scholarly journals A Comprehensive Evaluation of Flavor Instability of Beer (Part 1): Influence of Release of Bound State Aldehydes

Foods ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2432
Author(s):  
Florian Lehnhardt ◽  
Arndt Nobis ◽  
Andreas Skornia ◽  
Thomas Becker ◽  
Martina Gastl
Keyword(s):  
Bound States ◽  
De Novo ◽  
Comprehensive Evaluation ◽  
Early Stage ◽  
Active Form ◽  
Bound State ◽  
Free Form ◽  
Soluble Nitrogen ◽  
Strecker Aldehydes ◽  
Lager Beer

Flavor instability of pale lager beer depends decisively on aroma-active aldehydes from the Maillard reaction, Strecker degradation, and lipid oxidation, which are formed in various oxidative and non-oxidative reactions. Therein, aldehydes can be formed de novo and be released from bound states to a free, aroma-active form during aging. During malting and brewing, proteolysis affects the amount of soluble nitrogen and thus flavor instability in different ways (e.g., precursors for de novo formation and binding agents for bound states). To isolate nitrogen-related aging processes, beers from malts (two barley varieties, three proteolytic malt modifications) were produced on a 50 L scale in part 1 of this study. Sensory analysis revealed increased flavor instability for beers with higher amounts of soluble nitrogen. Especially Strecker aldehydes significantly increased with malt modification. The release of bound state aldehydes revealed most free aldehydes in fresh beers and with higher malt modification. During aging, the equilibrium between free and bound state aldehydes shifted toward the free form. These results reveal a nitrogen-dependent bound pool of aldehydes that is depleted during aging and is responsible for aged aroma, especially in the early and medium stages of aging. Therefore, bound state aldehydes are indicators of the early-stage prediction of flavor instability already in a fresh condition.

scholarly journals A Comprehensive Evaluation of Flavor Instability of Beer (Part 2): The Influence of De Novo Formation of Aging Aldehydes

Foods ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2668
Author(s):  
Arndt Nobis ◽  
Melanie Kwasnicki ◽  
Florian Lehnhardt ◽  
Michael Hellwig ◽  
Thomas Henle ◽  
...  
Keyword(s):  
Amino Acid ◽  
Free Amino ◽  
De Novo ◽  
Comprehensive Evaluation ◽  
Degradation Products ◽  
Amino Acid Content ◽  
Natural Aging ◽  
Bound State ◽  
Soluble Nitrogen ◽  
Oxidation Reactions

Flavor instability of beer is affected by the rise of aroma-active aldehydes during aging. Aldehydes can be either released from bound-state forms or formed de novo. This second part of our study focused on the de novo formation of aldehydes during the Maillard reaction, Strecker degradation, and oxidation reactions. Key precursor compounds for de novo pathways are free amino acids. This study varied the potential for reactions by varying free amino acid content in fresh beer using different proteolytic malt modification levels (569–731 mg/100 g d. m. of soluble nitrogen) of the used malt in brewing trials. Overall, six pale lager beers were produced from three malts (different malt modification levels), each was made from two different barley varieties and was naturally and forcibly aged. It was found that higher malt modification levels in fresh beer and during beer aging increased amino acid and dicarbonyl concentrations as aging precursors and Strecker aldehyde contents as aging indicators. Dicarbonyls were degraded during aging. Advanced glycation end products as possible degradation products showed no consistent formation during aging. Therefore, Strecker reactions were favored during beer aging. No alternative oxidative formation of Strecker aldehydes from their corresponding alcohols could be confirmed. Along with the preceding part one of our investigation, the results of this study showed that de novo formation and release occur simultaneously. After 4 months of natural aging, aldehyde rise is mainly accounted for by de novo formation.

scholarly journals Crystal structure of wild-type human thrombin in the Na+-free state

2005 ◽  
Vol 392 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Daniel J. D. Johnson ◽  
Ty E. Adams ◽  
Wei Li ◽  
James A. Huntington
Keyword(s):  
Crystal Structure ◽  
Protein C ◽  
Active Form ◽  
Bound State ◽  
Free Form ◽  
Wild Type ◽  
Thrombin Activity ◽  
Solution Studies ◽  
Human Thrombin ◽  
Anticoagulant Function

Regulation of thrombin activity is critical for haemostasis and the prevention of thrombosis. Thrombin has several procoagulant substrates, including fibrinogen and platelet receptors, and essential cofactors for stimulating its own formation. However, thrombin is also capable of serving an anticoagulant function by activating protein C. The specificity of thrombin is primarily regulated by binding to the cofactor TM (thrombomodulin), but co-ordination of Na+ can also affect thrombin activity. The Na+-free form is often referred to as ‘slow’ because of reduced rates of cleavage of procoagulant substrates, but the slow form is still capable of rapid activation of protein C in the presence of TM. The molecular basis of the slow proteolytic activity of thrombin has remained elusive, in spite of two decades of solution studies and many published crystallographic structures. In the present paper, we report the first structure of wild-type unliganded human thrombin grown in the absence of co-ordinating Na+. The Na+-binding site is observed in a highly ordered position 6 Å (1 Å=0.1 nm) removed from that seen in the Na+-bound state. The movement of the Na+ loop results in non-catalytic hydrogen-bonding in the active site and blocking of the S1 and S2 substrate-binding pockets. Similar, if more dramatic, changes were observed in a previous structure of the constitutively slow thrombin variant E217K. The slow behaviour of thrombin in solutions devoid of Na+ can now be understood in terms of an equilibrium between an inert species, represented by the crystal structure described in the present paper, and an active form, where the addition of Na+ populates the active state.

Association of the Non-Motor Burden with Patterns of Striatal Dopamine Loss in de novo Parkinson’s Disease

2020 ◽  
Vol 10 (4) ◽  
pp. 1541-1549
Author(s):  
Seok Jong Chung ◽  
Sangwon Lee ◽  
Han Soo Yoo ◽  
Yang Hyun Lee ◽  
Hye Sun Lee ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
De Novo ◽  
Early Stage ◽  
Striatal Dopamine ◽  
Motor Deficits ◽  
Dopamine Depletion ◽  
Severe Motor ◽  
Severe Group ◽  
Striatal Dopamine Depletion

Background: Striatal dopamine deficits play a key role in the pathogenesis of Parkinson’s disease (PD), and several non-motor symptoms (NMSs) have a dopaminergic component. Objective: To investigate the association between early NMS burden and the patterns of striatal dopamine depletion in patients with de novo PD. Methods: We consecutively recruited 255 patients with drug-naïve early-stage PD who underwent 18F-FP-CIT PET scans. The NMS burden of each patient was assessed using the NMS Questionnaire (NMSQuest), and patients were divided into the mild NMS burden (PDNMS-mild) (NMSQuest score <6; n = 91) and severe NMS burden groups (PDNMS-severe) (NMSQuest score >9; n = 90). We compared the striatal dopamine transporter (DAT) activity between the groups. Results: Patients in the PDNMS-severe group had more severe parkinsonian motor signs than those in the PDNMS-mild group, despite comparable DAT activity in the posterior putamen. DAT activity was more severely depleted in the PDNMS-severe group in the caudate and anterior putamen compared to that in the PDMNS-mild group. The inter-sub-regional ratio of the associative/limbic striatum to the sensorimotor striatum was lower in the PDNMS-severe group, although this value itself lacked fair accuracy for distinguishing between the patients with different NMS burdens. Conclusion: This study demonstrated that PD patients with severe NMS burden exhibited severe motor deficits and relatively diffuse dopamine depletion throughout the striatum. These findings suggest that the level of NMS burden could be associated with distinct patterns of striatal dopamine depletion, which could possibly indicate the overall pathological burden in PD.

scholarly journals Sequential fate-switches in stem-like cells drive the tumorigenic trajectory from human neural stem cells to malignant glioma

Cell Research ◽  
2021 ◽  
Author(s):  
Xiaofei Wang ◽  
Ran Zhou ◽  
Yanzhen Xiong ◽  
Lingling Zhou ◽  
Xiang Yan ◽  
...  
Keyword(s):  
Malignant Glioma ◽  
Single Cell ◽  
De Novo ◽  
Early Stage ◽  
Lineage Tracing ◽  
Human Neural Stem Cells ◽  
Transcriptional Reprogramming ◽  
Neural Stem Progenitor Cells ◽  
Human Gbm ◽  
End Stage

AbstractGlioblastoma (GBM) is an incurable and highly heterogeneous brain tumor, originating from human neural stem/progenitor cells (hNSCs/hNPCs) years ahead of diagnosis. Despite extensive efforts to characterize hNSCs and end-stage GBM at bulk and single-cell levels, the de novo gliomagenic path from hNSCs is largely unknown due to technical difficulties in early-stage sampling and preclinical modeling. Here, we established two highly penetrant hNSC-derived malignant glioma models, which resemble the histopathology and transcriptional heterogeneity of human GBM. Integrating time-series analyses of whole-exome sequencing, bulk and single-cell RNA-seq, we reconstructed gliomagenic trajectories, and identified a persistent NSC-like population at all stages of tumorigenesis. Through trajectory analyses and lineage tracing, we showed that tumor progression is primarily driven by multi-step transcriptional reprogramming and fate-switches in the NSC-like cells, which sequentially generate malignant heterogeneity and induce tumor phenotype transitions. We further uncovered stage-specific oncogenic cascades, and among the candidate genes we functionally validated C1QL1 as a new glioma-promoting factor. Importantly, the neurogenic-to-gliogenic switch in NSC-like cells marks an early stage characterized by a burst of oncogenic alterations, during which transient AP-1 inhibition is sufficient to inhibit gliomagenesis. Together, our results reveal previously undercharacterized molecular dynamics and fate choices driving de novo gliomagenesis from hNSCs, and provide a blueprint for potential early-stage treatment/diagnosis for GBM.

scholarly journals Bound states of a Klein–Gordon particle in the presence of a smooth potential well

2020 ◽  
Vol 35 (23) ◽  
pp. 2050140
Author(s):  
Eduardo López ◽  
Clara Rojas
Keyword(s):  
Bound States ◽  
Gordon Equation ◽  
Bound State ◽  
Potential Well ◽  
One Dimensional ◽  
Smooth Potential ◽  
Klein Gordon ◽  
The One ◽  
Potential Parameters ◽  
Klein Gordon Equation

We solve the one-dimensional time-independent Klein–Gordon equation in the presence of a smooth potential well. The bound state solutions are given in terms of the Whittaker [Formula: see text] function, and the antiparticle bound state is discussed in terms of potential parameters.

RETARDATION EFFECTS IN COVARIANT THREE-DIMENSIONAL BOUND STATE WAVE FUNCTIONS

2005 ◽  
Vol 14 (06) ◽  
pp. 931-947 ◽  
Author(s):  
F. PILOTTO ◽  
M. DILLIG
Keyword(s):  
Bound States ◽  
Three Dimensional ◽  
Bound State ◽  
Relative Energy ◽  
Wave Functions ◽  
Three Dimensions ◽  
State Wave ◽  
Scalar Diquark ◽  
Bound State Wave Function ◽  
Retardation Effects

We investigate the influence of retardation effects on covariant 3-dimensional wave functions for bound hadrons. Within a quark-(scalar) diquark representation of a baryon, the four-dimensional Bethe–Salpeter equation is solved for a 1-rank separable kernel which simulates Coulombic attraction and confinement. We project the manifestly covariant bound state wave function into three dimensions upon integrating out the non-static energy dependence and compare it with solutions of three-dimensional quasi-potential equations obtained from different kinematical projections on the relative energy variable. We find that for long-range interactions, as characteristic in QCD, retardation effects in bound states are of crucial importance.

THE NEXT STEP IN LEPTONIC DECAYS OF ETA AND KL BOUND STATES

1992 ◽  
Vol 07 (09) ◽  
pp. 1935-1951 ◽  
Author(s):  
G.A. KOZLOV
Keyword(s):  
Field Theory ◽  
Transition Form Factor ◽  
Bound States ◽  
Three Dimensional ◽  
Bound State ◽  
Quantum Field ◽  
Relative Momentum ◽  
Transition Form ◽  
Structure Transition ◽  
Leptonic Decays

A systematic discussion of the probability of eta and KL bound-state decays—[Formula: see text] and [Formula: see text](l=e, μ)—within a three-dimensional reduction to the two-body quantum field theory is presented. The bound-state vertex function depends on the relative momentum of constituent-like particles. A structure-transition form factor is defined by a confinement-type quark-antiquark wave function. The phenomenology of this kind of decays is analyzed.

scholarly journals In vivo assembly of tight junctions in fetal rat liver.

1975 ◽  
Vol 67 (2) ◽  
pp. 310-319 ◽  
Author(s):  
R Montesano ◽  
D S Friend ◽  
A Perrelet ◽  
L Orci
Keyword(s):  
Tight Junctions ◽  
De Novo ◽  
Early Stage ◽  
Fetal Life ◽  
Bile Canaliculi ◽  
Linear Arrays ◽  
Fetal Rat ◽  
Particle Aggregates ◽  
Fetal Rat Liver

Examination of glutaraldehyde-fixed, freeze-fractured livers from 14-15-day rat fetuses provided the basis for the following observations. Membrane particles align in otherwise poorly particulated areas of the presumptive pericanalicular plasma membrane (A face), frequently forming a discontinuous "honey-comb" network joining small particle islands. Even at this early stage, contiguous B-fracture faces contain furrows, rather than rows of pits, distinguishing the linear particle aggregates on the A face as developing tight junctions rather than gap junctions. Short segments of these linear arrays merge with smooth ridges clearly identifiable as segments of discontinuous tight junctions. With the continuing confluence of particulate and smooth ridge segments, mature tight junctions become fully appreciable. We conclude that tight junctions form de novo by the alignment and fusion of separate particles into beaded ridges which, in turn, become confluent and are transformed into continuous smooth ones. At 21 days of fetal life, most of the images of assembly have disappeared, and the liver reveals well-formed bile canaliculi sealed by mature tight junctions.

scholarly journals Structural insights into the mechanism of the DEAH-box RNA helicase Prp43

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Marcel J Tauchert ◽  
Jean-Baptiste Fourmann ◽  
Reinhard Lührmann ◽  
Ralf Ficner
Keyword(s):  
Conformational Changes ◽  
Bound States ◽  
Rna Binding ◽  
Atp Hydrolysis ◽  
Bound State ◽  
Rna Helicases ◽  
Large Rearrangements ◽  
Rna Complex ◽  
Structural Insights ◽  
Terminal Domains

The DEAH-box helicase Prp43 is a key player in pre-mRNA splicing as well as the maturation of rRNAs. The exact modus operandi of Prp43 and of all other spliceosomal DEAH-box RNA helicases is still elusive. Here, we report crystal structures of Prp43 complexes in different functional states and the analysis of structure-based mutants providing insights into the unwinding and loading mechanism of RNAs. The Prp43•ATP-analog•RNA complex shows the localization of the RNA inside a tunnel formed by the two RecA-like and C-terminal domains. In the ATP-bound state this tunnel can be transformed into a groove prone for RNA binding by large rearrangements of the C-terminal domains. Several conformational changes between the ATP- and ADP-bound states explain the coupling of ATP hydrolysis to RNA translocation, mainly mediated by a β-turn of the RecA1 domain containing the newly identified RF motif. This mechanism is clearly different to those of other RNA helicases.

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