Structural and Dynamical Characteristics of Short-Chain Branched Ring Polymer Melts at Interface under Shear Flow

Seung Heum Jeong; Soowon Cho; Tae Yong Ha; Eun Jung Roh; Chunggi Baig

doi:10.3390/polym12123068

Structural and Dynamical Characteristics of Short-Chain Branched Ring Polymer Melts at Interface under Shear Flow

Polymers ◽

10.3390/polym12123068 ◽

2020 ◽

Vol 12 (12) ◽

pp. 3068

Author(s):

Seung Heum Jeong ◽

Soowon Cho ◽

Tae Yong Ha ◽

Eun Jung Roh ◽

Chunggi Baig

Keyword(s):

Molecular Mechanisms ◽

Flow Direction ◽

Short Chain ◽

Wall Friction ◽

Nonequilibrium Molecular Dynamics ◽

Interfacial Slip ◽

Chain Branching ◽

Ring Geometry ◽

Wide Range ◽

Chain Conformations

We present a detailed analysis of the interfacial chain structure and dynamics of confined polymer melt systems under shear over a wide range of flow strengths using atomistic nonequilibrium molecular dynamics simulations, paying particular attention to the rheological influence of the closed-loop ring geometry and short-chain branching. We analyzed the interfacial slip, characteristic molecular mechanisms, and deformed chain conformations in response to the applied flow for linear, ring, short-chain branched (SCB) linear, and SCB ring polyethylene melts. The ring topology generally enlarges the interfacial chain dimension along the neutral direction, enhancing the dynamic friction of interfacial chains moving against the wall in the flow direction. This leads to a relatively smaller degree of slip (ds) for the ring-shaped polymers compared with their linear analogues. Furthermore, short-chain branching generally resulted in more compact and less deformed chain structures via the intrinsically fast random motions of the short branches. The short branches tend to be oriented more perpendicular (i.e., aligned in the neutral direction) than parallel to the backbone, which is mostly aligned in the flow direction, thereby enhancing the dynamic wall friction of the moving interfacial chains toward the flow direction. These features afford a relatively lower ds and less variation in ds in the weak-to-intermediate flow regimes. Accordingly, the interfacial SCB ring system displayed the lowest ds among the studied polymer systems throughout these regimes owing to the synergetic effects of ring geometry and short-chain branching. On the contrary, the structural disturbance exerted by the highly mobile short branches promotes the detachment of interfacial chains from the wall at strong flow fields, which results in steeper increasing behavior of the interfacial slip for the SCB polymers in the strong flow regime compared to the pure linear and ring polymers.

Download Full-text

Decreased Thermal Conductivity of Polyethylene Chain Influenced by Short Chain Branching

Journal of Heat Transfer ◽

10.1115/1.4038003 ◽

2017 ◽

Vol 140 (3) ◽

Cited By ~ 14

Author(s):

Danchen Luo ◽

Congliang Huang ◽

Zun Huang

Keyword(s):

Thermal Conductivity ◽

Molecular Dynamics ◽

Density Increase ◽

Short Chain ◽

Nonequilibrium Molecular Dynamics ◽

Side Chains ◽

Number Density ◽

Chain Branching ◽

Positive Effect

In this paper, we have studied the effect of short branches (side chains) on the thermal conductivity (TC) of a polyethylene (PE) chain. With a reverse nonequilibrium molecular dynamics (RNEMD) method, TCs of the pristine PE chain and the PE-ethyl chain are simulated and compared. It shows that the branch has a positive effect to decrease the TC of a PE chain. The TC of the PE-ethyl chain decreases with the number density increase of branches, until the density becomes larger than about eight ethyl per 200 segments, where the TC saturates to be only about 40% that of a pristine PE chain. Because of different weights, different branches will cause a different decrease of TCs, and a heavy branch will lead to a lower TC than a light one. This study is expected to provide some fundamental guidance to obtain a polymer with a low TC.

Download Full-text

SARS-CoV-2 and the Nervous System: From Clinical Features to Molecular Mechanisms

International Journal of Molecular Sciences ◽

10.3390/ijms21155475 ◽

2020 ◽

Vol 21 (15) ◽

pp. 5475 ◽

Cited By ~ 11

Author(s):

Manuela Pennisi ◽

Giuseppe Lanza ◽

Luca Falzone ◽

Francesco Fisicaro ◽

Raffaele Ferri ◽

...

Keyword(s):

Nervous System ◽

Molecular Mechanisms ◽

Neuronal Damage ◽

Neurological Complications ◽

Neurological Manifestations ◽

Wide Range ◽

Inflammatory State ◽

Acute Polyneuropathy ◽

The Central Nervous System ◽

The Impact

Increasing evidence suggests that Severe Acute Respiratory Syndrome-coronavirus-2 (SARS-CoV-2) can also invade the central nervous system (CNS). However, findings available on its neurological manifestations and their pathogenic mechanisms have not yet been systematically addressed. A literature search on neurological complications reported in patients with COVID-19 until June 2020 produced a total of 23 studies. Overall, these papers report that patients may exhibit a wide range of neurological manifestations, including encephalopathy, encephalitis, seizures, cerebrovascular events, acute polyneuropathy, headache, hypogeusia, and hyposmia, as well as some non-specific symptoms. Whether these features can be an indirect and unspecific consequence of the pulmonary disease or a generalized inflammatory state on the CNS remains to be determined; also, they may rather reflect direct SARS-CoV-2-related neuronal damage. Hematogenous versus transsynaptic propagation, the role of the angiotensin II converting enzyme receptor-2, the spread across the blood-brain barrier, the impact of the hyperimmune response (the so-called “cytokine storm”), and the possibility of virus persistence within some CNS resident cells are still debated. The different levels and severity of neurotropism and neurovirulence in patients with COVID-19 might be explained by a combination of viral and host factors and by their interaction.

Download Full-text

Targeting AURKA in Cancer: molecular mechanisms and opportunities for Cancer therapy

Molecular Cancer ◽

10.1186/s12943-020-01305-3 ◽

2021 ◽

Vol 20 (1) ◽

Cited By ~ 1

Author(s):

Ruijuan Du ◽

Chuntian Huang ◽

Kangdong Liu ◽

Xiang Li ◽

Zigang Dong

Keyword(s):

Cancer Therapy ◽

Molecular Mechanisms ◽

Aurora Kinase ◽

Interacting Proteins ◽

Multiple Tumor ◽

Oncogenic Pathways ◽

Wide Range ◽

The Family ◽

Tumor Types ◽

Cancer Tissues

AbstractAurora kinase A (AURKA) belongs to the family of serine/threonine kinases, whose activation is necessary for cell division processes via regulation of mitosis. AURKA shows significantly higher expression in cancer tissues than in normal control tissues for multiple tumor types according to the TCGA database. Activation of AURKA has been demonstrated to play an important role in a wide range of cancers, and numerous AURKA substrates have been identified. AURKA-mediated phosphorylation can regulate the functions of AURKA substrates, some of which are mitosis regulators, tumor suppressors or oncogenes. In addition, enrichment of AURKA-interacting proteins with KEGG pathway and GO analysis have demonstrated that these proteins are involved in classic oncogenic pathways. All of this evidence favors the idea of AURKA as a target for cancer therapy, and some small molecules targeting AURKA have been discovered. These AURKA inhibitors (AKIs) have been tested in preclinical studies, and some of them have been subjected to clinical trials as monotherapies or in combination with classic chemotherapy or other targeted therapies.

Download Full-text

Anti-NLRP3 Inflammasome Natural Compounds: An Update

Biomedicines ◽

10.3390/biomedicines9020136 ◽

2021 ◽

Vol 9 (2) ◽

pp. 136

Author(s):

Baolong Liu ◽

Jiujiu Yu

Keyword(s):

Nlrp3 Inflammasome ◽

Protein Complex ◽

Molecular Mechanisms ◽

Inflammatory Responses ◽

Natural Compounds ◽

Pyrin Domain ◽

Inflammatory Protein ◽

Wide Range ◽

Activation Mechanisms ◽

Stress Signals

The nucleotide-binding domain and leucine-rich repeat related (NLR) family, pyrin domain containing 3 (NLRP3) inflammasome is a multimeric protein complex that recognizes various danger or stress signals from pathogens, the host, and the environment, leading to activation of caspase-1 and inducing inflammatory responses. This pro-inflammatory protein complex plays critical roles in pathogenesis of a wide range of diseases including neurodegenerative diseases, autoinflammatory diseases, and metabolic disorders. Therefore, intensive efforts have been devoted to understanding its activation mechanisms and to searching for its specific inhibitors. Approximately forty natural compounds with anti-NLRP3 inflammasome properties have been identified. Here, we provide an update about new natural compounds that have been identified within the last three years to inhibit the NLRP3 inflammasome and offer an overview of the underlying molecular mechanisms of their anti-NLRP3 inflammasome activities.

Download Full-text

When the Balance Tips: Dysregulation of Mitochondrial Dynamics as a Culprit in Disease

International Journal of Molecular Sciences ◽

10.3390/ijms22094617 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4617

Author(s):

Styliana Kyriakoudi ◽

Anthi Drousiotou ◽

Petros P. Petrou

Keyword(s):

Insulin Resistance ◽

Mitochondrial Function ◽

Human Disease ◽

Molecular Mechanisms ◽

Mitochondrial Dynamics ◽

Mitochondrial Fusion ◽

Mitochondrial Morphology ◽

Disease Development ◽

Pathological Conditions ◽

Wide Range

Mitochondria are dynamic organelles, the morphology of which is tightly linked to their functions. The interplay between the coordinated events of fusion and fission that are collectively described as mitochondrial dynamics regulates mitochondrial morphology and adjusts mitochondrial function. Over the last few years, accruing evidence established a connection between dysregulated mitochondrial dynamics and disease development and progression. Defects in key components of the machinery mediating mitochondrial fusion and fission have been linked to a wide range of pathological conditions, such as insulin resistance and obesity, neurodegenerative diseases and cancer. Here, we provide an update on the molecular mechanisms promoting mitochondrial fusion and fission in mammals and discuss the emerging association of disturbed mitochondrial dynamics with human disease.

Download Full-text

Congenital adrenal hyperplasia: molecular mechanisms resulting in 21-hydroxylase deficiency

Acta Endocrinologica ◽

10.1530/acta.0.112s315 ◽

1986 ◽

Vol 113 (4_Suppl) ◽

pp. S315-S320 ◽

Cited By ~ 7

Author(s):

Patricia A. Donohoue ◽

Cornelis Van Dop ◽

Nicholas Jospe ◽

Claude J. Migeon

Keyword(s):

Congenital Adrenal Hyperplasia ◽

Molecular Mechanisms ◽

Sequence Data ◽

Phenotypic Expression ◽

Restriction Pattern ◽

Class Iii ◽

Adrenal Hyperplasia ◽

Hydroxylase Deficiency ◽

Wide Range ◽

21 Hydroxylase Deficiency

Abstract 21-Hydroxylase deficiency resulting in congenital adrenal hyperplasia (CAH) is a HLA-linked autosomal recessive disorder that has a wide range of phenotypic expression. Two homologous 21-hydroxylase genes (21-OHA and 21-OHB) occur within the Class III region of the major histocompatibility complex, but only one (21-OHB) appears to function in adrenal steroidogenesis. Our restriction maps, and initial sequence data from White et al. (Pediatr Res 20:274A (1986)) for the two human 21-OH genes reveal a high degree of homology between these genes and a reading frame shift mutation in the 21-OHA gene respectively. Among fourteen control subjects, the intragenic restriction patterns of the 21-OHA and 21-OHB genes are invariant. The few restriction fragment length polymorphisms (RFLPs) found in some controls result from polymorphic restriction sites outside the 21-OH genes. In patients with CAH, several different mechanisms for mutation of the 21-OHB gene have been described: 1) deletion of the unique sequences of the 21-OHB gene, 2) conversion of the unique sequences of the 21-OHB gene to those of 21-OHA, and 3) mutations of 21-OHB which do not result in a detectable alteration of restriction pattern (e.g., point mutations). Duplication of the 21-OHA gene has been found in some patients with attenuated CAH; however, the significance of this finding remains unclear.

Download Full-text

Correlation of Metabolic Profiles of Plasma and Cerebrospinal Fluid of High-Grade Glioma Patients

Metabolites ◽

10.3390/metabo11030133 ◽

2021 ◽

Vol 11 (3) ◽

pp. 133

Author(s):

Artem D. Rogachev ◽

Nikolay A. Alemasov ◽

Vladimir A. Ivanisenko ◽

Nikita V. Ivanisenko ◽

Evgeniy V. Gaisler ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Molecular Mechanisms ◽

High Grade Glioma ◽

Diagnostic Procedures ◽

Metabolic Profiles ◽

High Grade ◽

Wide Range ◽

Targeted Screening ◽

M Estimates ◽

Metabolite Content

This work compares the metabolic profiles of plasma and the cerebrospinal fluid (CSF) of the patients with high-grade (III and IV) gliomas and the conditionally healthy controls using the wide-range targeted screening of low molecular metabolites by HPLC-MS/MS. The obtained data were analyzed using robust linear regression with Huber’s M-estimates, and a number of metabolites with correlated content in plasma and CSF was identified. The statistical analysis shows a significant correlation of metabolite content in plasma and CSF samples for the majority of metabolites. Several metabolites were shown to have high correlation in the control samples, but not in the glioma patients. This can be due to the specific metabolic processes in the glioma patients or to the damaged integrity of blood-brain barrier. The results of our study may be useful for the understanding of molecular mechanisms underlying the development of gliomas, as well as for the search of potential biomarkers for the minimally invasive diagnostic procedures of gliomas.

Download Full-text

Could metabolomics drive the fate of COVID-19 pandemic? A narrative review on lights and shadows

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2021-0414 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Michele Mussap ◽

Vassilios Fanos

Keyword(s):

Molecular Mechanisms ◽

Vascular Dysfunction ◽

Asymptomatic Infection ◽

Multiple Organ ◽

Therapeutic Interventions ◽

Patient Specific ◽

Wide Range ◽

Life Threatening ◽

The Individual ◽

Host Metabolism

Abstract Human Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) infection activates a complex interaction host/virus, leading to the reprogramming of the host metabolism aimed at the energy supply for viral replication. Alterations of the host metabolic homeostasis strongly influence the immune response to SARS-CoV-2, forming the basis of a wide range of outcomes, from the asymptomatic infection to the onset of COVID-19 and up to life-threatening acute respiratory distress syndrome, vascular dysfunction, multiple organ failure, and death. Deciphering the molecular mechanisms associated with the individual susceptibility to SARS-CoV-2 infection calls for a system biology approach; this strategy can address multiple goals, including which patients will respond effectively to the therapeutic treatment. The power of metabolomics lies in the ability to recognize endogenous and exogenous metabolites within a biological sample, measuring their concentration, and identifying perturbations of biochemical pathways associated with qualitative and quantitative metabolic changes. Over the last year, a limited number of metabolomics- and lipidomics-based clinical studies in COVID-19 patients have been published and are discussed in this review. Remarkable alterations in the lipid and amino acid metabolism depict the molecular phenotype of subjects infected by SARS-CoV-2; notably, structural and functional data on the lipids-virus interaction may open new perspectives on targeted therapeutic interventions. Several limitations affect most metabolomics-based studies, slowing the routine application of metabolomics. However, moving metabolomics from bench to bedside cannot imply the mere determination of a given metabolite panel; rather, slotting metabolomics into clinical practice requires the conversion of metabolic patient-specific data into actionable clinical applications.

Download Full-text