Lee CH

References (39)

Title : Human Poisoning with Chlorpyrifos and Cypermethrin Pesticide Mixture: Assessment of Clinical Outcome of Cases Admitted in a Tertiary Care Hospital in Taiwan - Wu_2023_Int.J.Gen.Med_16_4795
Author(s) : Wu YJ , Chang SS , Chen HY , Tsai KF , Lee WC , Wang IK , Lee CH , Chen CY , Liu SH , Weng CH , Huang WH , Hsu CW , Yen TH
Ref : Int J Gen Med , 16 :4795 , 2023
Abstract : BACKGROUND AND PURPOSE: There is an overall paucity of data regarding the human toxicity of chlorpyrifos and cypermethrin pesticide mixture. Both organophosphate and pyrethroid insecticides are metabolized by carboxylesterases. Thus, its pesticide combination, organophosphates may boost the toxicity of pyrethroids via inhibited its detoxification by carboxylesterases. This study examined the clinical course, laboratory tests, and outcomes of patients with chlorpyrifos, cypermethrin or their pesticide mixture poisoning, and to determine what association, if any, might exist between these findings. PATIENTS AND METHODS: Between 2000 and 2021, 121 patients poisoned with chlorpyrifos, cypermethrin, or their pesticide mixture were treated at Chang Gung Memorial Hospital. Patients were categorized as chlorpyrifos (n=82), cypermethrin (n=27) or chlorpyrifos and cypermethrin (n=12) groups. Demographic, clinical, laboratory and mortality data were collected for analysis. RESULTS: The patients experienced a broad range of clinical symptoms, including aspiration pneumonia (44.6%), salivation (42.5%), acute respiratory failure (41.3%), acute kidney injury (13.9%), seizures (7.5%), hypotension (2.6%), etc. Leukocytosis (12,700+/-6600 /uL) and elevated serum C-reactive protein level (36.8+/-50.4 mg/L) were common. The acute respiratory failure rate was 41.3%, comprising 48.8% in chlorpyrifos, 11.1% in cypermethrin as well as 58.3% in chlorpyrifos and cypermethrin poisoning. Patients with chlorpyrifos and cypermethrin pesticide mixture poisoning suffered higher rates of acute respiratory failure (P=0.001) and salivation (P=0.001), but lower Glasgow Coma Scale score (P=0.011) and serum cholinesterase level (P<0.001) than other groups. A total of 17 (14.0%) patients expired. The mortality rate was 14.0%, including 17.1% in chlorpyrifos, 3.7% in cypermethrin as well as 16.7% in chlorpyrifos and cypermethrin poisoning. No significant differences in mortality rate were noted (P=0.214). CONCLUSION: Chlorpyrifos pesticide accounted for the major toxicity of the pesticide mixture. While the data show a higher rate of respiratory failure in the chlorpyrifos and cypermethrin pesticide mixture group than others, other measures of toxicity such as mortality and length of stay were not increased.
ESTHER : Wu_2023_Int.J.Gen.Med_16_4795
PubMedSearch : Wu_2023_Int.J.Gen.Med_16_4795
PubMedID: 37908758

Title : Synthesis and Biological Evaluation of O(6)-Aminoalkyl-Hispidol Analogs as Multifunctional Monoamine Oxidase-B Inhibitors towards Management of Neurodegenerative Diseases - Hassan_2023_Antioxidants.(Basel)_12_
Author(s) : Hassan AHE , Kim HJ , Park K , Choi Y , Moon S , Lee CH , Kim YJ , Cho SB , Gee MS , Lee D , Park JH , Lee JK , Ryu JH , Park KD , Lee YS
Ref : Antioxidants (Basel) , 12 : , 2023
Abstract : Oxidative catabolism of monoamine neurotransmitters by monoamine oxidases (MAOs) produces reactive oxygen species (ROS), which contributes to neuronal cells' death and also lowers monoamine neurotransmitter levels. In addition, acetylcholinesterase activity and neuroinflammation are involved in neurodegenerative diseases. Herein, we aim to achieve a multifunctional agent that inhibits the oxidative catabolism of monoamine neurotransmitters and, hence, the detrimental production of ROS while enhancing neurotransmitter levels. Such a multifunctional agent might also inhibit acetylcholinesterase and neuroinflammation. To meet this end goal, a series of aminoalkyl derivatives of analogs of the natural product hispidol were designed, synthesized, and evaluated against both monoamine oxidase-A (MAO-A) and monoamine oxidase-B (MAO-B). Promising MAO inhibitors were further checked for the inhibition of acetylcholinesterase and neuroinflammation. Among them, compounds 3aa and 3bc were identified as potential multifunctional molecules eliciting submicromolar selective MAO-B inhibition, low-micromolar AChE inhibition, and the inhibition of microglial PGE(2) production. An evaluation of their effects on memory and cognitive impairments using a passive avoidance test confirmed the in vivo activity of compound 3bc, which showed comparable activity to donepezil. In silico molecular docking provided insights into the MAO and acetylcholinesterase inhibitory activities of compounds 3aa and 3bc. These findings suggest compound 3bc as a potential lead for the further development of agents against neurodegenerative diseases.
ESTHER : Hassan_2023_Antioxidants.(Basel)_12_
PubMedSearch : Hassan_2023_Antioxidants.(Basel)_12_
PubMedID: 37237899

Title : Neuroprotective Effects of Davallia mariesii Roots and Its Active Constituents on Scopolamine-Induced Memory Impairment in In Vivo and In Vitro Studies - Lee_2023_Pharmaceuticals.(Basel)_16_
Author(s) : Lee CH , Ko MS , Kim YS , Ham JE , Choi JY , Hwang KW , Park SY
Ref : Pharmaceuticals (Basel) , 16 : , 2023
Abstract : Beta-amyloid (Abeta) proteins, major contributors to Alzheimer's disease (AD), are overproduced and accumulate as oligomers and fibrils. These protein accumulations lead to significant changes in neuronal structure and function, ultimately resulting in the neuronal cell death observed in AD. Consequently, substances that can inhibit Abeta production and/or accumulation are of great interest for AD prevention and treatment. In the course of an ongoing search for natural products, the roots of Davallia mariesii T. Moore ex Baker were selected as a promising candidate with anti-amyloidogenic effects. The ethanol extract of D. mariesii roots, along with its active constituents, not only markedly reduced Abeta production by decreasing beta-secretase expression in APP-CHO cells (Chinese hamster ovary cells which stably express amyloid precursor proteins), but also exhibited the ability to diminish Abeta aggregation while enhancing the disaggregation of Abeta aggregates, as determined through the Thioflavin T (Th T) assay. Furthermore, in an in vivo study, the extract of D. mariesii roots showed potential (a tendency) for mitigating scopolamine-induced memory impairment, as evidenced by results from the Morris water maze test and the passive avoidance test, which correlated with reduced Abeta deposition. Additionally, the levels of acetylcholine were significantly elevated, and acetylcholinesterase levels significantly decreased in the brains of mice (whole brains). The treatment with the extract of D. mariesii roots also led to upregulated brain-derived neurotrophic factor (BDNF) and phospho-cAMP response element-binding protein (p-CREB) in the hippocampal region. These findings suggest that the extract of D. mariesii roots, along with its active constituents, may offer neuroprotective effects against AD. Consequently, there is potential for the development of the extract of D. mariesii roots and its active constituents as effective therapeutic or preventative agents for AD.
ESTHER : Lee_2023_Pharmaceuticals.(Basel)_16_
PubMedSearch : Lee_2023_Pharmaceuticals.(Basel)_16_
PubMedID: 38004471

Title : Cholinesterase inhibitors associated with lower rate of mortality in dementia patients with heart failure: a nationwide propensity weighting study - Hsieh_2023_Clin.Auton.Res__
Author(s) : Hsieh MJ , Lee CH , Chen DY , Wu CL , Huang YT , Chang SH
Ref : Clin Auton Res , : , 2023
Abstract : PURPOSE: This study investigates the potential impact of cholinesterase inhibitors (ChEIs) on patients with heart failure (HF) and dementia. ChEIs are known to boost acetylcholine levels and benefit cognition in patients with dementia; however, their effect on patients with HF is uncertain. This study aimed to assess whether cardiovascular events and mortality among patients with HF and dementia are altered by ChEI therapy. METHODS: Data from the National Health Insurance Research Database in Taiwan were retrospectively analyzed. Dementia patients diagnosed with HF were followed for 5 years until all-cause mortality, cardiovascular mortality, hospitalization for worsening HF, or the end of the study. Multivariable Cox models and inverse probability of treatment weighting (IPTW) were employed. RESULTS: Out of 20,848 patients with dementia, 5138 had HF. Among them, 726 were ChEI users and 4412 were non-users. Based on IPTW, the ChEI users had significantly lower estimated risks of all-cause mortality [hazard ratio (HR) 0.43; 95% confidence interval (CI) 0.38-0.49, p < 0.001] and cardiovascular mortality (HR 0.41; 95% CI 0.33-0.53, p < 0.001) compared with the non-users, but there was no significant difference in hospitalization for worsening HF (HR 0.73; 95% CI 0.51-1.05, p = 0.091) after 5 years. The survival benefits of ChEIs were consistent across subgroups. CONCLUSIONS: The results of this retrospective cohort study suggest that ChEIs may be beneficial in reducing all-cause and cardiovascular mortality in patients with dementia with HF. Further research is needed to validate these findings and explore the potential benefits of ChEIs in all patients with HF, including those without dementia.
ESTHER : Hsieh_2023_Clin.Auton.Res__
PubMedSearch : Hsieh_2023_Clin.Auton.Res__
PubMedID: 37935929

Title : Glycogen Storage Disease Phenotypes Accompanying the Perturbation of the Methionine Cycle in NDRG3-Deficient Mouse Livers - Sohn_2022_Cells_11_
Author(s) : Sohn HA , Lee DC , Park A , Kang M , Yoon BH , Lee CH , Kim YH , Oh KJ , Kim CY , Park SH , Koo H , Kim HC , Yoon WK , Lim DS , Kim D , Park KC , Yeom YI
Ref : Cells , 11 : , 2022
Abstract : N-Myc downstream regulated gene 3 (NDRG3) is a unique pro-tumorigenic member among NDRG family genes, mediating growth signals. Here, we investigated the pathophysiological roles of NDRG3 in relation to cell metabolism by disrupting its functions in liver. Mice with liver-specific KO of NDRG3 (Ndrg3 LKO) exhibited glycogen storage disease (GSD) phenotypes including excessive hepatic glycogen accumulation, hypoglycemia, elevated liver triglyceride content, and several signs of liver injury. They suffered from impaired hepatic glucose homeostasis, due to the suppression of fasting-associated glycogenolysis and gluconeogenesis. Consistently, the expression of glycogen phosphorylase (PYGL) and glucose-6-phosphate transporter (G6PT) was significantly down-regulated in an Ndrg3 LKO-dependent manner. Transcriptomic and metabolomic analyses revealed that NDRG3 depletion significantly perturbed the methionine cycle, redirecting its flux towards branch pathways to upregulate several metabolites known to have hepatoprotective functions. Mechanistically, Ndrg3 LKO-dependent downregulation of glycine N-methyltransferase in the methionine cycle and the resultant elevation of the S-adenosylmethionine level appears to play a critical role in the restructuring of the methionine metabolism, eventually leading to the manifestation of GSD phenotypes in Ndrg3 LKO mice. Our results indicate that NDRG3 is required for the homeostasis of liver cell metabolism upstream of the glucose-glycogen flux and methionine cycle and suggest therapeutic values for regulating NDRG3 in disorders with malfunctions in these pathways.
ESTHER : Sohn_2022_Cells_11_
PubMedSearch : Sohn_2022_Cells_11_
PubMedID: 35563842
Gene_locus related to this paper: human-NDRG3 , mouse-ndr3

Title : Activation and closed-state inactivation mechanisms of the human voltage-gated K(V)4 channel complexes - Ye_2022_Mol.Cell_S1097-2765_00395
Author(s) : Ye W , Zhao H , Dai Y , Wang Y , Lo YH , Jan LY , Lee CH
Ref : Mol Cell , : , 2022
Abstract : The voltage-gated ion channel activity depends on both activation (transition from the resting state to the open state) and inactivation. Inactivation is a self-restraint mechanism to limit ion conduction and is as crucial to membrane excitability as activation. Inactivation can occur when the channel is open or closed. Although open-state inactivation is well understood, the molecular basis of closed-state inactivation has remained elusive. We report cryo-EM structures of human K(V)4.2 channel complexes in inactivated, open, and closed states. Closed-state inactivation of K(V)4 involves an unprecedented symmetry breakdown for pore closure by only two of the four S4-S5 linkers, distinct from known mechanisms of open-state inactivation. We further capture K(V)4 in a putative resting state, revealing how voltage sensor movements control the pore. Moreover, our structures provide insights regarding channel modulation by KChIP2 and DPP6 auxiliary subunits. Our findings elucidate mechanisms of closed-state inactivation and voltage-dependent activation of the K(V)4 channel.
ESTHER : Ye_2022_Mol.Cell_S1097-2765_00395
PubMedSearch : Ye_2022_Mol.Cell_S1097-2765_00395
PubMedID: 35597238
Gene_locus related to this paper: human-DPP6

Title : Association Between Cholinesterase Inhibitors and New-Onset Heart Failure in Patients With Alzheimer's Disease: A Nationwide Propensity Score Matching Study - Hsieh_2022_Front.Cardiovasc.Med_9_831730
Author(s) : Hsieh MJ , Chen DY , Lee CH , Wu CL , Chen YJ , Huang YT , Chang SH
Ref : Front Cardiovasc Med , 9 :831730 , 2022
Abstract : BACKGROUND: Autonomic nervous dysfunction is a shared clinical feature in Alzheimer's disease (AD) and heart failure (HF). Cholinesterase inhibitors (ChEIs) are widely used autonomic modulators in patients with AD, but their primary preventive benefit on new-onset HF is still uncertain. OBJECTIVE: This study examined whether ChEIs have a primary preventive effect on new-onset HF in patients with AD. METHODS: This propensity score matching (PSM) study was conducted using data from the National Health Insurance Research Database of Taiwan for 1995 to 2017. Certificated patients with AD and without a history of HF were divided into ChEI (donepezil, rivastigmine, or galantamine) users or nonusers. The primary endpoint was new-onset HF, and the secondary endpoints were myocardial infarction and cardiovascular death after 10-year follow-up. RESULTS: After screening 16,042 patients, 7,411 patients were enrolled, of whom 668 were ChEI users and 1,336 were nonusers after 1:2 PSM. Compared with nonusers, ChEI users exhibited a significantly lower incidence of new-onset HF (HR 0.48; 95% CI 0.34-0.68, p < 0.001) and cardiovascular death (HR 0.55; 95% CI 0.37-0.82, p = 0.003) but not of myocardial infarction (HR 1.09; 95% CI 0.52-1.62, p = 0.821) after 10-year follow-up. The preventive benefit of ChEI use compared with Non-use (controls) was consistent across all exploratory subgroups without statistically significant treatment-by-subgroup interactions. CONCLUSIONS: Prescription of ChEIs may provide a preventive benefit associated with lower incidence of new-onset HF in patients with AD after 10-year follow-up.
ESTHER : Hsieh_2022_Front.Cardiovasc.Med_9_831730
PubMedSearch : Hsieh_2022_Front.Cardiovasc.Med_9_831730
PubMedID: 35369359

Title : A Review on Properties and Application of Bio-Based Poly(Butylene Succinate) - Rafiqah_2021_Polymers.(Basel)_13_
Author(s) : Rafiqah SA , Khalina A , Harmaen AS , Tawakkal IA , Zaman K , Asim M , Nurrazi MN , Lee CH
Ref : Polymers (Basel) , 13 : , 2021
Abstract : Researchers and companies have increasingly been drawn to biodegradable polymers and composites because of their environmental resilience, eco-friendliness, and suitability for a range of applications. For various uses, biodegradable fabrics use biodegradable polymers or natural fibers as reinforcement. Many approaches have been taken to achieve better compatibility for tailored and improved material properties. In this article, PBS (polybutylene succinate) was chosen as the main topic due to its excellent properties and intensive interest among industrial and researchers. PBS is an environmentally safe biopolymer that has some special properties, such as good clarity and processability, a shiny look, and flexibility, but it also has some drawbacks, such as brittleness. PBS-based natural fiber composites are completely biodegradable and have strong physical properties. Several research studies on PBS-based composites have been published, including physical, mechanical, and thermal assessments of the properties and its ability to replace petroleum-based materials, but no systematic analysis of up-to-date research evidence is currently available in the literature. The aim of this analysis is to highlight recent developments in PBS research and production, as well as its natural fiber composites. The current research efforts focus on the synthesis, copolymers and biodegradability for its properties, trends, challenges and prospects in the field of PBS and its composites also reviewed in this paper.
ESTHER : Rafiqah_2021_Polymers.(Basel)_13_
PubMedSearch : Rafiqah_2021_Polymers.(Basel)_13_
PubMedID: 33946989

Title : Identification of a Second Type of AHL-lactonase from Rhodococcus sp. BH4, belonging to the alpha\/beta Hydrolase Superfamily - Ryu_2020_J.Microbiol.Biotechnol__
Author(s) : Ryu DH , Lee SW , Mikolaityte V , Kim YW , Jeong HY , Lee SJ , Lee CH , Lee JK
Ref : J Microbiol Biotechnol , : , 2020
Abstract : N-acyl-homoserine lactone (AHL)-mediated quorum sensing (QS) plays a major role in development of biofilms, which contribute to rise in infections and biofouling in water-related industries. Interference in QS, called quorum quenching (QQ), has recieved a lot of attention in recent years. Rhodococcus spp. are known to have prominent quorum quenching activity and in previous reports it was suggested that this genus possesses multiple QQ enzymes, but only one gene, qsdA, which encodes an AHL-lactonase belonging to phosphotriesterase family, has been identified. Therefore, we conducted a whole genome sequencing and analysis of Rhodococcus sp. BH4 isolated from a wastewater treatment plant. The sequencing revealed another gene encoding a QQ enzyme (named jydB) that exhibited a high AHL degrading activity. This QQ enzyme had a 46% amino acid sequence similarity with the AHL-lactonase (AidH) of Ochrobactrum sp. T63. HPLC analysis and AHL restoration experiments by acidification revealed that the jydB gene encodes an AHL-lactonase which shares the known characteristics of the alpha/beta hydrolase family. Purified recombinant JydB demonstrated a high hydrolytic activity against various AHLs. Kinetic analysis of JydB revealed a high catalytic efficiency (kcat/KM) against C4-HSL and 3-oxo-C6 HSL, ranging from 1.88 x 10(6) to 1.45 x 10(6) M(-1) s(-1), with distinctly low KM values (0.16 - 0.24 mM). This study affirms that the AHL degrading activity and biofilm inhibition ability of Rhodococcus sp. BH4 may be due to the presence of multiple quorum quenching enzymes, including two types of AHL-lactonases, in addition to AHL-acylase and oxidoreductase, for which the genes have yet to be described.
ESTHER : Ryu_2020_J.Microbiol.Biotechnol__
PubMedSearch : Ryu_2020_J.Microbiol.Biotechnol__
PubMedID: 32160697

Title : Reducing inflammation and rescuing FTD-related behavioral deficits in progranulin-deficient mice with alpha7 nicotinic acetylcholine receptor agonists - Minami_2015_Biochem.Pharmacol_97(4)_454
Author(s) : Minami SS , Shen V , Le D , Krabbe G , Asgarov R , Perez-Celajes L , Lee CH , Li J , Donnelly-Roberts D , Gan L
Ref : Biochemical Pharmacology , 97 :454 , 2015
Abstract : Mutations in the progranulin gene cause frontotemporal dementia (FTD), a debilitating neurodegenerative disease that involves atrophy of the frontal and temporal lobes and affects personality, behavior, and language. Progranulin-deficient mouse models of FTD exhibit deficits in compulsive and social behaviors reminiscent of patients with FTD, and develop excessive microgliosis and increased release of inflammatory cytokines. Activation of nicotinic acetylcholine receptors (nAChRs) by nicotine or specific alpha7 nAChR agonists reduces neuroinflammation. Here, we investigated whether activation of nAChRs by nicotine or alpha7 agonists improved the excessive inflammatory and behavioral phenotypes of a progranulin-deficient FTD mouse model. We found that treatment with selective alpha7 agonists, PHA-568487 or ABT-107, strongly suppressed the activation of NF-kappaB in progranulin-deficient cells. Treatment with ABT-107 also reduced microgliosis, decreased TNFalpha levels, and reduced compulsive behavior in progranulin-deficient mice. Collectively, these data suggest that targeting activation of the alpha7 nAChR pathway may be beneficial in decreasing neuroinflammation and reversing some of the behavioral deficits observed in progranulin-deficient FTD.
ESTHER : Minami_2015_Biochem.Pharmacol_97(4)_454
PubMedSearch : Minami_2015_Biochem.Pharmacol_97(4)_454
PubMedID: 26206194

Title : Effects of mood-stabilizing drugs on dendritic outgrowth and synaptic protein levels in primary hippocampal neurons - Park_2015_Bipolar.Disord_17_278
Author(s) : Park SW , Lee JG , Seo MK , Cho HY , Lee CH , Lee JH , Lee BJ , Baek JH , Seol W , Kim YH
Ref : Bipolar Disord , 17 :278 , 2015
Abstract : OBJECTIVES: Mood-stabilizing drugs, such as lithium (Li) and valproate (VPA), are widely used for the treatment of bipolar disorder, a disease marked by recurrent episodes of mania and depression. Growing evidence suggests that Li exerts neurotrophic and neuroprotective effects, leading to an increase in neural plasticity. The present study investigated whether other mood-stabilizing drugs produce similar effects in primary hippocampal neurons.
METHODS: The effects of the mood-stabilizing drugs Li, VPA, carbamazepine (CBZ), and lamotrigine (LTG) on hippocampal dendritic outgrowth were examined. Western blotting analysis was used to measure the expression of synaptic proteins - that is, brain-derived neurotrophic factor (BDNF), postsynaptic density protein-95 (PSD-95), neuroligin 1 (NLG1), beta-neurexin, and synaptophysin (SYP). To determine neuroprotective effects, we used a B27-deprivation cytotoxicity model which causes hippocampal cell death upon removal of B27 from the culture medium.
RESULTS: Li (0.5-2.0 mM), VPA (0.5-2.0 mM), CBZ (0.01-0.10 mM), and LTG (0.01-0.10 mM) significantly increased dendritic outgrowth. The neurotrophic effect of Li and VPA was blocked by inhibition of phosphatidylinositol 3-kinase, extracellular signal-regulated kinase, and protein kinase A signaling; the effects of CBZ and LTG were not affected by inhibition of these signaling pathways. Li, VPA, and CBZ prevented B27 deprivation-induced decreases in BDNF, PSD-95, NLG1, beta-neurexin, and SYP levels, whereas LTG did not.
CONCLUSIONS: These results suggest that Li, VPA, CBZ, and LTG exert neurotrophic effects by promoting dendritic outgrowth; however, the mechanism of action differs. Furthermore, certain mood-stabilizing drugs may exert neuroprotective effects by enhancing synaptic protein levels against cytotoxicity in hippocampal cultures.
ESTHER : Park_2015_Bipolar.Disord_17_278
PubMedSearch : Park_2015_Bipolar.Disord_17_278
PubMedID: 25307211

Title : Genomic makeup of the marine flavobacterium Nonlabens (Donghaeana) dokdonensis and identification of a novel class of rhodopsins - Kwon_2013_Genome.Biol.Evol_5_187
Author(s) : Kwon SK , Kim BK , Song JY , Kwak MJ , Lee CH , Yoon JH , Oh TK , Kim JF
Ref : Genome Biol Evol , 5 :187 , 2013
Abstract : Rhodopsin-containing marine microbes such as those in the class Flavobacteriia play a pivotal role in the biogeochemical cycle of the euphotic zone (Fuhrman JA, Schwalbach MS, Stingl U. 2008. Proteorhodopsins: an array of physiological roles? Nat Rev Microbiol. 6:488-494). Deciphering the genome information of flavobacteria and accessing the diversity and ecological impact of microbial rhodopsins are important in understanding and preserving the global ecosystems. The genome sequence of the orange-pigmented marine flavobacterium Nonlabens dokdonensis (basonym: Donghaeana dokdonensis) DSW-6 was determined. As a marine photoheterotroph, DSW-6 has written in its genome physiological features that allow survival in the oligotrophic environments. The sequence analysis also uncovered a gene encoding an unexpected type of microbial rhodopsin containing a unique motif in addition to a proteorhodopsin gene and a number of photolyase or cryptochrome genes. Homologs of the novel rhodopsin gene were found in other flavobacteria, alphaproteobacteria, a species of Cytophagia, a deinococcus, and even a eukaryote diatom. They all contain the characteristic NQ motif and form a phylogenetically distinct group. Expression analysis of this rhodopsin gene in DSW-6 indicated that it is induced at high NaCl concentrations, as well as in the presence of light and the absence of nutrients. Genomic and metagenomic surveys demonstrate the diversity of the NQ rhodopsins in nature and the prevalent occurrence of the encoding genes among microbial communities inhabiting hypersaline niches, suggesting its involvement in sodium metabolism and the sodium-adapted lifestyle.
ESTHER : Kwon_2013_Genome.Biol.Evol_5_187
PubMedSearch : Kwon_2013_Genome.Biol.Evol_5_187
PubMedID: 23292138

Title : Genome sequence of the leaf-colonizing Bacterium Bacillus sp. strain 5B6, isolated from a cherry tree - Kim_2012_J.Bacteriol_194_3758
Author(s) : Kim BK , Chung JH , Kim SY , Jeong H , Kang SG , Kwon SK , Lee CH , Song JY , Yu DS , Ryu CM , Kim JF
Ref : Journal of Bacteriology , 194 :3758 , 2012
Abstract : Plant growth-promoting bacteria colonize various habitats, including the phyllosphere. Here, we present the high-quality draft genome sequence of Bacillus sp. strain 5B6, which was isolated from the leaf of a cherry tree. The 3.9-Mb genome uncovers its potential for understanding the nature of leaf colonization as well as antibiosis against plant pathogens.
ESTHER : Kim_2012_J.Bacteriol_194_3758
PubMedSearch : Kim_2012_J.Bacteriol_194_3758
PubMedID: 22740678
Gene_locus related to this paper: baca2-a7z924 , bacsu-YVAK

Title : Genome sequence of the plant growth-promoting rhizobacterium Bacillus sp. strain JS - Song_2012_J.Bacteriol_194_3760
Author(s) : Song JY , Kim HA , Kim JS , Kim SY , Jeong H , Kang SG , Kim BK , Kwon SK , Lee CH , Yu DS , Kim BS , Kim SH , Kwon SY , Kim JF
Ref : Journal of Bacteriology , 194 :3760 , 2012
Abstract : Volatile and nonvolatile compounds emitted from the plant growth-promoting rhizobacterium Bacillus sp. strain JS enhance the growth of tobacco and lettuce. Here, we report the high-quality genome sequence of this bacterium. Its 4.1-Mb genome reveals a number of genes whose products are possibly involved in promotion of plant growth or antibiosis.
ESTHER : Song_2012_J.Bacteriol_194_3760
PubMedSearch : Song_2012_J.Bacteriol_194_3760
PubMedID: 22740679
Gene_locus related to this paper: bacsu-pnbae , bacsu-YVAK

Title : Complete genome sequence of the endophytic bacterium Burkholderia sp. strain KJ006 - Kwak_2012_J.Bacteriol_194_4432
Author(s) : Kwak MJ , Song JY , Kim SY , Jeong H , Kang SG , Kim BK , Kwon SK , Lee CH , Yu DS , Park SH , Kim JF
Ref : Journal of Bacteriology , 194 :4432 , 2012
Abstract : Endophytes live inside plant tissues without causing any harm and may even benefit plants. Here, we provide the high-quality genome sequence of Burkholderia sp. strain KJ006, an endophytic bacterium of rice with antifungal activity. The 6.6-Mb genome, consisting of three chromosomes and a single plasmid, contains genes related to plant growth promotion or degradation of aromatic compounds.
ESTHER : Kwak_2012_J.Bacteriol_194_4432
PubMedSearch : Kwak_2012_J.Bacteriol_194_4432
PubMedID: 22843575
Gene_locus related to this paper: 9burk-i2dyd7 , burvg-a4jmy2

Title : A cellular model of memory reconsolidation involves reactivation-induced destabilization and restabilization at the sensorimotor synapse in Aplysia - Lee_2012_Proc.Natl.Acad.Sci.U.S.A_109_14200
Author(s) : Lee SH , Kwak C , Shim J , Kim JE , Choi SL , Kim HF , Jang DJ , Lee JA , Lee K , Lee CH , Lee YD , Miniaci MC , Bailey CH , Kandel ER , Kaang BK
Ref : Proc Natl Acad Sci U S A , 109 :14200 , 2012
Abstract : The memory reconsolidation hypothesis suggests that a memory trace becomes labile after retrieval and needs to be reconsolidated before it can be stabilized. However, it is unclear from earlier studies whether the same synapses involved in encoding the memory trace are those that are destabilized and restabilized after the synaptic reactivation that accompanies memory retrieval, or whether new and different synapses are recruited. To address this issue, we studied a simple nonassociative form of memory, long-term sensitization of the gill- and siphon-withdrawal reflex in Aplysia, and its cellular analog, long-term facilitation at the sensory-to-motor neuron synapse. We found that after memory retrieval, behavioral long-term sensitization in Aplysia becomes labile via ubiquitin/proteasome-dependent protein degradation and is reconsolidated by means of de novo protein synthesis. In parallel, we found that on the cellular level, long-term facilitation at the sensory-to-motor neuron synapse that mediates long-term sensitization is also destabilized by protein degradation and is restabilized by protein synthesis after synaptic reactivation, a procedure that parallels memory retrieval or retraining evident on the behavioral level. These results provide direct evidence that the same synapses that store the long-term memory trace encoded by changes in the strength of synaptic connections critical for sensitization are disrupted and reconstructed after signal retrieval.
ESTHER : Lee_2012_Proc.Natl.Acad.Sci.U.S.A_109_14200
PubMedSearch : Lee_2012_Proc.Natl.Acad.Sci.U.S.A_109_14200
PubMedID: 22893682

Title : Learning-related synaptic growth mediated by internalization of Aplysia cell adhesion molecule is controlled by membrane phosphatidylinositol 4,5-bisphosphate synthetic pathway - Lee_2012_J.Neurosci_32_16296
Author(s) : Lee SH , Shim J , Choi SL , Lee N , Lee CH , Bailey CH , Kandel ER , Jang DJ , Kaang BK
Ref : Journal of Neuroscience , 32 :16296 , 2012
Abstract : Long-term facilitation in Aplysia is accompanied by the growth of new synaptic connections between the sensory and motor neurons of the gill-withdrawal reflex. One of the initial steps leading to the growth of these synapses is the internalization, induced by 5-HT, of the transmembrane isoform of Aplysia cell-adhesion molecule (TM-apCAM) from the plasma membrane of sensory neurons (Bailey et al., 1992). However, the mechanisms that govern the internalization of TM-apCAM and how this internalization is coupled to the molecular events that initiate the structural changes are not fully understood. Here, we report that the synthesis of membrane phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)], which is known to be mediated by a signaling cascade through Aplysia Sec7 protein (ApSec7) and phosphatidylinositol-4-phosphate 5-kinase type I alpha (PIP5KIalpha) is required for both the internalization of TM-apCAM and the initiation of synaptic growth during 5-HT-induced long-term facilitation. Pharmacological blockade of PI(4,5)P(2) synthesis by the application of the inhibitor phenylarsine oxide blocked the internalization of apCAM. Furthermore, perturbation of the endogenous activation of ApSec7 and its downstream target PIP5KIalpha also blocked 5-HT-mediated internalization of TM-apCAM and synaptic growth. Finally, long-term facilitation was specifically impaired by blocking the ApSec7 signaling pathway at sensory-to-motor neuron synapses. These data indicate that the ApSec7/PIP5KIalpha signaling pathway is actively recruited during learning-related 5-HT signaling and acts as a key regulator of apCAM internalization associated with the formation of new synaptic connections during long-term facilitation.
ESTHER : Lee_2012_J.Neurosci_32_16296
PubMedSearch : Lee_2012_J.Neurosci_32_16296
PubMedID: 23152613

Title : The memory ameliorating effects of INM-176, an ethanolic extract of Angelica gigas, against scopolamine- or Abeta(1-42)-induced cognitive dysfunction in mice - Park_2012_J.Ethnopharmacol_143_611
Author(s) : Park SJ , Jung JM , Lee HE , Lee YW , Kim DH , Kim JM , Hong JG , Lee CH , Jung IH , Cho YB , Jang DS , Ryu JH
Ref : J Ethnopharmacol , 143 :611 , 2012
Abstract : ETHNOPHARMACOLOGICAL RELEVANCE: Alzheimer's disease is a neurodegenerative disorder associated with cognitive impairment and cholinergic neuronal death. INM-176 is a standardized ethanolic extract of Angelica gigas Nakai that has been traditionally used in herbal medicine in China, Japan, and Korea to treat anemia or as a sedative. We investigated whether INM-176 exhibits anti-amnesic effects. MATERIALS AND METHODS: Memory impairment was induced by scopolamine, a cholinergic muscarinic receptor antagonist, or amyloid beta(1-42) (Abeta(1-42)) protein. Anti-amnesic effects of INM-176 were measured by the passive avoidance and the Morris water maze tasks in mice. We also examined the effect of INM-176 on the acetylcholinesterase activity, as well as Abeta(1-42) protein-induced astrogliosis or cholinergic neuronal loss in the brain. RESULTS: Scopolamine-induced cognitive dysfunction was significantly attenuated by a single or sub-chronic administration of INM-176 in the passive avoidance and the Morris water maze tasks. A single or sub-chronic administration of INM-176 also ameliorated memory impairments induced by Abeta(1-42) protein. INM-176 inhibited acetylcholinesterase activity in the hippocampal tissue in vitro and ex vivo. In addition, INM-176 attenuated the Abeta(1-42) protein-induced astrocyte activation in the hippocampus as well as cholinergic neuronal damage in the CA3 region of the hippocampus and the nucleus basalis of Meynert. CONCLUSION: These results suggest that the memory ameliorating effects of INM-176 on scopolamine- or Abeta(1-42) protein-induced memory impairment are mediated, in part, via acetylcholinesterase inhibition and neuroprotective activities.
ESTHER : Park_2012_J.Ethnopharmacol_143_611
PubMedSearch : Park_2012_J.Ethnopharmacol_143_611
PubMedID: 22846435

Title : Tea polyphenol (-)-epigallocatechin-3-gallate inhibits nicotine- and estrogen-induced alpha9-nicotinic acetylcholine receptor upregulation in human breast cancer cells - Tu_2011_Mol.Nutr.Food.Res_55_455
Author(s) : Tu SH , Ku CY , Ho CT , Chen CS , Huang CS , Lee CH , Chen LC , Pan MH , Chang HW , Chang CH , Chang YJ , Wei PL , Wu CH , Ho YS
Ref : Mol Nutr Food Res , 55 :455 , 2011
Abstract : SCOPE: The aim of this research was to explore whether the tea-polyphenol (-)-epigallocatechin-3-gallate (EGCG) could be used as a potential agent for blocking smoking (nicotine, Nic)- or hormone (estradiol, E2)-induced breast cancer cell proliferation through inhibition of a common signaling pathway. METHODS AND
RESULTS: To explore whether Nic (>0.1 muM, 24 h) and E2 (>1 nM, 24 h) significantly increased alpha9-nicotinic acetylcholine (alpha9-nicotinic acetylcholine receptor (nAChR)) mRNA and protein expression levels, real-time PCR and immunoblotting analysis experiments were performed in human breast cancer (MCF-7) cells. Luciferase promoter activity experiment was performed to test the alpha9-nAChR promoter activity affected by Nic, E2 or EGCG. The results indicate that treatment with EGCG (1 muM) profoundly decreases Nic- and E2-induced MCF-7 proliferation by down regulating alpha9-nAChR expression. The alpha9-nAChR promoter activity is significantly induced by 24-h treatment with Nic (10 muM) or E2 (10 nM) (>1.8 and approximately 2.3-fold, respectively) in MCF-7 cells. Pretreatment with EGCG eliminated the Nic- and E2-induced alpha9-nAChR promoter-dependent luciferase activity. We further demonstrate that combined treatment with EGCG profoundly inhibits [3H]-Nic/ alpha9-nAChR binding activity in breast cancer cells.
CONCLUSIONS: We found that the EGCG could be used as an agent for blocking smoking (Nic)- or hormone (E2)-induced breast cancer cell proliferation by inhibiting of alpha9-nAChR signaling pathway. This study reveals the novel antitumor mechanisms of EGCG, and these results may have significant applications for chemopreventive purposes in human breast cancer.
ESTHER : Tu_2011_Mol.Nutr.Food.Res_55_455
PubMedSearch : Tu_2011_Mol.Nutr.Food.Res_55_455
PubMedID: 21370452

Title : Structure-activity studies of diazabicyclo[3.3.0]octane-substituted pyrazines and pyridines as potent alpha4beta2 nicotinic acetylcholine receptor ligands - Scanio_2011_J.Med.Chem_54_7678
Author(s) : Scanio MJ , Shi L , Bunnelle WH , Anderson DJ , Helfrich RJ , Malysz J , Thorin-Hagene KK , Van Handel CE , Marsh KC , Lee CH , Gopalakrishnan M
Ref : Journal of Medicinal Chemistry , 54 :7678 , 2011
Abstract : A series of diazabicyclo[3.3.0]octane substituted pyridines and pyrazines was synthesized and characterized at the alpha4beta2 neuronal nicotinic acetylcholine receptor (nAChR). The compounds were designed to mimic the profile of ABT-089, high affinity binding ligand for the alpha4beta2 nAChR, with limited agonist activity. Carboxamide derivatives of 3-(diazabicyclo[3.3.0]octane)-substituted pyridines or 2-(diazabicyclo[3.3.0]octane)-substituted pyrazines were found to have the desired binding and activity profile. The structure-activity relationship of these compounds is presented.
ESTHER : Scanio_2011_J.Med.Chem_54_7678
PubMedSearch : Scanio_2011_J.Med.Chem_54_7678
PubMedID: 21962147

Title : Crosstalk between nicotine and estrogen-induced estrogen receptor activation induces alpha9-nicotinic acetylcholine receptor expression in human breast cancer cells - Lee_2011_Breast.Cancer.Res.Treat_129_331
Author(s) : Lee CH , Chang YC , Chen CS , Tu SH , Wang YJ , Chen LC , Chang YJ , Wei PL , Chang HW , Chang CH , Huang CS , Wu CH , Ho YS
Ref : Breast Cancer Research Treat , 129 :331 , 2011
Abstract : The primary aim of this study was to elucidate the role of the estrogen receptor (ER), a transcription factor involved in the nicotine- and 17beta-estradiol (E2)-mediated up-regulation of alpha9-nAChR gene expression. A real-time polymerase chain reaction (PCR) assay was used to quantify the alpha9-nAChR mRNA expression levels of surgically isolated (n=339) and laser-capture microdissected tissues (ER+ versus ER-, n= 6 per group). Chromatin immunoprecipitation (ChIP) and luciferase-promoter activity assays were used to investigate the ER-mediated transcriptional regulation of alpha9-nAChR gene expression. We observed that breast tumors with higher alpha9-nAChR mRNA expression levels (i.e., a mean fold ratio in the tumor/normal-paired samples of greater than tenfold) were associated with the lowest 5-year disease-specific survival rate (50%, dead/alive= 4/4, total = 8 patients, P= 0.006), in contrast to breast tumors with low levels (i.e., a mean fold ratio of less than onefold) of alpha9-nAChR expression (88%, dead/alive= 3/22, total= 25 patients). Furthermore, higher alpha9-nAChR mRNA expression levels were preferentially detected in ER+ tumor tissues in comparison to ER- tumor tissues (ER+ versus ER- patients: n=160 vs. 72; mean fold ratios of alpha9-nAChR expression = 11 +/- 3 vs. 6.7 +/- 2.3 fold, respectively). In vitro promoter-binding assays demonstrated that the ER is a major transcription factor that mediates nicotine- and E2-induced up-regulation of alpha9-nAChR gene expression in MCF-7 cells. In conclusion, our data indicate that the ER plays a central role in mediating alpha9-nAChR gene up-regulation in response to either nicotine or E2 stimulation.
ESTHER : Lee_2011_Breast.Cancer.Res.Treat_129_331
PubMedSearch : Lee_2011_Breast.Cancer.Res.Treat_129_331
PubMedID: 20953833

Title : alpha4beta2 neuronal nicotinic receptor positive allosteric modulation: an approach for improving the therapeutic index of alpha4beta2 nAChR agonists in pain - Lee_2011_Biochem.Pharmacol_82(8)_959
Author(s) : Lee CH , Zhu C , Malysz J , Campbell T , Shaughnessy T , Honore P , Polakowski J , Gopalakrishnan M
Ref : Biochemical Pharmacology , 82 :959 , 2011
Abstract : Nicotinic acetylcholine receptors (nAChRs) function as ligand-gated ion channels activated by the neurotransmitter acetylcholine. Gene knockout and antisense studies coupled with pharmacological studies with nAChR agonists have documented a role of alpha4beta2 nAChR activation in analgesia. ABT-594, for the first time, provided clinical validation to the nAChR agonist pharmacology as a novel mechanism for treatment of pain. However, ABT-594 was poorly tolerated at the efficacious doses, particularly with respect to the side effects of nausea and emesis, which is thought to be mediated by activation of the ganglionic-type (alpha3-containing) nAChRs. An alternate approach is to selectively modulate the alpha4beta2 nAChR via positive allosteric modulation. Positive allosteric modulators (PAMs) are compounds that do not interact with the agonist binding sites or possess intrinsic activity at the receptor per se, but potentiate the effects of the agonist. NS9283 (also known as A-969933), the first oxadiazole analog, was found to selectively enhance the potency of a range of nAChR agonists at alpha4beta2, but not alpha3beta4, nAChRs. Studies reported here, along with the accompanying manuscript [1] collectively point to the conclusion, based on preclinical models, that the analgesic efficacy of clinically well-tolerated doses of ABT-594 in humans can be significantly enhanced by co-administration with the alpha4beta2 PAM. Additionally, studies in ferrets demonstrate no exaggeration of emetic effect when ABT-594 is co-dosed with NS9283. Cardiovascular studies in anesthetized dogs achieve supra-therapeutic plasma concentrations of ABT-594 (>20-fold) without hemodynamic or electrophysiological effects using the co-administration paradigm.
ESTHER : Lee_2011_Biochem.Pharmacol_82(8)_959
PubMedSearch : Lee_2011_Biochem.Pharmacol_82(8)_959
PubMedID: 21763685

Title : Potentiation of analgesic efficacy but not side effects: co-administration of an alpha4beta2 neuronal nicotinic acetylcholine receptor agonist and its positive allosteric modulator in experimental models of pain in rats - Zhu_2011_Biochem.Pharmacol_82(8)_967
Author(s) : Zhu CZ , Chin CL , Rustay NR , Zhong C , Mikusa J , Chandran P , Salyers A , Gomez E , Simler G , Lewis LG , Gauvin D , Baker S , Pai M , Tovcimak A , Brown J , Komater V , Fox GB , Decker MW , Jacobson PB , Gopalakrishnan M , Lee CH , Honore P
Ref : Biochemical Pharmacology , 82 :967 , 2011
Abstract : Positive modulation of the neuronal nicotinic acetylcholine receptor (nAChR) alpha4beta2 subtype by selective positive allosteric modulator NS-9283 has shown to potentiate the nAChR agonist ABT-594-induced anti-allodynic activity in preclinical neuropathic pain. To determine whether this benefit can be extended beyond neuropathic pain, the present study examined the analgesic activity and adverse effect profile of co-administered NS-9283 and ABT-594 in a variety of preclinical models in rats. The effect of the combined therapy on drug-induced brain activities was also determined using pharmacological magnetic resonance imaging. In carrageenan-induced thermal hyperalgesia, co-administration of NS-9283 (3.5 mumol/kg, i.p.) induced a 6-fold leftward shift of the dose-response of ABT-594 (ED(50)=26 vs. 160 nmol/kg, i.p.). In the paw skin incision model of post-operative pain, co-administration of NS-9283 similarly induced a 6-fold leftward shift of ABT-594 (ED(50)=26 vs. 153 nmol/kg). In monoiodo-acetate induced knee joint pain, co-administration of NS-9283 enhanced the potency of ABT-594 by 5-fold (ED(50)=1.0 vs. 4.6 nmol/kg). In pharmacological MRI, co-administration of NS-9283 was shown to lead to a leftward shift of ABT-594 dose-response for cortical activation. ABT-594 induced CNS-related adverse effects were not exacerbated in presence of an efficacious dose of NS-9283 (3.5 mumol/kg). Acute challenge of NS-9283 produced no cross sensitization in nicotine-conditioned animals. These results demonstrate that selective positive allosteric modulation at the alpha4beta2 nAChR potentiates nAChR agonist-induced analgesic activity across neuropathic and nociceptive preclinical pain models without potentiating ABT-594-mediated adverse effects, suggesting that selective positive modulation of alpha4beta2 nAChR by PAM may represent a novel analgesic approach.
ESTHER : Zhu_2011_Biochem.Pharmacol_82(8)_967
PubMedSearch : Zhu_2011_Biochem.Pharmacol_82(8)_967
PubMedID: 21620806

Title : Alpha3* and alpha 7 nAChR-mediated Ca2+ transient generation in IMR-32 neuroblastoma cells - Ween_2010_Neurochem.Int_57_269
Author(s) : Ween H , Thorin-Hagene K , Andersen E , Gronlien JH , Lee CH , Gopalakrishnan M , Malysz J
Ref : Neurochem Int , 57 :269 , 2010
Abstract : Alpha3-containing (alpha 3*) and alpha 7 nicotinic acetylcholine receptors (nAChRs) are expressed in human IMR-32 neuroblastoma cells and implicated in Ca(2+) signaling. In this study, we investigated the intracellular Ca(2+) transient generation evoked by selective activation of alpha 3* (agonist potency rank order: epibatidine>varenicline>nicotine approximately cytisine) and alpha 7 (rank order in the presence of alpha 7 positive allosteric modulator or PAM: A-795723>NS6784 approximately PNU-282987) using, respectively, varenicline and NS6784 (+alpha 7 PAM) by Ca(2+) imaging. Effects of inhibitors of nAChRs (MLA and mecamylamine), ER Ca(2+) ATPase pump (CPA and thapsigargin), Ca(2+)-induced Ca(2+) release (ryanodine and dantrolene), Ca(2+) channels (nitrendipine, diltiazem, and Cd(2+)), and removal of extracellular Ca(2+) were examined. alpha 7 PAMs, when tested in the presence of NS6784, were more active when added first, followed by the agonist, than in the reverse order. Removal of extracellular Ca(2+) - but not CPA, thapsigargin, ryanodine, dantrolene, nitrendipine, diltiazem, or Cd(2+) - diminished the alpha 7 agonist-evoked Ca(2+) transients. In contrast, only diltiazem and nitrendipine and removal of extracellular Ca(2+) inhibited the alpha 3*-mediated Ca(2+) transients. The differential effect of diltiazem and nitrendipine versus Cd(2+) was due to direct inhibition of alpha 3* nAChRs as revealed by Ca(2+) imaging in HEK-293 cells expressing human alpha 3 beta 4 nAChRs and patch clamp in IMR-32 cells. In summary, this study provides evidence that alpha 3* and alpha 7 nAChR agonist-evoked global Ca(2+) transient generation in IMR-32 cells does not primarily involve voltage-dependent Ca(2+) channels, intracellular Ca(2+) stores, or Ca(2+)-induced Ca(2+) release. These mechanisms may, however, be still involved in other forms of nAChR-mediated Ca(2+) signaling.
ESTHER : Ween_2010_Neurochem.Int_57_269
PubMedSearch : Ween_2010_Neurochem.Int_57_269
PubMedID: 20558224

Title : Genome sequences of Escherichia coli B strains REL606 and BL21(DE3) - Jeong_2009_J.Mol.Biol_394_644
Author(s) : Jeong H , Barbe V , Lee CH , Vallenet D , Yu DS , Choi SH , Couloux A , Lee SW , Yoon SH , Cattolico L , Hur CG , Park HS , Segurens B , Kim SC , Oh TK , Lenski RE , Studier FW , Daegelen P , Kim JF
Ref : Journal of Molecular Biology , 394 :644 , 2009
Abstract : Escherichia coli K-12 and B have been the subjects of classical experiments from which much of our understanding of molecular genetics has emerged. We present here complete genome sequences of two E. coli B strains, REL606, used in a long-term evolution experiment, and BL21(DE3), widely used to express recombinant proteins. The two genomes differ in length by 72,304 bp and have 426 single base pair differences, a seemingly large difference for laboratory strains having a common ancestor within the last 67 years. Transpositions by IS1 and IS150 have occurred in both lineages. Integration of the DE3 prophage in BL21(DE3) apparently displaced a defective prophage in the lambda attachment site of B. As might have been anticipated from the many genetic and biochemical experiments comparing B and K-12 over the years, the B genomes are similar in size and organization to the genome of E. coli K-12 MG1655 and have >99% sequence identity over approximately 92% of their genomes. E. coli B and K-12 differ considerably in distribution of IS elements and in location and composition of larger mobile elements. An unexpected difference is the absence of a large cluster of flagella genes in B, due to a 41 kbp IS1-mediated deletion. Gene clusters that specify the LPS core, O antigen, and restriction enzymes differ substantially, presumably because of horizontal transfer. Comparative analysis of 32 independently isolated E. coli and Shigella genomes, both commensals and pathogenic strains, identifies a minimal set of genes in common plus many strain-specific genes that constitute a large E. coli pan-genome.
ESTHER : Jeong_2009_J.Mol.Biol_394_644
PubMedSearch : Jeong_2009_J.Mol.Biol_394_644
PubMedID: 19786035
Gene_locus related to this paper: eco57-b3a913 , ecoli-Aes , ecoli-rutD , ecoli-bioh , ecoli-dlhh , ecoli-entf , ecoli-fes , ecoli-mhpc , ecoli-pldb , ecoli-ptrb , ecoli-yafa , ecoli-yaim , ecoli-ybff , ecoli-ycfp , ecoli-ycjy , ecoli-yeiG , ecoli-YFBB , ecoli-yghX , ecoli-yhet , ecoli-yiel , ecoli-yjfp , ecoli-YNBC , ecoli-ypfh , ecoli-yqia , ecoli-YfhR

Title : Atromentin-induced apoptosis in human leukemia U937 cells - Kim_2009_J.Microbiol.Biotechnol_19_946
Author(s) : Kim JH , Lee CH
Ref : J Microbiol Biotechnol , 19 :946 , 2009
Abstract : In the course of screening for apoptotic substances that induce apoptosis in human leukemia U937 cells, a fungal strain, F000487, which exhibits potent inducible activity, was selected. The active compound was purified from an ethyl acetate extract of the microorganism by Sep-pak C18 column chromatography and HPLC, and was identified as atromentin by spectroscopic methods. This compound induced caspase-3 processing in human leukemia U937 cells. The caspase-3 and poly (ADP-ribose) polymerase (PARP) were induced by atromentin in a dose-dependent manner. Furthermore, DNA fragmentation was also induced by this compound in a dose-dependent manner. These results show that atromentin potently induces apoptosis in U937 cells and that atromentin-induced apoptosis is related to the selective activation of caspases.
ESTHER : Kim_2009_J.Microbiol.Biotechnol_19_946
PubMedSearch : Kim_2009_J.Microbiol.Biotechnol_19_946
PubMedID: 19809251
Gene_locus related to this paper: tappa-atra

Title : Red mold rice prevents the development of obesity, dyslipidemia and hyperinsulinemia induced by high-fat diet - Chen_2008_Int.J.Obes.(Lond)_32_1694
Author(s) : Chen WP , Ho BY , Lee CL , Lee CH , Pan TM
Ref : Int J Obes (Lond) , 32 :1694 , 2008
Abstract : OBJECTIVE: To investigate the influences of red mold rice (RMR) on obesity and related metabolic abnormalities.
METHODS AND RESULTS: The 3T3-L1 cell line was used to examine the effects of RMR extracts on preadipocytes and on mature adipocytes. Both water and ethanol extracts of RMR had inhibitory effects on 3T3-L1 preadipocyte proliferation and differentiation. Water extracts of RMR enhanced the lipolysis activity in mature adipocytes, which negatively correlated with the triglyceride content within cells. RMR treatment did not affect heparin-releasable lipoprotein lipase activity in mature adipocytes. Furthermore, animal studies were carried out to explore the antiobesity effects of RMR. The control group of male Wistar rats were fed regular laboratory feed, whereas the other groups were fed the high-fat (HF) diet supplemented with lovastatin, rice or RMR (0.4 and 2%, w w(-1)). The relative caloric intakes of the control and HF groups were 3.34 and 4.85 kcal g(-1), respectively. After 6 weeks, rats treated with RMR at the 0.4 and 2% doses had lower weight gain and less fat pads mass accompanied with smaller fat cells than did the HF-diet rats. These effects probably resulted from an increase in the lipolysis activity of adipose tissue and a reduction in food/energy consumption. On the other hand, the RMR supplement significantly reduced serum total cholesterol, serum low-density lipoprotein (LDL) cholesterol, the ratio of LDL to high-density lipoprotein (HDL) cholesterol and serum insulin in the HF group. Moreover, the 2% RMR treatment significantly increased serum HDL cholesterol.
CONCLUSION: This study reveals for the first time that RMR can prevent body fat accumulation and improve dyslipidemia. The antiobesity effects of RMR mainly derive from the lipolytic activity and mild antiappetite potency of RMR. In addition, extracts of RMR suppressed the proliferation and differentiation in 3T3-L1 preadipocytes, which might have contributed to the inhibition of new adipocyte formation or hyperplasia in adipose tissue.
ESTHER : Chen_2008_Int.J.Obes.(Lond)_32_1694
PubMedSearch : Chen_2008_Int.J.Obes.(Lond)_32_1694
PubMedID: 18794894

Title : The crystal structure of the estA protein, a virulence factor from Streptococcus pneumoniae -
Author(s) : Kim MH , Kang BS , Kim S , Kim KJ , Lee CH , Oh BC , Park SC , Oh TK
Ref : Proteins , 70 :578 , 2008
PubMedID: 17932928
Gene_locus related to this paper: strpn-SP0614

Title : Isolation and characterization of a novel lipase from a metagenomic library of tidal flat sediments: evidence for a new family of bacterial lipases - Lee_2006_Appl.Environ.Microbiol_72_7406
Author(s) : Lee MH , Lee CH , Oh TK , Song JK , Yoon JH
Ref : Applied Environmental Microbiology , 72 :7406 , 2006
Abstract : We cloned lipG, which encoded a lipolytic enzyme, from a Korean tidal flat metagenomic library. LipG was related to six putative lipases previously identified only in bacterial genome sequences. These enzymes comprise a new family. We partially characterized LipG, providing the first experimental data for a member of this family.
ESTHER : Lee_2006_Appl.Environ.Microbiol_72_7406
PubMedSearch : Lee_2006_Appl.Environ.Microbiol_72_7406
PubMedID: 16950897
Gene_locus related to this paper: 9bact-q1paf1

Title : Peroxisome proliferator-activated receptor delta promotes very low-density lipoprotein-derived fatty acid catabolism in the macrophage - Lee_2006_Proc.Natl.Acad.Sci.U.S.A_103_2434
Author(s) : Lee CH , Kang K , Mehl IR , Nofsinger R , Alaynick WA , Chong LW , Rosenfeld JM , Evans RM
Ref : Proc Natl Acad Sci U S A , 103 :2434 , 2006
Abstract : Significant attention has focused on the role of low-density lipoprotein (LDL) in the pathogenesis of atherosclerosis. However, recent advances have identified triglyceride-rich lipoproteins [e.g., very LDL (VLDL)] as independent risk predictors for this disease. We have previously demonstrated peroxisome proliferator-activated receptor (PPAR)delta, but not PPARgamma, is the major nuclear VLDL sensor in the macrophage, which is a crucial component of the atherosclerotic lesion. Here, we show that, in addition to beta-oxidation and energy dissipation, activation of PPARdelta by VLDL particles induces key genes involved in carnitine biosynthesis and lipid mobilization mediated by a recently identified TG lipase, transport secretion protein 2 (also named desnutrin, iPLA2zeta, and adipose triglyceride lipase), resulting in increased fatty acid catabolism. Unexpectedly, deletion of PPARdelta results in derepression of target gene expression, a phenotype similar to that of ligand activation, suggesting that unliganded PPARdelta suppresses fatty acid utilization through active repression, which is reversed upon ligand binding. This unique transcriptional mechanism assures a tight control of the homeostasis of VLDL-derived fatty acid and provides a therapeutic target for other lipid-related disorders, including dyslipidemia and diabetes, in addition to coronary artery disease.
ESTHER : Lee_2006_Proc.Natl.Acad.Sci.U.S.A_103_2434
PubMedSearch : Lee_2006_Proc.Natl.Acad.Sci.U.S.A_103_2434
PubMedID: 16467150

Title : Bacillus cibi sp. nov., isolated from jeotgal, a traditional Korean fermented seafood - Yoon_2005_Int.J.Syst.Evol.Microbiol_55_733
Author(s) : Yoon JH , Lee CH , Oh TK
Ref : Int J Syst Evol Microbiol , 55 :733 , 2005
Abstract : A Gram-variable, motile, endospore-forming, halotolerant bacillus, strain JG-30(T), was isolated from the traditional Korean fermented seafood jeotgal, and was subjected to a polyphasic taxonomic study. This organism grew optimally at 37 degrees C and in the presence of 0-1 % (w/v) NaCl. 16S rRNA gene sequence analysis showed that strain JG-30(T) forms a distinct phylogenetic lineage within the evolutionary radiation encompassed by the genus Bacillus. Strain JG-30(T) was characterized chemotaxonomically as having cell-wall peptidoglycan based on meso-diaminopimelic acid, MK-7 as the predominant menaquinone and iso-C(15 : 0) and iso-C(14 : 0) as the major fatty acids. The DNA G+C content was 45 mol%. Strain JG-30(T) exhibited levels of 16S rRNA gene sequence similarity of less than 95.7 % to Bacillus species with validly published names. On the basis of its phenotypic properties and phylogenetic distinctiveness, strain JG-30(T) (=KCTC 3880(T)=DSM 16189(T)) was classified within the genus Bacillus as a novel species, for which the name Bacillus cibi sp. nov. is proposed.
ESTHER : Yoon_2005_Int.J.Syst.Evol.Microbiol_55_733
PubMedSearch : Yoon_2005_Int.J.Syst.Evol.Microbiol_55_733
PubMedID: 15774653
Gene_locus related to this paper: 9baci-a0a084gmw3 , 9baci-a0a084gjz2 , 9baci-a0a084h1w6 , metid-a0a084gkg9

Title : Coenzyme q10 confers cardiovascular protection against acute mevinphos intoxication by ameliorating bioenergetic failure and hypoxia in the rostral ventrolateral medulla of the rat - Yen_2005_Shock_23_353
Author(s) : Yen DH , Chan JY , Huang CI , Lee CH , Chan SH , Chang AY
Ref : Shock , 23 :353 , 2005
Abstract : Coenzyme Q10 (CoQ10, ubiquinone) is a highly mobile electron carrier in the mitochondrial respiratory chain that also acts as an antioxidant. We evaluated the cardiovascular protective efficacy of CoQ10 at the rostral ventrolateral medulla (RVLM), a medullary site where sympathetic vasomotor tone originates and where the organophosphate poison mevinphos (Mev) acts to elicit cardiovascular intoxication. Experiments were carried out in adult male Sprague-Dawley rats that were maintained under propofol anesthesia. Microinjection bilaterally of Mev (10 nmol) into the RVLM induced progressive hypotension and minor bradycardia, alongside significant depression of the activity of NADH cytochrome c reductase (enzyme marker for Complexes I and III) or cytochrome c oxidase (enzyme marker for Complex IV) in the mitochondrial respiratory chain, reduction in ATP concentration, or tissue hypoxia in the RVLM. On the other hand, the activity of succinate cytochrome c reductase (enzyme marker for Complexes II and III) remained unaltered. The Mev-induced hypotension, bioenergetic failure, or hypoxia was significantly reversed when CoQ10 (4 microg) was coadministered bilaterally into the RVLM with the organophosphate poison. We conclude that CoQ10 confers cardiovascular protection against acute Mev intoxication by acting on the RVLM, whose neuronal activity is intimately related to the "life-and-death" process. We also showed that amelioration of the selective dysfunction of respiratory enzyme Complexes I and IV in the mitochondrial respiratory chain, the reduced ATP level, and the induced tissue hypoxia in the RVLM are among some of the underlying mechanisms for the elicited protection.
ESTHER : Yen_2005_Shock_23_353
PubMedSearch : Yen_2005_Shock_23_353
PubMedID: 15803059

Title : Depression of mitochondrial respiratory enzyme activity in rostral ventrolateral medulla during acute mevinphos intoxication in the rat - Yen_2004_Shock_21_358
Author(s) : Yen DH , Chan JY , Tseng HP , Huang CI , Lee CH , Chan SH , Chang AY
Ref : Shock , 21 :358 , 2004
Abstract : We investigated possible changes in bioenergetics at the rostral ventrolateral medulla (RVLM), a medullary site where sympathetic vasomotor tone originates and where the organophosphate poison mevinphos (Mev) acts to elicit cardiovascular intoxication. In Sprague-Dawley rats maintained under propofol anesthesia, microinjection bilaterally of Mev (10 nmol) into the RVLM induced progressive hypotension that was accompanied by an early augmentation (80-100 min post-Mev; Phase I), followed by a decrease (>100 min post-Mev; Phase II) in the power density of the vasomotor components (0-0.8 Hz) in systemic arterial pressure (SAP) signals. Enzyme assay revealed that local application of Mev into the RVLM also significantly and progressively depressed the activity of NADH cytochrome c reductase (marker for Complexes I and III) and cytochrome c oxidase (marker for Complex IV) in the mitochondrial respiratory chain of the RVLM, but not the heart. On the other hand, the activity of succinate cytochrome c reductase (marker for Complexes II and III) remained unaltered. Both the cardiovascular consequences and depression of mitochondrial respiratory chain enzymes elicited by Mev were significantly antagonized on comicroinjection of atropine (3.5 or 7 nmol) bilaterally into the RVLM. We conclude that Mev adversely effects cardiovascular control by acting as a cholinesterase inhibitor in the RVLM, whose neuronal activity is intimately related to the death process. The resulting accumulation of acetylcholine and prolonged activation of muscarinic receptors in the RVLM is manifested by a selective dysfunction of respiratory enzyme Complexes I and IV in the mitochondrial respiratory chain that underlies cardiovascular toxicity associated with organophosphate poisons such as Mev.
ESTHER : Yen_2004_Shock_21_358
PubMedSearch : Yen_2004_Shock_21_358
PubMedID: 15179137

Title : Gene expression analysis of the pro-oestrous-stage rat uterus reveals neuroligin 2 as a novel steroid-regulated gene - Kang_2004_Reprod.Fertil.Dev_16_763
Author(s) : Kang HS , Lee CK , Kim JR , Yu SJ , Kang SG , Moon DH , Lee CH , Kim DK
Ref : Reprod Fertil Dev , 16 :763 , 2004
Abstract : In the present study, differential gene expression in the uteri of ovariectomised (OVX) and pro-oestrous rats (OVX v. pro-oestrus pair) was investigated using cDNA expression array analysis. Differential uterine gene expression in OVX rats and progesterone (P(4))-injected OVX rats (OVX v. OVX + P(4) pair) was also examined. The uterine gene expression profiles of these two sets of animals were also compared for the effects of P(4) treatment. RNA samples were extracted from uterine tissues and reverse transcribed in the presence of [alpha(32)P]-dATP. Membrane sets of rat arrays were hybridised with cDNA probe sets. Northern blot analysis was used to validate the relative gene expression patterns obtained from the cDNA array. Of the 1176 cDNAs examined, 23 genes showed significant (>two-fold) changes in expression in the OVX v. pro-oestrus pair. Twenty of these genes were upregulated during pro-oestrus compared with their expression in the OVX rat uterus. In the OVX v. OVX + P(4) pair, 22 genes showed significant (>two-fold) changes in gene expression. Twenty of these genes were upregulated in the OVX + P(4) animals. The genes for nuclear factor I-XI, afadin, neuroligin 2, semaphorin Z, calpain 4, cyclase-associated protein homologue, thymosin beta-4X and p8 were significantly upregulated in the uteri of the pro-oestrus and OVX + P(4) rats of both experimental pairs compared with the OVX rat uteri. These genes appear to be under the control of P(4). One of the most interesting findings of the present study is the unexpected and marked expression of the neuroligin 2 gene in the rat uterus. This gene is expressed at high levels in the central nervous system and acts as a nerve cell adhesion factor. According to Northern blot analysis, neuroligin 2 gene expression was higher during the pro-oestrus and metoestrus stages than during the oestrus and dioestrus stages of the oestrous cycle. In addition, neuroligin 2 mRNA levels were increased by both 17beta-oestradiol (E(2)) and P(4), although P(4) administration upregulated gene expression to a greater extent than injection of E(2). These results indicate that neuroligin 2 gene expression in the rat uterus is under the control of both E(2) and P(4), which are secreted periodically during the oestrous cycle.
ESTHER : Kang_2004_Reprod.Fertil.Dev_16_763
PubMedSearch : Kang_2004_Reprod.Fertil.Dev_16_763
PubMedID: 15740699

Title : Transdermal delivery of physostigmine: effects of enhancers and pressure-sensitive adhesives - Kim_2002_Drug.Dev.Ind.Pharm_28_833
Author(s) : Kim JH , Lee CH , Choi HK
Ref : Drug Dev Ind Pharm , 28 :833 , 2002
Abstract : The purpose of this study was to investigate the effects of various pressure-sensitive adhesives (PSA) on the percutaneous absorption of physostigmine across hairless mouse skin. In addition, the influences of various vehicles and polyvinylpyrrolidone (PVP) on the percutaneous absorption of physostigmine from PSA matrix across hairless mouse skin were evaluated using a flow-through diffusion cell system at 37 degrees C. Physostigmine showed the highest permeability from silicone adhesive matrix, followed by polyisobutylene (PIB), styrene-isoprene-styrene (SIS), acrylic, and styrene-butadiene-styrene (SBS) matrix. Among acrylic adhesives, the permeability of physostigmine was the highest from grafted acrylic adhesive. Polyvinyl pyrrolidone inhibited the crystallization of physostigmine in the PIB adhesive matrix and enhanced the permeability of physostigmine from the PIB adhesive matrix. When esters of sorbitol and fatty acid, polyethylene glycol (PEG) alkyl esters, and caprylic/capric triglycerides were tested, the more lipophilic was a surfactant, the higher the permeation rate within the same group of surfactants. The enhancement effect of PEG derivatives was lower than that of non-PEG derivatives. Among non-linear fatty acid derivatives, linoleate derivatives showed higher permeability of physostigmine than oleate derivatives. This study showed that several non-ionic surfactants, including PEG-20 evening primrose glyceride, enhanced the permeation of physostigmine across hairless mouse skin better than oleic acid.
ESTHER : Kim_2002_Drug.Dev.Ind.Pharm_28_833
PubMedSearch : Kim_2002_Drug.Dev.Ind.Pharm_28_833
PubMedID: 12236069

Title : Induction of microsomal epoxide hydrolase by sulfur amino acid deprivation via the pathway of C-Jun N-terminal kinase and its extracellular exposure during cell death - Kang_2002_Free.Radic.Biol.Med_32_1017
Author(s) : Kang KW , Novak RF , Lee CH , Kim SG
Ref : Free Radic Biol Med , 32 :1017 , 2002
Abstract : Microsomal epoxide hydrolase (mEH), an epoxide detoxifying enzyme and putative cell surface autoantigen, is inducible by xenobiotics and by certain pathophysiological conditions (e.g., tumorigenesis and protein-calorie malnutrition). The present study was designed to determine mEH expression in H4IIE cells during cell death initiated by sulfur amino acid deprivation (SAAD) and to identify the signaling pathway for the enzyme induction. SAAD induced cell death at 48-72 h with translocation of Bax to mitochondria and increased mitochondrial permeability with cytochrome c release, both of which were prevented by SB203580 or by dominant-negative JNK1 [JNK1(-)] stable transfection. Caspase-3 activity was only marginally increased by SAAD. Neither genomic DNA fragmentation nor poly(ADP-ribose) polymerase cleavage was observed during SAAD-induced cell death. Thus, SAAD induced cell death independent of caspase activation. This was supported by the observation that benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a general caspase inhibitor, did not prevent cell death. The levels of mEH mRNA and protein were notably increased in cells under SAAD for 48-72 h. The induction of mEH occurred in parallel with cell death. Whereas SAAD-induced cell death resulted from both JNK1 and p38 kinase activation, mEH induction was decreased only by JNK1(-) transfection. Immunocytochemistry revealed that mEH protein was intensely stained in dying cells, cellular fragments and cell debris. Furthermore, the number of cells positive for surface mEH substantially increased by SAAD, as evidenced by flow cytometry analysis. These results demonstrated that SAAD induced nonapoptotic cell death with Bax translocation to mitochondria and mitochondrial cytochrome c release, but not through caspase-3 activation, and that mEH was induced by SAAD via the pathway of JNK1, but not ERK1/2 or p38 kinase, in parallel with cell death.
ESTHER : Kang_2002_Free.Radic.Biol.Med_32_1017
PubMedSearch : Kang_2002_Free.Radic.Biol.Med_32_1017
PubMedID: 12008117

Title : Spectral changes in systemic arterial pressure signals during acute mevinphos intoxication in the rat - Yen_2001_Shock_15_35
Author(s) : Yen DH , Yen JC , Len WB , Wang LM , Lee CH , Chan SH
Ref : Shock , 15 :35 , 2001
Abstract : We investigated the cardiovascular consequences of acute intoxication by the organophosphate poison, mevinphos (Mev), and delineated the underlying mechanism. Based on on-line power spectral analysis of systemic arterial pressure (SAP) signals in rats anesthetized and maintained by propofol, we identified two distinct phases after intravenous administration of Mev (160 or 320 microg/kg). Phase I was characterized by transient hypertension and mild tachycardia, concurrent with an increase in the very high-frequency (BVHF; 5-9 Hz), high-frequency (BHF; 0.8-2.4 Hz), low-frequency (BLF; 0.25-0.8 Hz),and very low-frequency (BVLF; 0-0.25 Hz) components of SAP signals. Phase II exhibited significant hypotension, a reversal of the BVHF and BVLF power to control levels, and further reduction in the power density of both BHF and BLF components to below baseline. Microinjection of Mev (2 microg) into the bilateral nucleus reticularis ventrolateralis (NRVL), the medullary origin of sympathetic neurogenic vasomotor tone, essentially duplicated those phasic cardiovascular changes. Similarly, sympathoexcitatory NRVL neurons exhibited respectively an elevation and a decline in their spontaneous activities during Phase I and Phase II Mev intoxication. We conclude that the progressive accumulation of acetylcholine over time induced by a direct inhibition of Mev on cholinesterase in the NRVL may be responsible for the phasic changes in cardiovascular events over the course of acute Mev intoxication. Whereas the initial amount of acetylcholine is excitatory to NRVL neurons, overstimulation by the amassed acetylcholine results instead of an inhibitory action.
ESTHER : Yen_2001_Shock_15_35
PubMedSearch : Yen_2001_Shock_15_35
PubMedID: 11198355

Title : A Pseudomonas stutzeri gene cluster encoding the biosynthesis of the CCl4-dechlorination agent pyridine-2,6-bis(thiocarboxylic acid) - Lewis_2000_Environ.Microbiol_2_407
Author(s) : Lewis TA , Cortese MS , Sebat JL , Green TL , Lee CH , Crawford RL
Ref : Environ Microbiol , 2 :407 , 2000
Abstract : A spontaneous mutant of Pseudomonas stutzeri strain KC lacked the carbon tetrachloride (CCl4) transformation ability of wild-type KC. Analysis of restriction digests separated by pulsed-field gel electrophoresis (PFGE) indicated that the mutant strain CTN1 differed from strain KC by deletion of approximately 170 kb of chromosomal DNA. CTN1 did not produce pyridine-2,6-bis(thiocarboxylic acid) (PDTC), the agent determined to be responsible for CCl4 dechlorination in cultures of strain KC. Cosmids from a genomic library of strain KC containing DNA from within the deleted region were identified by hybridization with a 148 kb genomic Spel fragment absent in strain CTN1. Several cosmids identified in this manner were further screened for complementation of the PDTC biosynthesis-negative (Pdt -) phenotype. One cosmid (pT31) complemented the Pdt- phenotype of CTN1 and conferred CCl4 transformation activity and PDTC production upon other pseudomonads. Southern analysis showed that none of three other P. stutzeri strains representing three genomovars contained DNA that would hybridize with the 25,746 bp insert of pT31. Transposon mutagenesis of pT31 identified open reading frames (ORFs) whose disruption affected the ability to make PDTC in the strain CTN1 background. These data describe the pdt locus of strain KC as residing in a non-essential region of the chromosome subject to spontaneous deletion. The pdt locus is necessary for PDTC biosynthesis in strain KC and is sufficient for PDTC biosynthesis by other pseudomonads but is not a common feature of P. stutzeri strains.
ESTHER : Lewis_2000_Environ.Microbiol_2_407
PubMedSearch : Lewis_2000_Environ.Microbiol_2_407
PubMedID: 11234929
Gene_locus related to this paper: psest-PDTORFB

Title : Spectral analysis of systemic arterial pressure and heart rate signals of patients with acute respiratory failure induced by severe organophosphate poisoning - Yen_2000_Crit.Care.Med_28_2805
Author(s) : Yen DH , Yien HW , Wang LM , Lee CH , Chan SH
Ref : Critical Care Medicine , 28 :2805 , 2000
Abstract : OBJECTIVE: Spectral analysis of systemic arterial pressure (BP) and heart rate (HR) signals may be an alternative prognostic tool for predicting patient outcome in the intensive care unit (ICU). We evaluated the applicability of the same analysis in the emergency department for predicting mortality in patients with acute respiratory failure induced by severe organophosphate poisoning. DESIGN: Prospective collection of data from 14 emergency service patients. SETTING: Emergency service at a large, university-affiliated medical center. PATIENTS: Consecutive patients who, after attempting suicide by ingesting organophosphates, were admitted to the ICU of the emergency service with acute respiratory failure and remained for > or =2 days INTERVENTIONS: None. MEASUREMENTS AND MAIN
RESULTS: Demographic and survival data and day 1 Acute Physiology and Chronic Health Evaluation (APACHE) II and Glasgow Coma Scale scores were recorded. Continuous, on-line, real-time spectral analysis of BP and HR signals was carried out during the first 12 hrs after admission. We then computed the total sum of power density during this period of the low-frequency (0.04-0.15 Hz) and very low-frequency (0.004-0.04 Hz) components in the BP and HR spectra, along with the averaged values of mean BP and HR. Eight patients who recovered exhibited vigorous power in the low-frequency and very low-frequency components of their BP and HR signals. There was a significant reduction in the power density of those four spectral components in three patients who eventually died. Three patients discharged in a vegetative state manifested significantly reduced power in the low-frequency component in their BP spectra, with maintained power in the other three spectral components. APACHE II and Glasgow Coma Scale scores of the recovered patients were discernibly different from those of patients who eventually died or who became vegetative. None of the 14 patients showed appreciable differences in mean BP, mean HR, erythrocyte or plasma cholinesterase concentration, or atropine requirement during the first 24 hrs. CONCLUSION: The low-frequency and very low-frequency components of BP and HR signals may be a sensitive alternative index for early prediction of mortality in patients with acute respiratory failure induced by severe organophosphate poisoning.
ESTHER : Yen_2000_Crit.Care.Med_28_2805
PubMedSearch : Yen_2000_Crit.Care.Med_28_2805
PubMedID: 10966254