Elucidating the Temporal Patterns of Gene Expression in the Inferred Regulatory Interactions of GmCOL1b in Glycine max.

The CONSTANS ( CO ) gene in Arabidopsis thaliana has a central role in photoperiodic regulation of flowering. However, the roles of CO genes in mediating flowering in soybeans ( Glycine max ) remain uncertain. We previously inferred regulatory interactions of a soybean CO homolog, GmCOL1b , using in-house RNA-seq data and the network inference algorithm package CausNet. Here, we identify potential GmCOL1b downstream genes and experimentally verify them by expressing GmCOL1b in soybean protoplast cells. Temporal expression patterns of these genes indicate the regulatory effects of GmCOL1b on the expression of the circadian clock genes GmLCL1 and GmLCL4 and the flowering regulator GmTEM1a .

Clarifying the Temporal Dynamics of the Circadian Clock and Flowering Gene Network Using Overexpression and Targeted Mutagenesis of Soybean EARLY FLOWERING 3-1 ( GmELF3-1 ).

With progressing climate fluctuations, an understanding of the molecular mechanisms of crop plants that regulate their flowering responses to environments is crucial. To achieve this goal, we aimed at clarifying the gene regulatory networks among the circadian clock and flowering genes in soybean ( Glycine max ). Based on our network inference approach , we hypothesize that GmELF3-1 , one of the Evening Complex (EC) gene homologs in soybean's circadian clock, may have an integrative role in transcriptional regulation of the circadian clock and flowering gene network. In this study, we verify GmELF3-1 ' s regulatory roles in its potential downstream genes by modulating the activity of GmELF3-1 using overexpression and CRISPR-Cas9 in soybean protoplasts. Our results indicate that GmELF3-1 may control the expression of the PRR genes in the circadian clock and the flowering gene GmCOL1a .

Opposite Surface and Bulk Solvatochromic Effects in a Molecular Spin-Crossover Compound Revealed by Ambient Pressure X-ray Absorption Spectroscopy.

We investigate the solvatochromic effect of a Fe-based spin-crossover (SCO) compound via ambient pressure soft X-ray absorption spectroscopy (AP-XAS) and atomic force microscopy (AFM). AP-XAS provides the direct evidence of the spin configuration for the Fe(II) 3d states of the SCO material upon in situ exposure to specific gas or vapor mixtures; concurrent changes in nanoscale topography and mechanical characteristics are revealed via AFM imaging and AFM-based force spectroscopy, respectively. We find that exposing the SCO material to gaseous helium promotes an effective decrease of the transition temperature of its surface layers, while the exposure to methanol vapor causes opposite surfacial and bulk solvatochromic effects. Surfacial solvatochromism is accompanied by a dramatic reduction of the surface layers stiffness. We propose a rationalization of the observed effects based on interfacial dehydration and solvation phenomena.

Evaluation of the efficiency under current use of human fibrinogen concentrate in trauma patients with life-threatening hemorrhagic disorders.

The aim of the study was to assess the influence of fibrinogen concentrate on survival when it is used in trauma patients with life-threatening hemorrhagic disorders. Secondly, to evaluate when the fibrinogen concentrate administration maximizes its efficacy, and to describe what other concomitant treatment the patients received in order to control their life-threatening hemorrhage. Retrospective, observational, and multicenter study was carried out in three trauma areas between June 2012 and June 2014. The totality of trauma patients with a documented life-threatening hemorrhage who received a fibrinogen concentrate prescription was included in the study. Demographic and analytical data, admission diagnosis, treatment indication, fibrinogen concentrate dose, survival after 1 and 7 days, hospitalization time, and concomitant blood product treatment were collected. One hundred and twenty-three patients were finally included. The mean dose of fibrinogen concentrate administered was 2.87 g. The mean initial fibrinogen plasma level was 1.49 g/l, which rose to 2.26 g/l. The number of patients who survived after 24 h was 80.49%, and 69.11% after 7 days. Lower fibrinogen plasma levels are statistically associated with a higher probability of death after 7 days (P = 0.004). The most suitable threshold to recommend the fibrinogen concentrate administration has been found to be 1.5 g/dl (P = 0006, after 24 h; P = 0.032, after 7 days). Finally, the most common concomitant treatment was the erythrocytes concentrate. A statistically significant relationship between lower fibrinogen plasma levels and a higher probability of death after 7 days has been found. Our data support the threshold of 1.5 g/l as the recommended level to administer fibrinogen concentrate in trauma patients.

Physiopathology and treatment of critical bleeding: a literature review.

OBJECTIVES: to develop the different factors involved in the physiopathology of trauma-induced coagulopathy, through a review of publications on the matter; as well as to assess the evidence available on the treatment of critical bleeding and the recommendations by clinical practice guidelines. METHODS: a search has been conducted on the bibliography published about the physiopathology and treatment of critical bleeding in the PUBMED, BestPractice, UpToDate databases and the Cochrane Plus Library. The main key words used for this search were "early trauma induced coagulopathy", "mechanisms of early trauma-induced coagulopathy", "blood transfusion guidelines", "massive transfusion guidelines" and "fibrinogen replacement therapy". The most clinically relevant articles were selected for this review. CONCLUSIONS: the physiopathology of the trauma-induced coagulopathy is a more complex matter and involves more factors than was initially assumed. The early treatment of the coagulopathy is critical for the initial management of the critical bleeding. However, the use of blood derivatives should be rational and based on homogeneous and high-quality scientific evidence. The main cornerstones for the treatment of critical bleeding are: fluid therapy, fibrinogen concentrate, prothrombin complex concentrate, plasma, erythrocyte or platelet concentrates, tranexamic acid, and calcium. Their administration should be assessed depending on the clinical condition of each patient.

Objetivos: desarrollar los factores implicados en la fisiopatología de la coagulopatía asociada al traumatismo (CAT) mediante una revisión de la literatura publicada al respecto; además de revisar la evidencia disponible sobre el tratamiento de la hemorragia crítica y las recomendaciones de las guías de práctica clínica. Métodos: se ha realizado una búsqueda de la bibliografía publicada sobre la fisiopatología y tratamiento de la hemorragia crítica en las bases de datos PUBMED, BestPractice, UpToDate y la Biblioteca Cochrane Plus. Las principales palabras clave utilizadas para la búsqueda han sido: "early trauma induced coagulopathy", "mechanisms of early trauma-induced coagulopathy", "blood transfusión guidelines", "massive transfusion guidelines" y "fibrinogen replacement therapy". Los artículos más clínicamente relevantes han sido seleccionados para la revisión. Conclusiones: la fisiopatología de la coagulopatía asociada al traumatismo se trata de un cuadro más complejo y multifactorial de lo que inicialmente se había aceptado. El tratamiento precoz de la coagulopatía es imprescindible para el manejo inicial de la hemorragia crítica. No obstante, el uso de hemoderivados debería ser racional y basado en una evidencia científica homogénea y de alta calidad. Los principales pilares del tratamiento de la hemorragia crítica son la fluidoterapia, el concentrado de fibrinógeno, el concentrado de complejo protrombínico, el plasma, los concentrados de hematíes o de plaquetas, el ácido tranexámico y el calcio. Su administración debería valorarse en función de las condiciones clínicas de cada paciente.

Physiopathology and treatment of critical bleeding: a literature review / Fisiopatología y tratamiento de la hemorragia crítica: una revisión de la literatura

Objectives: to develop the different factors involved in the physiopathology of trauma-induced coagulopathy, through a review of publications on the matter; as well as to assess the evidence available on the treatment of critical bleeding and the recommendations by clinical practice guidelines. Methods: a search has been conducted on the bibliography published about the physiopathology and treatment of critical bleeding in the PUBMED, BestPractice, UpToDate databases and the Cochrane Plus Library. The main key words used for this search were 'early trauma induced coagulopathy', 'mechanisms of early trauma-induced coagulopathy', 'blood transfusion guidelines', 'massive transfusion guidelines' and 'fibrinogen replacement therapy'. The most clinically relevant articles were selected for this review. Conclusions: the physiopathology of the trauma-induced coagulopathy is a more complex matter and involves more factors than was initially assumed. The early treatment of the coagulopathy is critical for the initial management of the critical bleeding. However, the use of blood derivatives should be rational and based on homogeneous and high-quality scientific evidence. The main cornerstones for the treatment of critical bleeding are: fluid therapy, fibrinogen concentrate, prothrombin complex concentrate, plasma, erythrocyte or platelet concentrates, tranexamic acid, and calcium. Their administration should be assessed depending on the clinical condition of each patient (AU)

Objetivos: desarrollar los factores implicados en la fisiopatología de la coagulopatía asociada al traumatismo (CAT) mediante una revisión de la literatura publicada al respecto; además de revisar la evidencia disponible sobre el tratamiento de la hemorragia crítica y las recomendaciones de las guías de práctica clínica. Métodos: se ha realizado una búsqueda de la bibliografía publicada sobre la fisiopatología y tratamiento de la hemorragia crítica en las bases de datos PUBMED, BestPractice, UpToDate y la Biblioteca Cochrane Plus. Las principales palabras clave utilizadas para la búsqueda han sido: 'early trauma induced coagulopathy', 'mechanisms of early trauma-induced coagulopathy', 'blood transfusión guidelines', 'massive transfusion guidelines' y 'fibrinogen replacement therapy'. Los artículos más clínicamente relevantes han sido seleccionados para la revisión. Conclusiones: la fisiopatología de la coagulopatía asociada al traumatismo se trata de un cuadro más complejo y multifactorial de lo que inicialmente se había aceptado. El tratamiento precoz de la coagulopatía es imprescindible para el manejo inicial de la hemorragia crítica. No obstante, el uso de hemoderivados debería ser racional y basado en una evidencia científica homogénea y de alta calidad. Los principales pilares del tratamiento de la hemorragia crítica son la fluidoterapia, el concentrado de fibrinógeno, el concentrado de complejo protrombínico, el plasma, los concentrados de hematíes o de plaquetas, el ácido tranexámico y el calcio. Su administración debería valorarse en función de las condiciones clínicas de cada paciente (AU)