RESUMEN
Gonadotropin-releasing hormone agonist (GnRHa) therapy is used to control puberty progression and it preserves height potential in patients with idiopathic central precocious puberty (ICPP). This study evaluated the correlation between weight and height gain at menarche following GnRHa treatment among girls with ICPP and relatively central early puberty (EP). We investigated height/weight trends and changes in height from diagnosis to menarche in girls with ICPP and EP treated with GnRHa. The mean difference in height (Δheight) from treatment cessation to menarche was 9.79 ± 3.53 cm. Girls were divided into girls with Δheight ≥ 9.79 cm (Group 1) and girls with Δheight < 9.79 cm (Group 2). Although near adult height was significantly higher in Group 1, the mean body mass index (BMI) and weight were significantly lower at diagnosis, treatment discontinuation, and menarche. The BMI and weight at the three time points were negatively correlated with height. Girls with higher BMI at all three time points had slower growth rates during the study period. Considering that BMI and body weight were closely related to Δheight, proper management of BMI and body weight of girls receiving early puberty treatment might contribute to growth during and after GnRHa treatment.
RESUMEN
Myxococcus xanthus, a myxobacterium, displays phase variation between yellow phase and tan phase. We found that deletion of the encA gene encoding encapsulin and the encF gene encoding a metalloprotease causes formation of tan colonies that never transform into yellow colonies. The encA and encF mutants were defective in the production of DK-xanthene and myxovirescin. They did not produce extracellular polysaccharides; hence, the cells did not aggregate in liquid and showed reduced swarming on agar plates. The mutants had defective sporulation, but were rescued extracellularly by wild type cells. All these traits indicate that the encA and encF mutants are likely to be tan-phase-locked, and encapsulin has a close relationship with phase variation in M. xanthus. The encA and encF genes are localized in the same gene cluster, encBAEFG (MXAN_3557~MXAN_3553). Unlike the encA and encF genes, deletion of other genes in the cluster did not show tan-phase-locked phenotype.
Asunto(s)
Proteínas Bacterianas/metabolismo , Myxococcus xanthus/crecimiento & desarrollo , Myxococcus xanthus/genética , Proteínas Bacterianas/genética , Color , Eliminación de Gen , Macrólidos/metabolismo , Metaloproteasas/genética , Metaloproteasas/metabolismo , Mutación , Myxococcus xanthus/metabolismo , Fenotipo , Polisacáridos Bacterianos/biosíntesis , Xantenos/metabolismoRESUMEN
The measurement of oxygen consumption rate (OCR) provides a comprehensive understanding of mitochondrial metabolism. However, no study has been conducted to investigate the mitochondrial dysfunction caused by organophosphate flame retardants (OPFRs). The objectives of this study were to optimize the experimental conditions to measure OCR in zebrafish embryos using the Seahorse XFe 24 Extracellular Flux Analyzer, and to investigate the changes of OCR in zebrafish embryos exposed to OPFRs. We first optimized the experimental conditions such as the number of embryos, concentrations of inhibitors, and time points. We determined the factors, i.e., three embryos, 12.5⯵M of oligomycin, 8⯵M of carbonyl cyanaide 4-(trifluoromethoxy) phenylhydrazone (FCCP), and 24 hpf (hours post-fertilization) time point, for obtaining the typical pattern of OCR in dechorinated zebrafish embryos. After confirming the determinants upon exposure of triclosan, the inhibition of OCR was measured in zebrafish embryos exposed to two major OPFRs, triphenyl phosphate (TPHP) and tris (1,3-dichloro-2-propyl) phosphate (TDCIPP). We found that significant inhibition of OCR was observed in basal respiration for TPHP, and in basal and maximal respiration for TDCIPP exposure, respectively. We suggest the optimum conditions of the Seahorse XFe 24 analyzer to better evaluate OCR in zebrafish embryos, and demonstrate the potential of TPHP and TDCIPP to cause the disruption of energy metabolism associated with mitochondrial dysfunction.
Asunto(s)
Embrión no Mamífero/efectos de los fármacos , Retardadores de Llama/toxicidad , Organofosfatos/toxicidad , Consumo de Oxígeno/efectos de los fármacos , Pez Cebra/metabolismo , Animales , Embrión no Mamífero/metabolismo , Desarrollo Embrionario/efectos de los fármacos , Metabolismo Energético/efectos de los fármacos , Modelos TeóricosRESUMEN
DKxanthenes are a class of yellow secondary metabolites produced by myxobacterial genera Myxococcus and Stigmatella. We identified a putative 49.5 kb DKxanthene biosynthetic gene cluster from Myxococcus stipitatus DSM 14675 by genomic sequence and mutational analysis. The cluster was comprisedof 15 genes (MYSTI_06004-MYSTI_06018) encoding polyketide synthases, non-ribosomal peptide synthases, and proteins with unknown functions. Disruption of the genes by plasmid insertion resulted in defects in the production of yellow pigments. High-performance liquid chromatography and liquid chromatography-tandem mass spectrometry analysis indicated that the yellow pigments produced by M. stipitatus DSM 14675 might be noble DKxanthene derivatives. M. stipitatus did not require DKxanthenes for the formation of heat-resistant viable spores, unlike Myxococcus xanthus. Furthermore, DKxanthenes showed growth inhibitory activity against the fungi Aspergillus niger, Candida albicans, and Rhizopus stolonifer.
Asunto(s)
Vías Biosintéticas/genética , Familia de Multigenes/genética , Myxococcus/enzimología , Myxococcus/genética , Myxococcus/metabolismo , Xantenos/metabolismo , Xantenos/farmacología , Antiinfecciosos/química , Antiinfecciosos/metabolismo , Antiinfecciosos/farmacología , Aspergillus niger/efectos de los fármacos , Aspergillus niger/crecimiento & desarrollo , Proteínas Bacterianas/genética , Candida albicans/efectos de los fármacos , Candida albicans/crecimiento & desarrollo , Cuerpos Fructíferos de los Hongos/efectos de los fármacos , Genes Bacterianos/genética , Mutación , Myxococcus xanthus/metabolismo , Péptido Sintasas/genética , Pigmentos Biológicos/genética , Pigmentos Biológicos/metabolismo , Plásmidos/genética , Sintasas Poliquetidas/genética , Rhizopus/efectos de los fármacos , Rhizopus/crecimiento & desarrollo , Metabolismo Secundario/genética , Análisis de Secuencia , Esporas/efectos de los fármacos , Xantenos/químicaRESUMEN
Herein, we report the pathogenic and phylogenetic characteristics of seven Shiga toxin (Stx)-producing Escherichia coli (STEC) isolates from 434 retail meats collected in Korea during 2006 to 2012. The experimental analyses revealed that all isolates (i) were identified as non-O157 STEC, including O91:H14 (3 isolates), O121:H10 (2 isolates), O91:H21 (1 isolate), and O18:H20 (1 isolate), (ii) carried diverse Stx subtype genes (stx1, stx2c, stx2e, or stx1 + stx2b) whose expression levels varied strain by strain, and (iii) lacked the locus of enterocyte effacement (LEE) pathogenicity island, a major virulence factor of STEC, but they possessed one or more alternative virulence genes encoding cytotoxins (Cdt and SubAB) and/or adhesins (Saa, Iha, and EcpA). Notably, a significant heterogeneity in glutamate-induced acid resistance was observed among the STEC isolates (p ï¼ 0.05). In addition, phylogenetic analyses demonstrated that all three STEC O91:H14 isolates were categorized into sequence type (ST) 33, of which two beef isolates were identical in their pulsotypes. Similar results were observed with two O121:H10 pork isolates (ST641; 88.2% similarity). Interestingly, 96.0% of the 100 human STEC isolates collected in Korea during 2003 to 2014 were serotyped as O91:H14, and the ST33 lineage was confirmed in approximately 72.2% (13/18 isolates) of human STEC O91:H14 isolates from diarrheal patients.
Asunto(s)
Escherichia coli O157/genética , Carne Roja/microbiología , Escherichia coli Shiga-Toxigénica/genética , Animales , Western Blotting , Bovinos , Electroforesis en Gel de Campo Pulsado , Escherichia coli O157/aislamiento & purificación , Escherichia coli O157/patogenicidad , Pruebas de Fijación de Látex , Tipificación de Secuencias Multilocus , Filogenia , República de Corea , Escherichia coli Shiga-Toxigénica/aislamiento & purificación , Escherichia coli Shiga-Toxigénica/patogenicidad , PorcinosRESUMEN
We report here a new virulent Salmonella enterica serovar Typhimurium (S Typhimurium) bacteriophage, GG32, which was isolated from the Guem River in the Republic of Korea. The strain can infect both S Typhimurium and Escherichia coli (E. coli) O157:H7 and may be a good candidate for a bio-control agent.
RESUMEN
Here, we announce the complete genome sequence of Salmonella enterica serovar Enteritidis (S Enteritidis) bacteriophage MA12, a 41-Kb chromosome. The strain can infect both Campylobacter jejuni (C. jejuni) and S Enteritidis and can be used in phage therapy experiments with poultry and poultry meat.
RESUMEN
INTRODUCTION: Despite the crucial role of endothelial progenitor cells (EPCs) in vascular regeneration, the specific interactions between EPCs and hematopoietic cells remain unclear. METHODS: In EPC colony forming assays, we first demonstrated that the formation of EPC colonies was drastically increased in the coculture of CD34+ and CD34- cells, and determined the optimal concentrations of CD34+ cells and CD34- cells for spindle-shaped EPC differentiation. RESULTS: Functionally, the coculture of CD34+ and CD34- cells resulted in a significant enhancement of adhesion, tube formation, and migration capacity compared with culture of CD34+ cells alone. Furthermore, blood flow recovery and capillary formation were remarkably increased by the coculture of CD34+ and CD34- cells in a murine hind-limb ischemia model. To elucidate further the role of hematopoietic cells in EPC differentiation, we isolated different populations of hematopoietic cells. T lymphocytes (CD3+) markedly accelerated the early EPC status of CD34+ cells, while macrophages (CD11b+) or megakaryocytes (CD41+) specifically promoted large EPC colonies. CONCLUSION: Our results suggest that specific populations of hematopoietic cells play a role in the EPC differentiation of CD34+ cells, a finding that may aid in the development of a novel cell therapy strategy to overcome the quantitative and qualitative limitations of EPC therapy.
Asunto(s)
Antígenos CD34/metabolismo , Células Progenitoras Endoteliales/fisiología , Sangre Fetal/citología , Miembro Posterior/irrigación sanguínea , Isquemia/terapia , Animales , Diferenciación Celular , Células Cultivadas , Técnicas de Cocultivo , Trasplante de Células Madre de Sangre del Cordón Umbilical , Modelos Animales de Enfermedad , Células Progenitoras Endoteliales/citología , Sangre Fetal/metabolismo , Células Endoteliales de la Vena Umbilical Humana , Humanos , Masculino , Ratones , Ratones Endogámicos BALB CRESUMEN
Cell fate decisions during embryogenesis and adult life govern tissue formation, homeostasis and repair. Two key decisions that must be tightly coordinated are proliferation and differentiation. Overproliferation can lead to hyperplasia or tumor formation while premature differentiation can result in a depletion of proliferating cells and organ failure. Maintaining this balance is especially important in tissues that undergo rapid turnover like skin however, despite recent advances, the genetic mechanisms that balance cell differentiation and proliferation are still unclear. In an unbiased genetic screen to identify genes affecting early development, we identified an essential regulator of the proliferation-differentiation balance in epidermal progenitor cells, the Keratinocyte differentiation factor 1 (Kdf1; 1810019J16Rik) gene. Kdf1 is expressed in epidermal cells from early stages of epidermis formation through adulthood. Specifically, Kdf1 is expressed both in epidermal progenitor cells where it acts to curb the rate of proliferation as well as in their progeny where it is required to block proliferation and promote differentiation. Consequently, Kdf1 mutants display both uncontrolled cell proliferation in the epidermis and failure to develop terminal fates. Our findings reveal a dual role for the novel gene Kdf1 both as a repressive signal for progenitor cell proliferation through its inhibition of p63 and a strong inductive signal for terminal differentiation through its interaction with the cell cycle regulator Stratifin.
Asunto(s)
Diferenciación Celular , Epidermis/patología , Proteínas/metabolismo , Células Madre/metabolismo , Proteínas 14-3-3/metabolismo , Alelos , Animales , Secuencia de Bases , Diferenciación Celular/genética , Proliferación Celular , Fisura del Paladar/embriología , Fisura del Paladar/genética , Fisura del Paladar/patología , Pérdida del Embrión/genética , Pérdida del Embrión/patología , Epidermis/metabolismo , Femenino , Regulación del Desarrollo de la Expresión Génica , Genes Recesivos/genética , Prueba de Complementación Genética , Heterocigoto , Queratinocitos/metabolismo , Queratinocitos/patología , Masculino , Ratones , Ratones Endogámicos C57BL , Datos de Secuencia Molecular , Fenotipo , Fosfoproteínas/metabolismo , Mutación Puntual/genética , Unión Proteica , Proteínas/genética , Empalme del ARN/genética , Transactivadores/metabolismoRESUMEN
Sunsik, a ready-to-eat food in Korea, is comprised of various agricultural and marine products, and has been an important concern in Bacillus cereus food poisoning. The aim of this study was to investigate the toxin profiles, genotypic and phenotypic patterns as well as antibiotic resistance of B. cereus strains isolated from Sunsik. A subtyping method known as automated repetitive sequence-based PCR system (DiversiLab™) was used to assess the intraspecific biodiversity of these isolates. Thirty-five B. cereus strains were isolated from 100 commercial Sunsik samples, all of which harbored at least 1 enterotoxin gene. The detection rates of nheABC, hblCDA, cytK, and entFM enterotoxin gene among all isolates were 97%, 86%, 77%, and 100%, respectively. Most strains also produced corresponding enterotoxins such as HBL (83%) and NHE (94%). One strain (2.9%) carried the emetic toxin genes, including ces and EM1, and was positive for the HEp-2 cell emetic toxin assay. Most strains were positive for various biochemical tests such as salicin hydrolysis (86%), starch fermentation (89%), hemolysis (89%), motility test (100%) and lecithinase hydrolysis (89%). All isolates were susceptible to most antibiotics although they were highly resistant to ß-lactam antibiotics. By using the automated rep-PCR system, all isolates were successfully differentiated, indicating the diversity of B. cereus strains present in Sunsik.
Asunto(s)
Antibacterianos/farmacología , Bacillus cereus/efectos de los fármacos , Bacillus cereus/aislamiento & purificación , Toxinas Bacterianas/metabolismo , Farmacorresistencia Bacteriana , Microbiología de Alimentos , Bacillus cereus/crecimiento & desarrollo , Bacillus cereus/metabolismo , Proteínas Bacterianas/genética , Proteínas Bacterianas/metabolismo , Toxinas Bacterianas/toxicidad , Contaminación de Alimentos/análisis , Células Hep G2 , Humanos , Fenotipo , República de CoreaRESUMEN
arl13b was initially cloned as the novel cystic kidney gene scorpion (sco) in zebrafish and was shown to be required for cilia formation in the kidney duct. In mouse, a null mutant of Arl13b shows abnormal ultrastructure of the cilium and defective sonic hedgehog (Shh) signaling. Importantly, a recent study linked mutations in ARL13B to a classical form of Joubert syndrome (JS), an autosomal recessive disorder characterized by a distinctive cerebellar malformation. In this study, we analyzed the zebrafish arl13b (sco) mutant and gene products in detail. We first demonstrate that Arl13b is a protein that is highly enriched in the cilium and is required for cilia formation in multiple organs in zebrafish, and that knockdown of arl13b leads to multiple cilia-associated phenotypes. We additionally show that multiple regions of Arl13b are required for its localization to the cilium. By means of rescuing experiments with a series of deletion and point mutants, we further demonstrate that the ciliary localization is crucial for the in vivo function of Arl13b. Together, these results strongly support the hypothesis that JS-related disease (JSRD) is a ciliopathy, or a disease caused by ciliary defects, and that Arl13b functions mainly through the cilium.
Asunto(s)
Cilios/metabolismo , Proteínas de Pez Cebra/genética , Proteínas de Pez Cebra/metabolismo , Factores de Ribosilacion-ADP/genética , Factores de Ribosilacion-ADP/metabolismo , Alelos , Animales , Cilios/genética , Cilios/ultraestructura , Embrión no Mamífero/ultraestructura , Eliminación de Gen , Genes Recesivos , Humanos , Inmunohistoquímica , Hibridación in Situ , Enfermedades Renales Quísticas/genética , Enfermedades Renales Quísticas/metabolismo , Mutación , Mutación Puntual , Síndrome , Pez Cebra/genética , Pez Cebra/metabolismoRESUMEN
Chlamydophila pneumoniae is a Gram-negative intracellular obligate human pathogen and accounts for 5-10% of cases of community-acquired pneumonia. However, isolating and culturing this pathogen is difficult, so there have been several studies searching for new biomarkers for its diagnosis. In this study, we obtained immunogenic proteins of C. pneumoniae KNIH-1 for diagnosis using immunoproteomics. C. pneumoniae infection sera were selected for the highest index value of C. pneumoniae-specific IgG using microimmunofluorescence (MIF). The detected protein spots in common from C. pneumoniae infection sera using proteome analysis were identified as Omp11, type III secretion system ATPase, and PmpG by LC-MS/MS and MS databases. They were selected as candidate antigens. In addition, using in silico prediction we also identified proteins encoded by Omp11, PmpG and IncA as antigens. And then, IncA acts as an effector by a type III secretion system ATPase, as identified by mass spectrometry, and was selected as a candidate antigen. Thus, we predict proteins encoded by Omp11, the PmpG family and by IncA as candidate diagnostic immunogens.