Variability of global net sea–air CO₂ fluxes over the last three decades using empirical relationships

PARK, GEUN‐,HA,WANNINKHOF, RIK,DONEY, SCOTT C.,TAKAHASHI, TARO,LEE, KITACK,FEELY, RICHARD A.,SABINE, CHRISTOPHER L.,TRIÑ,ANES, JOAQUIN,LIMA, IVAN D. Blackwell Publishing Ltd 2010 Tellus. Series B, Chemical and physical meteorolog Vol.62 No.5

<P><B>ABSTRACT</B></P><P>The interannual variability of net sea–air CO<SUB>2</SUB> flux for the period 1982–2007 is obtained from a diagnostic model using empirical subannual relationships between climatological CO<SUB>2</SUB> partial pressure in surface seawater (<I>p</I>CO<SUB>2SW</SUB>) and sea surface temperature (SST), along with interannual changes in SST and wind speed. These optimum subannual relationships show significantly better correlation between <I>p</I>CO<SUB>2SW</SUB> and SST than the previous relationships using fixed monthly boundaries. Our diagnostic model yields an interannual variability of ±0.14 PgC yr<SUP>−1</SUP> (1σ) with a 26‐year mean of −1.48 PgC yr<SUP>−1</SUP>. The greatest interannual variability is found in the Equatorial Pacific, and significant variability is also found at northern and southern high‐latitudes, depending in part, on which wind product is used. We provide an assessment of our approach by applying it to <I>p</I>CO<SUB>2SW</SUB> and SST output from a prognostic global biogeochemical ocean model. Our diagnostic approach applied to this model output shows reasonable agreement with the prognostic model net sea–air CO<SUB>2</SUB> fluxes in terms of magnitude and phase of variability, suggesting that our diagnostic approach can capture much of the observed variability on regional to global scale. A notable exception is that our approach shows significantly less variability than the prognostic model in the Southern Ocean.</P>

Artificial intelligence-based heritage tree disease diagnosis using transfer learning: A case study of Zelkova serrata

Sabin Lee,Bogyeom Park,Daejung Kim,Kyoungwon Seo 한국HCI학회 2024 한국HCI학회 학술대회 Vol.2024 No.1

Heritage trees are highly valued and protected by national laws because of their cultural and historical significance. However, due to the financial and time constraints associated with the continuous monitoring of the heritage trees, unnecessary losses are reported annually. As a solution, this study suggests an artificial intelligence(AI)-based heritage tree disease diagnosis system on Zelkova serrata. We have compared several state-of-the-art deep learning models with transfer learning on the Zelkova Serrata Dataset which consists of 680 images. All models achieved outstanding classification results even only using pre-trained weights of ImageNet, with F1 scores ranging from 92.00% to 96.26%. Particularly when additionally leveraging the plant disease datasets, model performances improved to a range of 93.78% to 99.45%. Through this research, we proposed the concept of AI-based heritage tree disease diagnosis using transfer learning. This system is expected to reduce the aforementioned financial and time constraints.

Evaluating the Sensitivity of <i>Mycobacterium tuberculosis</i> to Biotin Deprivation Using Regulated Gene Expression

Woong Park, Sae,Klotzsche, Marcus,Wilson, Daniel J.,Boshoff, Helena I.,Eoh, Hyungjin,Manjunatha, Ujjini,Blumenthal, Antje,Rhee, Kyu,Barry III, Clifton E.,Aldrich, Courtney C.,Ehrt, Sabine,Schnappinger Public Library of Science 2011 PLoS pathogens Vol.7 No.9

<▼1><P>In the search for new drug targets, we evaluated the biotin synthetic pathway of <I>Mycobacterium tuberculosis (Mtb)</I> and constructed an <I>Mtb</I> mutant lacking the biotin biosynthetic enzyme 7,8-diaminopelargonic acid synthase, BioA. In biotin-free synthetic media, <I>ΔbioA</I> did not produce wild-type levels of biotinylated proteins, and therefore did not grow and lost viability. <I>ΔbioA</I> was also unable to establish infection in mice. Conditionally-regulated knockdown strains of <I>Mtb</I> similarly exhibited impaired bacterial growth and viability <I>in vitro</I> and in mice, irrespective of the timing of transcriptional silencing. Biochemical studies further showed that BioA activity has to be reduced by approximately 99% to prevent growth. These studies thus establish that <I>de novo</I> biotin synthesis is essential for <I>Mtb</I> to establish and maintain a chronic infection in a murine model of TB. Moreover, these studies provide an experimental strategy to systematically rank the <I>in vivo</I> value of potential drug targets in <I>Mtb</I> and other pathogens.</P></▼1><▼2><P><B>Author Summary</B></P><P>We evaluated the biotin synthetic pathway of <I>Mycobacterium tuberculosis</I> (<I>Mtb</I>) as a new drug target by first generating an <I>Mtb</I> deletion mutant, <I>ΔbioA</I>, in which the biotin biosynthetic enzyme 7,8-diaminopelargonic acid synthase (BioA) has been inactivated. This mutant grew in the presence of biotin or <I>des</I>-thiobiotin, but not with an intermediate of the biotin biosynthesis pathway that requires BioA to be converted into biotin. Without exogenous biotin or <I>des</I>-thiobiotin, <I>ΔbioA,</I> was unable to produce biotinylated proteins, which are required for the biosynthesis of fatty acids, and thus died in biotin-free media. Using a regulatable promoter and different ribosome binding sequences we next constructed tightly controlled TetON mutants, in which expression of BioA could be induced with tetracyclines, but was inhibited in their absence. Characterization of these mutants during infections demonstrated that <I>de novo</I> biotin synthesis is not only required to establish infections but also to maintain bacterial persistence. Inhibition of BioA or other enzymes of the biotin biosynthesis pathways could thus be used to kill <I>Mtb</I> during both acute and chronic infections. Biochemical and immunological analyses of different <I>Mtb</I> mutants indicate that drugs targeting BioA would have to inactive approximately 99% of its activity to be effective.</P></▼2>

Genomic characteristics of triple negative apocrine carcinoma: a comparison to triple negative breast cancer

Kim Ji-Yeon,Park Sabin,Cho Eun Yoon,Lee Jeong Eon,Jung Hae Hyun,Chae Byung Joo,Kim Seok Won,Nam Seok Jin,Cho Soo Youn,Park Yeon Hee,Ahn Jin Seok,Lee Semin,Im Young-Hyuck 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

Apocrine carcinoma is a rare breast cancer subtype. As such, the genomic characteristics of apocrine carcinoma with triple negative immunohistochemical results (TNAC), which has been treated as triple negative breast cancer (TNBC), have not been revealed. In this study, we evaluated the genomic characteristics of TNAC compared to TNBC with low Ki-67 (LK-TNBC). In the genetic analysis of 73 TNACs and 32 LK-TNBCs, the most frequently mutated driver gene in TNAC was TP53 (16/56, 28.6%), followed by PIK3CA (9/56, 16.1%), ZNF717 (8/56, 14.3%), and PIK3R1 (6/56, 10.71%). Mutational signature analysis showed enrichment of defective DNA mismatch repair (MMR)-related signatures (SBS6 and SBS21) and the SBS5 signature in TNAC, whereas an APOBEC activity-associated mutational signature (SBS13) was more prominent in LK-TNBC (Student’s t test, p < 0.05). In intrinsic subtyping, 38.4% of TNACs were classified as luminal A, 27.4% as luminal B, 26.0% as HER2-enriched (HER2-E), 2.7% as basal, and 5.5% as normal-like. The basal subtype was the most dominant subtype (43.8%) in LK-TNBC (p < 0.001), followed by luminal B (21.9%), HER2-E (21.9%), and luminal A (12.5%). In the survival analysis, TNAC had a five-year disease-free survival (DFS) rate of 92.2% compared to 59.1% for LK-TNBC (P = 0.001) and a five-year overall survival (OS) rate of 95.3% compared to 74.6% for LK-TNBC (P = 0.0099). TNAC has different genetic characteristics and better survival outcomes than LK-TNBC. In particular, normal-like and luminal A subtypes in TNAC have much better DFS and OS than other intrinsic subtypes. Our findings are expected to impact medical practice for patients diagnosed with TNAC.

Alterations in cardiac DNA methylation in human dilated cardiomyopathy

Haas, Jan,Frese, Karen S,Park, Yoon Jung,Keller, Andreas,Vogel, Britta,Lindroth, Anders M,Weichenhan, Dieter,Franke, Jennifer,Fischer, Simon,Bauer, Andrea,Marquart, Sabine,Sedaghat-Hamedani, Farbod,Ka WILEY-VCH Verlag 2013 EMBO molecular medicine Vol.5 No.3

<P>Dilated cardiomyopathies (DCM) show remarkable variability in their age of onset, phenotypic presentation, and clinical course. Hence, disease mechanisms must exist that modify the occurrence and progression of DCM, either by genetic or epigenetic factors that may interact with environmental stimuli. In the present study, we examined genome-wide cardiac DNA methylation in patients with idiopathic DCM and controls. We detected methylation differences in pathways related to heart disease, but also in genes with yet unknown function in DCM or heart failure, namely <I>Lymphocyte antigen 75</I> (<I>LY75</I>), <I>Tyrosine kinase-type cell surface receptor HER3</I> (<I>ERBB3</I>), <I>Homeobox B13</I> (<I>HOXB13</I>) and <I>Adenosine receptor A2A</I> (<I>ADORA2A</I>). Mass-spectrometric analysis and bisulphite-sequencing enabled confirmation of the observed DNA methylation changes in independent cohorts. Aberrant DNA methylation in DCM patients was associated with significant changes in <I>LY75</I> and <I>ADORA2A</I> mRNA expression, but not in <I>ERBB3</I> and <I>HOXB13</I>. <I>In vivo</I> studies of orthologous <I>ly75</I> and <I>adora2a</I> in zebrafish demonstrate a functional role of these genes in adaptive or maladaptive pathways in heart failure.</P>

Global relationships of total alkalinity with salinity and temperature in surface waters of the world's oceans

Lee, Kitack,Tong, Lan T.,Millero, Frank J.,Sabine, Christopher L.,Dickson, Andrew G.,Goyet, Catherine,Park, Geun-Ha,Wanninkhof, Rik,Feely, Richard A.,Key, Robert M. American Geophysical Union 2006 Geophysical research letters Vol.33 No.19

Biosynthesis and Recycling of Nicotinamide Cofactors in<i>Mycobacterium tuberculosis</i> : <i>AN ESSENTIAL ROLE FOR NAD IN NONREPLICATING BACILLI</i>

Boshoff, Helena I. M.,Xu, Xia,Tahlan, Kapil,Dowd, Cynthia S.,Pethe, Kevin,Camacho, Luis R.,Park, Tae-Ho,Yun, Chang-Soo,Schnappinger, Dirk,Ehrt, Sabine,Williams, Kerstin J.,Barry III, Clifton E. American Society for Biochemistry and Molecular Bi 2008 The Journal of biological chemistry Vol.283 No.28

<P>Despite the presence of genes that apparently encode NAD salvage-specific enzymes in its genome, it has been previously thought that Mycobacterium tuberculosis can only synthesize NAD de novo. Transcriptional analysis of the de novo synthesis and putative salvage pathway genes revealed an up-regulation of the salvage pathway genes in vivo and in vitro under conditions of hypoxia. [14C]Nicotinamide incorporation assays in M. tuberculosis isolated directly from the lungs of infected mice or from infected macrophages revealed that incorporation of exogenous nicotinamide was very efficient in in vivo-adapted cells, in contrast to cells grown aerobically in vitro. Two putative nicotinic acid phosphoribosyltransferases, PncB1 (Rv1330c) and PncB2 (Rv0573c), were examined by a combination of in vitro enzymatic activity assays and allelic exchange studies. These studies revealed that both play a role in cofactor salvage. Mutants in the de novo pathway died upon removal of exogenous nicotinamide during active replication in vitro. Cell death is induced by both cofactor starvation and disruption of cellular redox homeostasis as electron transport is impaired by limiting NAD. Inhibitors of NAD synthetase, an essential enzyme common to both recycling and de novo synthesis pathways, displayed the same bactericidal effect as sudden NAD starvation of the de novo pathway mutant in both actively growing and nonreplicating M. tuberculosis. These studies demonstrate the plasticity of the organism in maintaining NAD levels and establish that the two enzymes of the universal pathway are attractive chemotherapeutic targets for active as well as latent tuberculosis.</P>