells in PNGD from two patients with systemic lupus erythematosus (SLE) and reviewed the previous published reports in order to provide a comprehensive summary on the clinical features of PNGD in SLE. Methods The immunohistochemical features of granulomatous cells in PNGD associated with SLE were analyzed. Immunohistochemical studies were performed on sections from our two cases using antibodies against CD68, CD163, CD15, Factor XIIIa, myeloperoxidase and neutrophil elastase. The clinical characteristics of the SLE patients who developed PNGD were also evaluated. We included all cases retrieved through a PubMed search with the key words PNGD and SLE. Results Cutaneous lesions consisted of erythematous plaques distributed on the face and upper limbs in both cases. The infiltrated cells were mainly positive for CD68 and CD163, a phenotype suggestive of M2 macrophages. Some mature neutrophils and lymphocytes were also present. A review of the literature of PNGD associated with SLE revealed a predominance in females, high prevalence of lupus nephritis and a good response to systemic steroids, with frequent skin lesions relapses during tapering of the treatment. Limitations This study examined only two cases; the pathogenesis of the disease remains to be clarified. Conclusion PNGD lesions were abundantly infiltrated by M2 macrophages, suggesting that they may have a role in this condition. SLE accompanied by PNGD might be associated with lupus nephritis and frequent relapses of skin lesions.

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Duong, Tien Q. "USABC and PNGV test procedures." Journal of Power Sources 89, no. 2 (August 2000): 244–48. http://dx.doi.org/10.1016/s0378-7753(00)00439-0.

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Akagawa, Mai, Yuki Hattori, Yoko Mizutani, En Shu, Tatsuhiko Miyazaki, and Mariko Seishima. "Palisaded Neutrophilic and Granulomatous Dermatitis in a Patient with Granulomatosis with Polyangiitis." Case Reports in Dermatology 12, no. 1 (March 20, 2020): 52–56. http://dx.doi.org/10.1159/000506670.

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Palisaded neutrophilic and granulomatous dermatitis (PNGD) shows various clinical features and is histologically characterized by palisaded granulomas surrounding degenerated collagen. PNGD is known to be associated with a variety of systemic conditions such as rheumatoid arthritis and systemic lupus erythematosus. Furthermore, PNGD has been reported to be associated with antineutrophilic cytoplasmic antibody-associated vasculitis, including granulomatosis with polyangiitis (GPA) and microscopic polyangiitis. Here, we report a case of PNGD associated with GPA, which showed the infiltration of CD163-positive M2 macrophages in the skin lesion with elevated serum level of soluble CD163 (sCD163). The serum sCD163 level was reduced to normal range after systemic steroid therapy. Thus, M2 macrophages may play a role in the pathomechanisms of PNGD associated with GPA.

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Xie, Zhu, Dong, Nan, Meng, Zhou, Sun, and Sun. "HMGB1-triggered inflammation inhibition of notoginseng leaf triterpenes against cerebral ischemia and reperfusion injury via MAPK and NF-κB signaling pathways." Biomolecules 9, no. 10 (September 20, 2019): 512. http://dx.doi.org/10.3390/biom9100512.

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Ischemic stroke is a clinically common cerebrovascular disease whose main risks include necrosis, apoptosis and cerebral infarction, all caused by cerebral ischemia and reperfusion (I/R) injury. This process has particular significance for the treatment of stroke patients. Notoginseng leaf triterpenes (PNGL), as a valuable medicine, have been discovered to have neuroprotective effects. However, it was not confirmed that whether PNGL may possess neuroprotective effects against cerebral I/R injury. To explore the neuroprotective effects of PNGL and their underlying mechanisms, a middle cerebral artery occlusion/reperfusion (MCAO/R) model was established. In vivo results suggested that in MCAO/R model rats, PNGL pretreatment (73.0, 146, 292 mg/kg) remarkably decreased infarct volume, reduced brain water content, and improved neurological functions; moreover, PNGL (73.0, 146, 292 mg/kg) significantly alleviated blood-brain barrier (BBB) disruption and inhibited neuronal apoptosis and neuronal loss caused by cerebral I/R injury, while PNGL with a different concertation (146, 292 mg/kg) significantly reduced the concentrations of IL-6, TNF-α, IL-1 β, and HMGB1 in serums in a dose-dependent way, which indicated that inflammation inhibition could be involved in the neuroprotective effects of PNGL. The immunofluorescence and western blot analysis showed PNGL decreased HMGB1 expression, suppressed the HMGB1-triggered inflammation, and inhibited microglia activation (IBA1) in hippocampus and cortex, thus dose-dependently downregulating inflammatory cytokines including VCAM-1, MMP-9, MMP-2, and ICAM-1 concentrations in ischemic brains. Interestingly, PNGL administration (146 mg/kg) significantly downregulated the levels of p-P44/42, p-JNK1/2 and p-P38 MAPK, and also inhibited expressions of the total NF-κB and phosphorylated NF-κB in ischemic brains, which was the downstream pathway triggered by HMGB1. All of these results indicated that the protective effects of PNGL against cerebral I/R injury could be associated with inhibiting HMGB1-triggered inflammation, suppressing the activation of MAPKs and NF-κB, and thus improved cerebral I/R-induced neuropathological changes. This study may offer insight into discovering new active compounds for the treatment of ischemic stroke.

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Abbasi, Afshan, Manikkavasagar Thamotharan, Bo-Chul Shin, Maria C. Jordan, Kenneth P. Roos, Andreas Stahl, and Sherin U. Devaskar. "Myocardial macronutrient transporter adaptations in the adult pregestational female intrauterine and postnatal growth-restricted offspring." American Journal of Physiology-Endocrinology and Metabolism 302, no. 11 (June 1, 2012): E1352—E1362. http://dx.doi.org/10.1152/ajpendo.00539.2011.

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Associations between exponential childhood growth superimposed on low birth weight and adult onset cardiovascular disease with glucose intolerance/type 2 diabetes mellitus exist in epidemiological investigations. To determine the metabolic adaptations that guard against myocardial failure on subsequent exposure to hypoxia, we compared with controls (CON), the effect of intrauterine (IUGR), postnatal (PNGR), and intrauterine and postnatal (IPGR) calorie and growth restriction ( n = 6/group) on myocardial macronutrient transporter (fatty acid and glucose) -mediated uptake in pregestational young female adult rat offspring. A higher myocardial FAT/CD36 protein expression in IUGR, PNGR, and IPGR, with higher FATP1 in IUGR, FATP6 in PNGR, FABP-c in PNGR and IPGR, and no change in GLUT4 of all groups was observed. These adaptive macronutrient transporter protein changes were associated with no change in myocardial [3H]bromopalmitate accumulation but a diminution in 2-deoxy-[14C]glucose uptake. Examination of the sarcolemmal subfraction revealed higher basal concentrations of FAT/CD36 in PNGR and FATP1 and GLUT4 in IUGR, PNGR, and IPGR vs. CON. Exogenous insulin uniformly further enhanced sarcolemmal association of these macronutrient transporter proteins above that of basal, with the exception of insulin resistance of FATP1 and GLUT4 in IUGR and FAT/CD36 in PNGR. The basal sarcolemmal macronutrient transporter adaptations proved protective against subsequent chronic hypoxic exposure (7 days) only in IUGR and PNGR, with notable deterioration in IPGR and CON of the echocardiographic ejection fraction. We conclude that the IUGR and PNGR pregestational adult female offspring displayed a resistance to insulin-induced translocation of FATP1, GLUT4, or FAT/CD36 to the myocardial sarcolemma due to preexistent higher basal concentrations. This basal adaptation of myocardial macronutrient transporters ensured adequate fatty acid uptake, thereby proving protective against chronic hypoxia-induced myocardial compromise.

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Garg, Meena, Manikkavasagar Thamotharan, Gerald Pan, Paul W. N. Lee, and Sherin U. Devaskar. "Early exposure of the pregestational intrauterine and postnatal growth-restricted female offspring to a peroxisome proliferator-activated receptor-γ agonist." American Journal of Physiology-Endocrinology and Metabolism 298, no. 3 (March 2010): E489—E498. http://dx.doi.org/10.1152/ajpendo.00361.2009.

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Prenatal nutrient restriction with intrauterine growth restriction (IUGR) alters basal and glucose-stimulated insulin response and hepatic metabolic adaptation. The effect of early intervention with insulin-sensitizing peroxisome proliferator-activated receptor γ agonists was examined in the metabolically maladapted F1 pregestational IUGR offspring with a propensity toward pregnancy-induced gestational diabetes. The effect of rosiglitazone maleate [RG; 11 μmol/day from postnatal day (PN) 21 to PN60] vs. placebo (PL) on metabolic adaptations in 2-mo-old F1 female rats subjected to prenatal (IUGR), postnatal (PNGR), or pre- and postnatal (IUGR + PNGR) nutrient restriction was investigated compared with control (CON). RG vs. PL had no effect on body weight or plasma glucose concentrations but increased subcutaneous white and brown adipose tissue and plasma cholesterol concentrations in all three experimental groups. Glucose tolerance tests with a 1:1 mixture of [2-2H2]- and [6,6-2H2]glucose in RG IUGR vs. PL IUGR revealed glucose tolerance with a lower glucose-stimulated insulin release (GSIR) and suppressed endogenous hepatic glucose production (HGP) with no difference in glucose clearance (GC) and recycling (GR). RG PNGR, although similar to PL CON, was hyperglycemic vs. PL PNGR with reduced GR but no difference in the existent low GSIR, HGP, and GC. RG IUGR + PNGR overall was no different from the PL counterpart. Insulin tolerance tests revealed perturbed recovery to baseline from the exaggerated hypoglycemia in RG vs. the PL groups with the only exception being RG PNGR where further worsening of hypoglycemia over PL PNGR was minimal with full recovery to baseline. These observations support that early intervention with RG suppressed HGP in IUGR vs. PL IUGR, without increasing GSIR similar to that seen in CON. Although RG reversed PNGR to the PL CON metabolic state, no such insulin-sensitizing effect was realized in IUGR + PNGR.

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HALL, PETER DUNBAR. "MODERN PNG MUSIC." Perfect Beat 2, no. 2 (October 7, 2015): 92–95. http://dx.doi.org/10.1558/prbt.v2i2.28791.

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Stevenson, Daniel E. "PNG palette permuter." ACM SIGCSE Bulletin 38, no. 3 (September 26, 2006): 143–47. http://dx.doi.org/10.1145/1140123.1140164.

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Hoekwater, Taco. "MetaPost: PNG Output." Zpravodaj Československého sdružení uživatelů TeXu 27, no. 1-2 (2017): 98–100. http://dx.doi.org/10.5300/2017-1-2/98.

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Lugli, Licia, Maria Carolina Bariola, Luca Ori, Laura Lucaccioni, Alberto Berardi, and Fabrizio Ferrari. "Further Delineation of Pyridoxine-Responsive Pyridoxine Phosphate Oxidase Deficiency Epilepsy: Report of a New Case and Review of the Literature With Genotype-Phenotype Correlation." Journal of Child Neurology 34, no. 14 (August 9, 2019): 937–43. http://dx.doi.org/10.1177/0883073819863992.

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In recent years, the clinical spectrum of pyridoxine phosphate oxidase (PNPO) deficiency has broadened. There are a growing number of patients with a transient or lasting response to pyridoxine in addition to cases that respond more traditionally to pyridoxal-phosphate. However, among pyridoxine-responsive patients with PNPO gene mutation, there are only a few reports on electroencephalogram (EEG) ictal/interictal patterns, and data regarding the outcomes are inconsistent. We describe a case of neonatal onset epilepsy with missense mutation c(674G>A) p(R225 H) in PNPO gene and pyridoxine responsiveness. Comparing this patient with 24 cases of previously described pyridoxine-responsive pyridoxine phosphate oxidase deficiency epilepsy, we found that patients carrying the missense mutation c(674G>A) p(R225 H) of the PNPO gene might have a more severe epileptic phenotype, possibly because of their lower residual PNPO activity. Indeed, pyridoxine-responsive pyridoxine phosphate oxidase deficiency epilepsy remains a challenge, with neurodevelopmental disabilities occurring in about half of the cases.

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Oak, Shilpa, Cang Tran, Maria-Olivia Castillo, Shanthie Thamotharan, Manikkavasagar Thamotharan, and Sherin U. Devaskar. "Peroxisome proliferator-activated receptor-γ agonist improves skeletal muscle insulin signaling in the pregestational intrauterine growth-restricted rat offspring." American Journal of Physiology-Endocrinology and Metabolism 297, no. 2 (August 2009): E514—E524. http://dx.doi.org/10.1152/ajpendo.00008.2009.

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The effect of early intervention with a peroxisome proliferator-activated receptor-γ (PPARγ) agonist on skeletal muscle GLUT4 translocation and insulin signaling was examined in intrauterine (IUGR) and postnatal (PNGR) growth-restricted pregestational female rat offspring. Rosiglitazone [11 μmol/day provided from postnatal day (PN)21 to PN60] improved skeletal muscle insulin sensitivity and GLUT4 translocation in prenatal nutrient restriction [50% calories from embryonic day (e)11 to e21; IUGR] with (IUGR+PNGR) and without (IUGR) postnatal nutrient restriction (50% calories from PN1 to PN21; PNGR) similar to that of control (ad libitum feeds throughout; Con) ( n = 6 each). This was accomplished by diminished basal and improved insulin-responsive GLUT4 association with the plasma membrane in IUGR, IUGR+PNGR, and PNGR mimicking that in Con ( P < 0.005). While no change in p85-phosphatidylinositol 3-kinase (PI3-K) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was observed, a decrease in protein tyrosine phosphatase 1B (PTP1B; P < 0.0002) and SH2-containing protein tyrosine phosphatase 2 (SHP2; P < 0.05) contributing to the rosiglitazone-induced insulin sensitivity was seen only in IUGR+PNGR. In contrast, an increase in phosphorylated 5′-adenosine monophosphate kinase (pAMPK; P < 0.04) and insulin responsiveness of phosphorylated phosphoinositide-dependent protein kinase-1 (pPDK1; P < 0.05), pAkt ( P < 0.01), and particularly pPKCζ ( P < 0.0001) and its corresponding enzyme activity ( P < 0.005) were observed in all four experimental groups. We conclude that early introduction of PPARγ agonist improved skeletal muscle activation of AMPK and insulin signaling, resulting in insulin-independent AMPK and insulin-responsive GLUT4 association with plasma membranes in IUGR, IUGR+PNGR, and PNGR adult offspring, similar to that of Con. These findings support a role for insulin sensitizers in preventing the subsequent development of gestational or type 2 diabetes mellitus in intrauterine and postnatal growth-restricted offspring.

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Chen, Yi Ning, Juan Zhang, and Chong Guo. "Analysis of Lithium Battery Model for Electric Vehicle." Advanced Materials Research 986-987 (July 2014): 1755–58. http://dx.doi.org/10.4028/www.scientific.net/amr.986-987.1755.

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The establishment of an accurate battery model is crucial to the design and research of battery and battery management system. This paper takes 180Ah LiFePO4 as research object, adopts PNGV model to describe the working characteristics of the battery,establishes PNGV simulation model in MATLAB/Simulink, recognizes the model parameters based on the experiment of HPPC pulse, verifies the accuracy of model in different conditions. The results show that PNGV model can show the dynamic characteristic of battery well.

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Millichap, J. Gordon, and John J. Millichap. "Pyridoxine Responsiveness and PNPO Gene Mutations." Pediatric Neurology Briefs 28, no. 6 (June 1, 2014): 42. http://dx.doi.org/10.15844/pedneurbriefs-28-6-2.

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Mckenzie, E. H., W. A. Volkert, and R. A. Holmes. "Biodistribution of [I4C]PnAO in rats." International Journal of Nuclear Medicine and Biology 12, no. 2 (January 1985): 133–34. http://dx.doi.org/10.1016/0047-0740(85)90168-8.

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Cheon, Keunsu, and Jungjai Lee. "N = 2 PNGB quintessence dark energy." Journal of the Korean Physical Society 79, no. 3 (July 9, 2021): 336–42. http://dx.doi.org/10.1007/s40042-021-00235-7.

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Xie, Weijie, Ting Zhu, Ping Zhou, Huibo Xu, Xiangbao Meng, Tao Ding, Fengwei Nan, Guibo Sun, and Xiaobo Sun. "Notoginseng Leaf Triterpenes Ameliorates OGD/R-Induced Neuronal Injury via SIRT1/2/3-Foxo3a-MnSOD/PGC-1α Signaling Pathways Mediated by the NAMPT-NAD Pathway." Oxidative Medicine and Cellular Longevity 2020 (October 23, 2020): 1–15. http://dx.doi.org/10.1155/2020/7308386.

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Background. Cerebral ischemic stroke (CIS) is a common cerebrovascular disease whose main risks include necrosis, apoptosis, and cerebral infarction. But few therapeutic advances and prominent drugs seem to be of value for ischemic stroke in the clinic yet. In the previous study, notoginseng leaf triterpenes (PNGL) from Panax notoginseng stem and leaf have been confirmed to have neuroprotective effects against mitochondrial damages caused by cerebral ischemia in vivo. However, the potential mechanisms of mitochondrial protection have not been fully elaborated yet. Methods. The oxygen and glucose deprivation and reperfusion (OGD/R)-induced SH-SY5Y cells were adopted to explore the neuroprotective effects and the potential mechanisms of PNGL in vitro. Cellular cytotoxicity was measured by MTT, viable mitochondrial staining, and antioxidant marker detection in vitro.Mitochondrial functions were analyzed by ATP content measurement, MMP determination, ROS, NAD, and NADH kit in vitro. And the inhibitor FK866 was adopted to verify the regulation of PNGL on the target NAMPT and its key downstream. Results. In OGD/R models, treatment with PNGL strikingly alleviated ischemia injury, obviously preserved redox balance and excessive oxidative stress, inhibited mitochondrial damage, markedly alleviated energy metabolism dysfunction, improved neuronal mitochondrial functions, obviously reduced neuronal loss and apoptosis in vitro, and thus notedly raised neuronal survival under ischemia and hypoxia. Meanwhile, PNGL markedly increased the expression of nicotinamide phosphoribosyltransferase (NAMPT) in the ischemic regions and OGD/R-induced SH-SY5Y cells and regulated the downstream SIRT1/2-Foxo3a and SIRT1/3-MnSOD/PGC-1α pathways. And FK866 further verified that the protective effects of PNGL might be mediated by the NAMPT in vitro. Conclusions. The mitochondrial protective effects of PNGL are, at least partly, mediated via the NAMPT-NAD+ and its downstream SIRT1/2/3-Foxo3a-MnSOD/PGC-1α signaling pathways. PNGL, as a new drug candidate, has a pivotal role in mitochondrial homeostasis and energy metabolism therapy via NAMPT against OGD-induced SH-SY5Y cell injury.

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Walker, Paul S., Paul M. Bergin, Martin C. Grossel, and Peter N. Horton. "Modeling Novel Radiopharmaceuticals: Mono-C6-Substituted PnAO Ligands (PnAO = 3,3,9,9-Tetramethyl-4,8-diazaundecane-2,10-dione Dioxime)." Inorganic Chemistry 43, no. 14 (July 2004): 4145–53. http://dx.doi.org/10.1021/ic0497634.

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Marbaix, Alexandre Y., Georges Chehade, Gaëtane Noël, Pierre Morsomme, Didier Vertommen, Guido T. Bommer, and Emile Van Schaftingen. "Pyridoxamine-phosphate oxidases and pyridoxamine-phosphate oxidase-related proteins catalyze the oxidation of 6-NAD(P)H to NAD(P)+." Biochemical Journal 476, no. 20 (October 28, 2019): 3033–52. http://dx.doi.org/10.1042/bcj20190602.

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Abstract 6-NADH and 6-NADPH are strong inhibitors of several dehydrogenases that may form spontaneously from NAD(P)H. They are known to be oxidized to NAD(P)+ by mammalian renalase, an FAD-linked enzyme mainly present in heart and kidney, and by related bacterial enzymes. We partially purified an enzyme oxidizing 6-NADPH from rat liver, and, surprisingly, identified it as pyridoxamine-phosphate oxidase (PNPO). This was confirmed by the finding that recombinant mouse PNPO oxidized 6-NADH and 6-NADPH with catalytic efficiencies comparable to those observed with pyridoxine- and pyridoxamine-5′-phosphate. PNPOs from Escherichia coli, Saccharomyces cerevisiae and Arabidopsis thaliana also displayed 6-NAD(P)H oxidase activity, indicating that this ‘side-activity’ is conserved. Remarkably, ‘pyridoxamine-phosphate oxidase-related proteins’ (PNPO-RP) from Nostoc punctiforme, A. thaliana and the yeast S. cerevisiae (Ygr017w) were not detectably active on pyridox(am)ine-5′-P, but oxidized 6-NADH, 6-NADPH and 2-NADH suggesting that this may be their main catalytic function. Their specificity profiles were therefore similar to that of renalase. Inactivation of renalase and of PNPO in mammalian cells and of Ygr017w in yeasts led to the accumulation of a reduced form of 6-NADH, tentatively identified as 4,5,6-NADH3, which can also be produced in vitro by reduction of 6-NADH by glyceraldehyde-3-phosphate dehydrogenase or glucose-6-phosphate dehydrogenase. As 4,5,6-NADH3 is not a substrate for renalase, PNPO or PNPO-RP, its accumulation presumably reflects the block in the oxidation of 6-NADH. These findings indicate that two different classes of enzymes using either FAD (renalase) or FMN (PNPOs and PNPO-RPs) as a cofactor play an as yet unsuspected role in removing damaged forms of NAD(P).

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Dai, Yun, Shanthie Thamotharan, Meena Garg, Bo-Chul Shin, and Sherin U. Devaskar. "Superimposition of Postnatal Calorie Restriction Protects the Aging Male Intrauterine Growth- Restricted Offspring from Metabolic Maladaptations." Endocrinology 153, no. 9 (September 1, 2012): 4216–26. http://dx.doi.org/10.1210/en.2012-1206.

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Intrauterine growth restriction (IUGR) results in dysregulated glucose homeostasis and adiposity in the adult. We hypothesized that with aging, these perturbations will wane, and superimposition of postnatal growth restriction (PNGR) on IUGR [intrauterine and postnatal growth restriction (IPGR)] will reverse the residual IUGR phenotype. We therefore undertook hyperinsulinemic-euglycemic clamp, energy balance, and physical activity studies during fed, fasted, and refed states, in light and dark cycles, on postweaned chow diet-fed more than 17-month aging male IUGR, PNGR, and IPGR vs. control (CON) rat offspring. Hyperinsulinemic-euglycemic clamp revealed similar whole-body insulin sensitivity and physical activity in the nonobese IUGR vs. CON, despite reduced heat production and energy expenditure. Compared with CON and IUGR, IPGR mimicking PNGR was lean and growth restricted with increased physical activity, O2 consumption (VO2), energy intake, and expenditure. Although insulin sensitivity was no different in IPGR and PNGR, skeletal muscle insulin-induced glucose uptake was enhanced. This presentation proved protective against the chronologically earlier (5.5 months) development of obesity and dysregulated energy homeostasis after 19 wk on a postweaned high-fat diet. This protective role of PNGR on the metabolic IUGR phenotype needs future fine tuning aimed at minimizing unintended consequences.

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KRIKKEN, J., and J. HUIJBREGTS. "New Guinea Onthophagus: taxonomy of ten small, unicolored new species (Coleoptera: Scarabaeidae: Scarabaeinae)." Zootaxa 3619, no. 5 (March 4, 2013): 501–25. http://dx.doi.org/10.11646/zootaxa.3619.5.1.

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The taxonomy of small, unicolor brown to black Papuasian species of the genus Onthophagus Latreille, 1802 is discussed. Two multi-species groups are defined in the nominotypical subgenus Onthophagus, one with broad and one with narrow dorsal eye foramina (O. acerus and O. kokodentatus groups, respectively). Twelve species are listed, keyed, and diagnosed. Ten of these are new species from Papua New Guinea (PNG) and West New Guinea (WNG, Indonesia), here described in the Onthophagus acerus group: O. aceroides (WNG), O. baiyericus (PNG), O. bituberoculus (WNG), O. daymanus (PNG), O. kokocellosus (PNG), O. kokopygus (PNG); in the Onthophagus kokodentatus group: O. dissidentatus (PNG), O. kokodentatus (PNG), O. kukali (PNG); and an ungrouped new species: Onthophagus ofianus (PNG). Two previously named species, O. acer Gillet, 1930 and O. mimikanus Balthasar, 1969, are briefly diagnosed and discussed.

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Park, Kwang Seung, Myoung-Ki Hong, Jin Wan Jeon, Ji Hwan Kim, Jeong Ho Jeon, Jung Hun Lee, Tae Yeong Kim, et al. "The novel metallo-β-lactamase PNGM-1 from a deep-sea sediment metagenome: crystallization and X-ray crystallographic analysis." Acta Crystallographica Section F Structural Biology Communications 74, no. 10 (September 19, 2018): 644–49. http://dx.doi.org/10.1107/s2053230x18012268.

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Metallo-β-lactamases (MBLs) are present in major Gram-negative pathogens and environmental species, and pose great health risks because of their ability to hydrolyze the β-lactam rings of antibiotics such as carbapenems. PNGM-1 was the first reported case of a subclass B3 MBL protein that was identified from a metagenomic library from deep-sea sediments that predate the antibiotic era. In this study, PNGM-1 was overexpressed, purified and crystallized. Crystals of native and selenomethionine-substituted PNGM-1 diffracted to 2.10 and 2.30 Å resolution, respectively. Both the native and the selenomethionine-labelled PNGM-1 crystals belonged to the monoclinic space group P21, with unit-cell parameters a = 122, b = 83, c = 163 Å, β = 110°. Matthews coefficient (V M) calculations suggested the presence of 6–10 molecules in the asymmetric unit, corresponding to a solvent content of ∼31–58%. Structure determination is currently in progress.

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Stoneking, M., L. B. Jorde, K. Bhatia, and A. C. Wilson. "Geographic variation in human mitochondrial DNA from Papua New Guinea." Genetics 124, no. 3 (March 1, 1990): 717–33. http://dx.doi.org/10.1093/genetics/124.3.717.

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Abstract High resolution mitochondrial DNA (mtDNA) restriction maps, consisting of an average of 370 sites per mtDNA map, were constructed for 119 people from 25 localities in Papua New Guinea (PNG). Comparison of these PNG restriction maps to published maps from Australian, Caucasian, Asian and African mtDNAs reveals that PNG has the lowest amount of mtDNA variation, and that PNG mtDNA lineages originated from Southeast Asia. The statistical significance of geographic structuring of populations with respect to mtDNA was assessed by comparing observed GST values to a distribution of GST values generated by random resampling of the data. These analyses show that there is significant structuring of mtDNA variation among worldwide populations, between highland and coastal PNG populations, and even between two highland PNG populations located approximately 200 km apart. However, coastal PNG populations are essentially panmictic, despite being spread over several hundred kilometers. Highland PNG populations also have more mtDNA variability and more mtDNA types represented per founding lineage than coastal PNG populations. All of these observations are consistent with a more ancient, restricted origin of highland PNG populations, internal isolation of highland PNG populations from one another and from coastal populations, and more recent and extensive population movements through coastal PNG. An apparent linguistic effect on PNG mtDNA variation disappeared when geography was taken into account. The high resolution technique for examining mtDNA variation, coupled with extensive geographic sampling within a single defined area, leads to an enhanced understanding of the influence of geography on mtDNA variation in human populations.

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Alghamdi, Malak, Stefan T. Arold, Hamdi Hasan, and Fahad Bashiri. "Pyridox(am)ine 5′-Phosphate Oxidase Deficiency: Severe Prenatal Presentation with Hypoxic Ischemic Encephalopathy." Journal of Pediatric Epilepsy 08, no. 02 (June 2019): 049–55. http://dx.doi.org/10.1055/s-0039-1697676.

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AbstractPyridox(am)ine 5′-phosphate oxidase (PNPO) deficiency is a rare autosomal recessive vitamin-responsive epileptic encephalopathy that manifests with a clinically and electrographically observable antiepileptic response to pyridoxine or pyridoxal 5′-phosphate (P5P). We report a preterm infant who presented with fetal distress and hypoxic ischemic encephalopathy (HIE) as well as seizures that responded to pyridoxine in the first day of life. The patient was diagnosed with PNPO deficiency and homozygosity for a missense-mutation in exon 7 of the PNPO gene, c.673 c > T (Arg225Cys), which disrupts the P5P binding site on PNPO. P5P with folinic acid achieved good control of the seizures. Riboflavin was introduced in the second year of life. The patient continued to have episodes of breakthrough seizures with sickness. P5P therapy resulted in marked seizure cessation but did not improve neurocognitive function in this patient, who had significant global psychomotor delay at the age of 3 years despite early treatment. We conclude from this report and other reports that HIE is a co-occurring condition with some inborn errors of metabolism. Therefore, PNPO deficiency should be investigated and P5P trial should be considered in case of presumed HIE particularly with familial recurrence of epileptic encephalopathy and refractory seizure.

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Vatsikopoulous, Helen. "PNG: Under the spell." Pacific Journalism Review : Te Koakoa 2, no. 1 (November 1, 1995): 24–36. http://dx.doi.org/10.24135/pjr.v2i1.533.

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Corruption and law and order problems beset Papua New Guinea in its 20th year of independence. Says former Governor of the Central Bank, Sir Mekere Morauta: 'This nation is under the spell of the statement that we are rich. So our riches will deliver us from the evils, from our own evils. They didn't. Where are we now?' [Transcript of an SBS Dateline programme PNG: Under the Spell, broadcast on 6 May 1995, and rebroadcast on PNG's EM TV on May 15, amid controversy].

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Nion, S. "PNG Transect 1998-2001." Journal of Asian Earth Sciences 15, no. 1 (February 1997): 103. http://dx.doi.org/10.1016/s1367-9120(97)88145-x.

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Nion, S. T. S. "PNG Transect 1998–2001." Journal of Asian Earth Sciences 15, no. 1 (February 1997): 103. http://dx.doi.org/10.1016/s0743-9547(97)87719-7.

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39

Wilbur, Charlton. "PNG: The definitive guide." Journal of Computing in Higher Education 12, no. 2 (March 2001): 94–97. http://dx.doi.org/10.1007/bf02940959.

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Lee, Laura A., Lisa K. Elfring, Giovanni Bosco, and Terry L. Orr-Weaver. "A Genetic Screen for Suppressors and Enhancers of the Drosophila PAN GU Cell Cycle Kinase Identifies Cyclin B as a Target." Genetics 158, no. 4 (August 1, 2001): 1545–56. http://dx.doi.org/10.1093/genetics/158.4.1545.

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Abstract The early cell cycles of Drosophila embryogenesis involve rapid oscillations between S phase and mitosis. These unique S-M cycles are driven by maternal stockpiles of components necessary for DNA replication and mitosis. Three genes, pan gu (png), plutonium (plu), and giant nuclei (gnu) are required to control the cell cycle specifically at the onset of Drosophila development by inhibiting DNA replication and promoting mitosis. PNG is a protein kinase that is in a complex with PLU. We employed a sensitized png mutant phenotype to screen for genes that when reduced in dosage would dominantly suppress or enhance png. We screened deficiencies covering over 50% of the autosomes and identified both enhancers and suppressors. Mutations in eIF-5A and PP1 87B dominantly suppress png. Cyclin B was shown to be a key PNG target. Mutations in cyclin B dominantly enhance png, whereas png is suppressed by cyclin B overexpression. Suppression occurs via restoration of Cyclin B protein levels that are decreased in png mutants. The plu and gnu phenotypes are also suppressed by cyclin B overexpression. These studies demonstrate that a crucial function of PNG in controlling the cell cycle is to permit the accumulation of adequate levels of Cyclin B protein.

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West, Hannah, Michelle Coffey, Michael J. Wagner, Howard L. McLeod, James P. Colley, Richard A. Adams, Oliver Fleck, et al. "Role for Nucleotide Excision Repair Gene Variants in Oxaliplatin-Induced Peripheral Neuropathy." JCO Precision Oncology, no. 2 (November 2018): 1–18. http://dx.doi.org/10.1200/po.18.00090.

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Purpose Oxaliplatin forms part of routine treatment of advanced colorectal cancer; however, it often causes severe peripheral neuropathy, resulting in treatment discontinuation. We sought to determine the molecular and cellular mechanism underlying this toxicity. Patients and Methods We exome resequenced blood DNA samples from nine patients with advanced colorectal cancer who had severe peripheral neuropathy associated with oxaliplatin (PNAO) within 12 weeks of treatment. We Sanger sequenced the ERCC4 and ERCC6 open reading frames in 63 patients with PNAO and carried out targeted genotyping in 1,763 patients without PNAO. We tested the functionality of ERCC4 variants using viability and DNA repair assays in Schizosaccharomyces pombe and human cell lines after exposure to oxaliplatin and ultraviolet light. Results Exome resequencing identified one patient carrying a novel germline truncating mutation in the nucleotide excision repair (NER) gene ERCC4. This mutation was functionally associated with sensitivity to oxaliplatin ( P = 3.5 × 10−2). We subsequently found that multiple rare ERCC4 nonsynonymous variants were over-represented in affected individuals ( P = 7.7 × 10−3) and three of these were defective in the repair of ultraviolet light–induced DNA damage ( P < 1 × 10−3). We validated a role for NER genes in PNAO by finding that multiple rare ERCC6 nonsynonymous variants were similarly over-represented in affected individuals ( P = 2.4 × 10−8). Excluding private variants, 22.2% of patients (14 of 63 patients) with PNAO carried Pro379Ser or Glu875Gly in ERCC4 or Asp425Ala, Gly446Asp, or Ser797Cys in ERCC6, compared with 8.7% of unaffected patients (152 of 1,750 patients; odds ratio, 3.0; 95% CI, 1.6 to 5.6; P = 2.5 × 10−4). Conclusion Our study provides evidence for a role of NER genes in PNAO, together with mechanistic insights.

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Suzuki, Tadashi, Hangil Park, Nancy M. Hollingsworth, Rolf Sternglanz, and William J. Lennarz. "PNG1, a Yeast Gene Encoding a Highly Conserved Peptide:N-Glycanase." Journal of Cell Biology 149, no. 5 (May 29, 2000): 1039–52. http://dx.doi.org/10.1083/jcb.149.5.1039.

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It has been proposed that cytoplasmic peptide:N-glycanase (PNGase) may be involved in the proteasome-dependent quality control machinery used to degrade newly synthesized glycoproteins that do not correctly fold in the ER. However, a lack of information about the structure of the enzyme has limited our ability to obtain insight into its precise biological function. A PNGase-defective mutant (png1-1) was identified by screening a collection of mutagenized strains for the absence of PNGase activity in cell extracts. The PNG1 gene was mapped to the left arm of chromosome XVI by genetic approaches and its open reading frame was identified. PNG1 encodes a soluble protein that, when expressed in Escherichia coli, exhibited PNGase activity. PNG1 may be required for efficient proteasome-mediated degradation of a misfolded glycoprotein. Subcellular localization studies indicate that Png1p is present in the nucleus as well as the cytosol. Sequencing of expressed sequence tag clones revealed that Png1p is highly conserved in a wide variety of eukaryotes including mammals, suggesting that the enzyme has an important function.

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Kim, Ikjin, Jungmi Ahn, Chang Liu, Kaori Tanabe, Jennifer Apodaca, Tadashi Suzuki, and Hai Rao. "The Png1–Rad23 complex regulates glycoprotein turnover." Journal of Cell Biology 172, no. 2 (January 9, 2006): 211–19. http://dx.doi.org/10.1083/jcb.200507149.

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Misfolded proteins in the endoplasmic reticulum (ER) are destroyed by a pathway termed ER-associated protein degradation (ERAD). Glycans are often removed from glycosylated ERAD substrates in the cytosol before substrate degradation, which maintains the efficiency of the proteasome. Png1, a deglycosylating enzyme, has long been suspected, but not proven, to be crucial in this process. We demonstrate that the efficient degradation of glycosylated ricin A chain requires the Png1–Rad23 complex, suggesting that this complex couples protein deglycosylation and degradation. Rad23 is a ubiquitin (Ub) binding protein involved in the transfer of ubiquitylated substrates to the proteasome. How Rad23 achieves its substrate specificity is unknown. We show that Rad23 binds various regulators of proteolysis to facilitate the degradation of distinct substrates. We propose that the substrate specificity of Rad23 and other Ub binding proteins is determined by their interactions with various cofactors involved in specific degradation pathways.

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Artyukhov, V. Ya, and A. I. Galeeva. "Spectroscopic parametrization of the method of PNDO." Soviet Physics Journal 29, no. 11 (November 1986): 949–52. http://dx.doi.org/10.1007/bf00898453.

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Farmania, Rajni, Ankit Gupta, Kumar Ankur, Sanjeev Chetry, and Suvasini Sharma. "Complexities of pyridoxine response in PNPO deficiency." Epilepsy & Behavior Reports 16 (2021): 100443. http://dx.doi.org/10.1016/j.ebr.2021.100443.

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Ngo, Emily O., Garrett R. LePage, John W. Thanassi, Natalie Meisler, and Louise M. Nutter. "Absence of Pyridoxine-5‘-Phosphate Oxidase (PNPO) Activity in Neoplastic Cells: Isolation, Characterization, and Expression of PNPO cDNA†." Biochemistry 37, no. 21 (May 1998): 7741–48. http://dx.doi.org/10.1021/bi972983r.

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47

Choi, Won Il, Youngwoo Nam, Cha Young Lee, Byoung Ki Choi, Yu Jin Shin, Jong-Hwan Lim, Sang-Hyun Koh, and Young-Seuk Park. "Changes in Major Insect Pests of Pine Forests in Korea Over the Last 50 Years." Forests 10, no. 8 (August 15, 2019): 692. http://dx.doi.org/10.3390/f10080692.

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Understanding the occurrence patterns of forest pests is fundamental for effective forest management from both economic and ecological perspectives. Here, we review the history of the occurrence patterns and causes of outbreaks and declines of pests in Korean pine forests over the last 50 years. During this period, the major pests of pine forests in Korea have shifted from pine caterpillar (Dendrolimus spectabilis Butler) to the pine needle gall midge (PNGM, Thecodiplosis japonensis (Uchida and Inouye)) and finally to pine wilt disease (PWD) caused by the pine wood nematode (Bursaphelenchus xylophilus (Steiner and Buhrer) Nickle). Outbreaks of pine caterpillar, a native species in Korea, have been recorded as far back as 900 years, and it was the most relevant forest pest in Korea until the 1970s. The decline of its importance has been attributed to reforestation and higher levels of subsequent natural enemy activity. The PNGM is an invasive species, first discovered in Korea in 1929, that became widely distributed by 1992 and the major forest pest in the 1980s and 1990s. A suite of parasitic wasps attacking the PNGM contributed at least partially to the decline of PNGM densities. Following the decline of the PNGM, damage from PWD has increased since 2003. These shifts in major forest pests might be related to changes in forest composition and interactions among forest pests. Therefore, a new management strategy for controlling forest pests is required to mitigate the decline of pine forests in Korea.

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Williams, Ged, Rose Jaspers, Veronica Wohuinangu, Svatka Micik, and Adrian De Luca. "Critical Care Nursing in Papua New Guinea." Connect: The World of Critical Care Nursing 14, no. 1 (March 1, 2020): 35–44. http://dx.doi.org/10.1891/wfccn-d-20-00011.

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ObjectiveTo explore and understand the current context of critical care nursing in Papua New Guinea (PNG).MethodA three day fact finding mission and consulation process with leaders of critical care and health services in PNG.ResultsAlthough challenged by limited resources and healthcare infrastructure there is a determination among local health care providers to growth and improve the provision of critical care services from the major hospitals of PNG. The PNG Critical Care Nurses Society (PNG CCNS) was officially formed in March 2020, providing hope and optimism for a renewed emphasis on this important speciality in PNG.ConclusionThe authors and the PNG CCNS recommend the establishment of active and supportive partnerships with other critical care leaders of the world to help guide future developments in PNG.

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Hasegawa, Takuya, Kentaro Ando, and Hideharu Sasaki. "Cold Water Flow and Upper-Ocean Currents in the Bismarck Sea from December 2001 to January 2002." Journal of Physical Oceanography 41, no. 4 (April 1, 2011): 827–34. http://dx.doi.org/10.1175/2010jpo4421.1.

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Abstract The authors investigated the upper-ocean currents in the Bismarck Sea and related oceanic thermal changes in the western equatorial South Pacific for December 2001–January 2002; during this period, coastal upwelling occurred along the Papua New Guinea (PNG) coast. Southeastward and northwestward coastal currents toward the central PNG coast appeared along northern and southern PNG, respectively. In addition, westward currents extended toward central PNG in the southern part of the Bismarck Sea. A northeastward outflow toward the equator from the PNG coastal area, which is compensated for by such flows, was also found. Volume budget analysis in the upper ocean showed that, during the analysis period, the northeastward outflow ranged from +1.0 to +2.0 Sv (1 Sv ≡ 106 m3 s−1). This northeastward outflow brought relatively cool coastal water, which is related to PNG coastal upwelling, to the western equatorial South Pacific near PNG during this period. In addition, the upper-ocean temperature in this region showed a cooling tendency in line with a negative heat transport from the PNG coastal region. The present results indicate that northeastward transport of the cold water is related to the complicated upper-ocean currents in the Bismarck Sea and may have strongly affected the upper-ocean thermal change in the western equatorial Pacific near PNG for December 2001–January 2002.

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MEI, JUN, QIZHEN GUO, YAN WU, and YUNFEI LI. "Evaluation of Chitosan-Starch–Based Edible Coating To Improve the Shelf Life of Bod Ljong Cheese." Journal of Food Protection 78, no. 7 (July 1, 2015): 1327–34. http://dx.doi.org/10.4315/0362-028x.jfp-14-402.

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The objective of this work was to evaluate the effectiveness of antimicrobial edible coatings to improve the quality of Bod ljong cheese throughout 25 days of storage. Coatings were prepared using chitosan, water chestnut starch, and glycerol as a base matrix, together with several combinations of antimicrobial substances: Cornus officinalis fruit extract (COFE), pine needle essential oil (PNEO), and nisin. Application of coating on cheese decreased water loss, lipid oxidation, changes in headspace gas composition, and color. Moreover, the edible coatings with COFE or PNEO had increased antimicrobial activity and did not permit growth of microorganisms. COFE and PNEO are manufactured from food-grade materials so they can be consumed as an integral part of the cheese, which represents a competitive advantage over nonedible coatings.

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Journal articles on the topic 'PNGO'

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