From NWChem to NWChemEx: Evolving with the Computational Chemistry Landscape.

Since the advent of the first computers, chemists have been at the forefront of using computers to understand and solve complex chemical problems. As the hardware and software have evolved, so have the theoretical and computational chemistry methods and algorithms. Parallel computers clearly changed the common computing paradigm in the late 1970s and 80s, and the field has again seen a paradigm shift with the advent of graphical processing units. This review explores the challenges and some of the solutions in transforming software from the terascale to the petascale and now to the upcoming exascale computers. While discussing the field in general, NWChem and its redesign, NWChemEx, will be highlighted as one of the early codesign projects to take advantage of massively parallel computers and emerging software standards to enable large scientific challenges to be tackled.

TAMM: Tensor algebra for many-body methods.

Tensor algebra operations such as contractions in computational chemistry consume a significant fraction of the computing time on large-scale computing platforms. The widespread use of tensor contractions between large multi-dimensional tensors in describing electronic structure theory has motivated the development of multiple tensor algebra frameworks targeting heterogeneous computing platforms. In this paper, we present Tensor Algebra for Many-body Methods (TAMM), a framework for productive and performance-portable development of scalable computational chemistry methods. TAMM decouples the specification of the computation from the execution of these operations on available high-performance computing systems. With this design choice, the scientific application developers (domain scientists) can focus on the algorithmic requirements using the tensor algebra interface provided by TAMM, whereas high-performance computing developers can direct their attention to various optimizations on the underlying constructs, such as efficient data distribution, optimized scheduling algorithms, and efficient use of intra-node resources (e.g., graphics processing units). The modular structure of TAMM allows it to support different hardware architectures and incorporate new algorithmic advances. We describe the TAMM framework and our approach to the sustainable development of scalable ground- and excited-state electronic structure methods. We present case studies highlighting the ease of use, including the performance and productivity gains compared to other frameworks.

Spalling-Induced Liftoff and Transfer of Electronic Films Using a van der Waals Release Layer.

Heterogeneous integration strategies are increasingly being employed to achieve more compact and capable electronics systems for multiple applications including space, electric vehicles, and wearable and medical devices. To enable new integration strategies, the growth and transfer of thin electronic films and devices, including III-nitrides, metal oxides, and 2D materials, using 2D boron nitride (BN)-on-sapphire templates are demonstrated. The van der Waals (vdW) BN layer, in this case, acts as a preferred mechanical release layer for precise separation at the substrate-film interface and leaves a smooth surface suitable for vdW bonding. A tensilely stressed Ni layer sputtered on top of the film induces controlled spalling fracture that propagates at the BN/sapphire interface. By incorporating controlled spalling, the process yield and sensitivity are greatly improved, owed to the greater fracture energy provided by the stressed metal layer relative to a soft tape or rubber stamp. With stress playing a critical role in this process, the influence of residual stress on detrimental cracking and bowing is investigated. Additionally, a back-end selected area lift-off technique is developed which allows for isolation and transfer of individual devices or arbitrary shapes.

Prognostic scoring system and risk stratification in patients with emphysematous pyelonephritis: an 11-year prospective study at a tertiary referral centre.

OBJECTIVES: To define pre-morbid, clinical, laboratory, and imaging features and identify prognostic factors associated with morbidity and mortality in patients with emphysematous pyelonephritis (EPN) and develop a prognostic scoring system for improving management outcomes. PATIENTS AND METHODS: From January 2009 to December 2019, we performed a prospective study of all patients with a suspected diagnosis of EPN referred to a specialist tertiary centre in South India. All patients who underwent non-contrast computed tomography of the abdomen and those diagnosed with EPN were included in this study. Demographic parameters, imaging, haematological and microbiology results were recorded. Patients were divided into three groups: Group 1, patients who survived without any intervention; Group 2, those who survived with surgical intervention; and Group 3, those who died with or without intervention. A prognostic scoring system was developed from 18 different parameters and risk stratification was developed. The scores were correlated with overall prognosis. RESULTS: Data from 131 patients with EPN enrolled in the study were analysed: Group 1 (n = 22), Group 2 (n = 102) and Group 3 (n = 7). By using univariate analysis, 10 factors were identified to be significantly associated with prognosis. Diabetes mellitus was the most common comorbidity. Shock at initial admission indicated a poor prognosis and warranted immediate attention (P < 0.001). CONCLUSIONS: A multi-disciplinary approach, a high index of clinical suspicion, an early diagnosis and administration of culture-specific antibiotics with identification of prognostic indicators and risk stratification, allows prompt and appropriate medical and surgical treatments that could improve EPN management outcomes.

Green's function coupled cluster simulation of the near-valence ionizations of DNA-fragments.

Accurate description of the ionization process in DNA is crucial to the understanding of the DNA damage under exposure to ionizing radiation and the exploration of the potential application of DNA strands in nanoelectronics. In this work, by employing our recently developed Green's function coupled-cluster library on supercomputing facilities, we have studied the spectral functions of several guanine-cytosine (G-C) base pair structures ([G-C]n, n = 1-3) for the first time in a relatively broad near-valence regime ([-25.0, -5.0] eV) in the coupled-cluster with singles and doubles level. Our focus is to give a preliminary many-body coupled-cluster understanding and guideline of the vertical ionization energy (VIE), spectral profile, and ionization feature changes of these systems as the system size expands in this near-valence regime. The results show that, as the system size expands, even though the lowest VIEs keep decreasing, the changes of spectral function profile and the relative peak positions get unexpectedly smaller. Further analysis of the ionized states associated with the most intensive peak in the spectral functions reveals non-negligible |2h, 1p⟩'s in the ionized wave functions of the considered G-C base pair systems. The leading |2h, 1p⟩'s associated with the main ionizations from the cytosine part of the G-C base pairs feature a transition from the intra-base-pair cytosine π → π* excitation to the inter-base-pair electron excitation as the size of G-C base pairs expands, which also indicates the minimum quantum region in the many-body calculations of DNA systems.

Downfolding of many-body Hamiltonians using active-space models: Extension of the sub-system embedding sub-algebras approach to unitary coupled cluster formalisms.

In this paper, we discuss the extension of the recently introduced subsystem embedding subalgebra coupled cluster (SES-CC) formalism to unitary CC formalisms. In analogy to the standard single-reference SES-CC formalism, its unitary CC extension allows one to include the dynamical (outside the active space) correlation effects in an SES induced complete active space (CAS) effective Hamiltonian. In contrast to the standard single-reference SES-CC theory, the unitary CC approach results in a Hermitian form of the effective Hamiltonian. Additionally, for the double unitary CC (DUCC) formalism, the corresponding CAS eigenvalue problem provides a rigorous separation of external cluster amplitudes that describe dynamical correlation effects-used to define the effective Hamiltonian-from those corresponding to the internal (inside the active space) excitations that define the components of eigenvectors associated with the energy of the entire system. The proposed formalism can be viewed as an efficient way of downfolding many-electron Hamiltonian to the low-energy model represented by a particular choice of CAS. In principle, this technique can be extended to any type of CAS representing an arbitrary energy window of a quantum system. The Hermitian character of low-dimensional effective Hamiltonians makes them an ideal target for several types of full configuration interaction type eigensolvers. As an example, we also discuss the algebraic form of the perturbative expansions of the effective DUCC Hamiltonians corresponding to composite unitary CC theories and discuss possible algorithms for hybrid classical and quantum computing. Given growing interest in quantum computing, we provide energies for H2 and Be systems obtained with the quantum phase estimator algorithm available in the Quantum Development Kit for the approximate DUCC Hamiltonians.

VLA-4 blockade by natalizumab inhibits sickle reticulocyte and leucocyte adhesion during simulated blood flow.

Very Late Antigen-4 (VLA-4, α4ß1-integrin, ITGA4) orchestrates cell-cell and cell-endothelium adhesion. Given the proposed role of VLA-4 in sickle cell disease (SCD) pathophysiology, we evaluated the ability of the VLA-4 blocking antibody natalizumab to inhibit SCD blood cell adhesion. Natalizumab recognized surface VLA-4 on leucocytes and reticulocytes in whole blood from SCD subjects. SCD reticulocytes were positive for VLA-4, while VLA-4 staining of non-SCD reticulocytes was undetectable. Titrations with natalizumab revealed the presence of saturable levels of VLA-4 on both SCD reticulocytes and leucocytes similar to healthy subject leucocytes. Under physiological flow conditions, the adhesion of SCD whole blood cells and isolated SCD leucocytes to immobilized vascular cell adhesion molecule 1 (VCAM-1) was blocked by natalizumab in a dose-dependent manner, which correlated with cell surface receptor binding. Natalizumab also inhibited >50% of whole blood cell binding to TNF-α activated human umbilical vein endothelial cell monolayers under physiological flow at clinically relevant concentrations (10 to 100 µg/ml). This indicates that VLA-4 is the dominant receptor that drives SCD reticulocyte and mononuclear cell adhesion to VCAM-1 and that the VLA-4 adhesion to VCAM-1 is a significant contributor to SCD blood cell adhesion to endothelium. Thus, VLA-4 blockade may be beneficial in sickle cell disease.

Recombinant factor VIII Fc (rFVIIIFc) fusion protein reduces immunogenicity and induces tolerance in hemophilia A mice.

Anti-factor VIII (FVIII) antibodies is a major complication of FVIII replacement therapy for hemophilia A. We investigated the immune response to recombinant human factor VIII Fc (rFVIIIFc) in comparison to BDD-rFVIII and full-length rFVIII (FL-rFVIII) in hemophilia A mice. Repeated administration of therapeutically relevant doses of rFVIIIFc in these mice resulted in significantly lower antibody responses to rFVIII compared to BDD-rFVIII and FL-rFVIII and reduced antibody production upon subsequent challenge with high doses of rFVIIIFc. The induction of a tolerogenic response by rFVIIIFc was associated with higher percentage of regulatory T-cells, a lower percentage of pro-inflammatory splenic T-cells, and up-regulation of tolerogenic cytokines and markers. Disruption of Fc interactions with either FcRn or Fcγ receptors diminished tolerance induction, suggesting the involvement of these pathways. These results indicate that rFVIIIFc reduces immunogenicity and imparts tolerance to rFVIII demonstrating that recombinant therapeutic proteins may be modified to influence immunogenicity and facilitate tolerance.

Resolvin E2 formation and impact in inflammation resolution.

Acute inflammation and its resolution are essential processes for tissue protection and homeostasis. In this context, specialized proresolving mediators derived from polyunsaturated fatty acids are of interest. In this study, we report that resolvin E2 (RvE2) from eicosapentaenoic acid is endogenously produced during self-limited murine peritonitis in both the initiation and resolution phases. RvE2 (1-10 nM) carries potent leukocyte-directed actions that include: 1) regulating chemotaxis of human neutrophils; and 2) enhancing phagocytosis and anti-inflammatory cytokine production. These actions appear to be mediated by leukocyte G-protein-coupled receptors as preparation of labeled RvE2 gave direct evidence for specific binding of radiolabeled RvE2 to neutrophils (K(d) 24.7 ± 10.1 nM) and resolvin E1 activation of recombinant G-protein-coupled receptors was assessed. In addition to the murine inflammatory milieu, RvE2 was also identified in plasma from healthy human subjects. RvE2 rapidly downregulated surface expression of human leukocyte integrins in whole blood and dampened responses to platelet-activating factor. Together, these results indicate that RvE2 can stimulate host-protective actions throughout initiation and resolution in the innate inflammatory responses.

A quantitative trait locus for ascites on chromosome 9 in broiler chicken lines.

A genome-wide SNP survey was used to identify chromosomal regions that showed linkage disequilibrium with respect to ascites susceptibility and ventricular hypertrophy in an F2 cross between previously described ascites-resistant and -susceptible lines. Variable number tandem repeats were used to obtain genotype data to further characterize these regions. A region on chromosome 9 (12 to 13 Mbp in 2011 assembly) shows association with ascites in the ascites lines and in several commercial broiler breeder lines with a significant sex effect. There are 2 candidate genes, AGTR1 (an angiotensin II type 1 receptor) and UTS2D (urotensin 2 domain containing), in this region that have been associated with hypertension and hypoxic response in mammals.

GdN nanoisland-based GaN tunnel junctions.

Tunnel junctions could have a great impact on gallium nitride and aluminum nitride-based devices such as light-emitting diodes and lasers by overcoming critical challenges related to hole injection and p-contacts. This paper demonstrates the use of GdN nanoislands to enhance interband tunneling and hole injection into GaN p-n junctions by several orders of magnitude, resulting in low tunnel junction specific resistivity (1.3 × 10(-3) Ω-cm(2)) compared to the previous results in wide band gap semiconductors. Tunnel injection of holes was confirmed by low-temperature operation of GaN p-n junction with a tunneling contact layer, and strong electroluminescence down to 20 K. The low tunnel junction resistance combined with low optical absorption loss in GdN is very promising for incorporation in GaN-based light emitters.

Resolvin D1 receptor stereoselectivity and regulation of inflammation and proresolving microRNAs.

Resolution of acute inflammation is an active process that involves the biosynthesis of specialized proresolving lipid mediators. Among them, resolvin D1 (RvD1) actions are mediated by two G protein-coupled receptors (GPCRs), ALX/FPR2 and GPR32, that also regulate specific microRNAs (miRNAs) and their target genes in novel resolution circuits. We report the ligand selectivity of RvD1 activation of ALX/FPR2 and GPR32. In addition to RvD1, its aspirin-triggered epimer and RvD1 analogs each dose dependently and effectively activated ALX/FPR2 and GPR32 in GPCR-overexpressing ß-arrestin systems using luminescence and electric cell-substrate impedance sensing. To corroborate these findings in vivo, neutrophil infiltration in self-limited peritonitis was reduced in human ALX/FPR2-overexpressing transgenic mice that was further limited to 50% by RvD1 treatment with as little as 10 ng of RvD1 per mouse. Analysis of miRNA expression revealed that RvD1 administration significantly up-regulated miR-208a and miR-219 in exudates isolated from ALX/FPR2 transgenic mice compared with littermates. Overexpression of miR-208a in human macrophages up-regulated IL-10. In comparison, in ALX/FPR2 knockout mice, RvD1 neither significantly reduced leukocyte infiltration in zymosan-induced peritonitis nor regulated miR-208a and IL-10 in these mice. Together, these results demonstrate the selectivity of RvD1 interactions with receptors ALX/FPR2 and GPR32. Moreover, they establish a new molecular circuit that is operative in the resolution of acute inflammation activated by the proresolving mediator RvD1 involving specific GPCRs and miRNAs.

Resolvin D1 binds human phagocytes with evidence for proresolving receptors.

Endogenous mechanisms that act in the resolution of acute inflammation are essential for host defense and the return to homeostasis. Resolvin D1 (RvD1), biosynthesized during resolution, displays potent and stereoselective anti-inflammatory actions, such as limiting neutrophil infiltration and proresolving actions. Here, we demonstrate that RvD1 actions on human polymorphonuclear leukocytes (PMNs) are pertussis toxin sensitive, decrease actin polymerization, and block LTB(4)-regulated adhesion molecules (beta2 integrins). Synthetic [(3)H]-RvD1 was prepared, which revealed specific RvD1 recognition sites on human leukocytes. Screening systems to identify receptors for RvD1 gave two candidates--ALX, a lipoxin A(4) receptor, and GPR32, an orphan--that were confirmed using a beta-arrestin-based ligand receptor system. Nuclear receptors including retinoid X receptor-alpha and peroxisome proliferator-activated receptor-alpha, -delta, -gamma were not activated by either resolvin E1 or RvD1 at bioactive nanomolar concentrations. RvD1 enhanced macrophage phagocytosis of zymosan and apoptotic PMNs, which increased with overexpression of human ALX and GPR32 and decreased with selective knockdown of these G-protein-coupled receptors. Also, ALX and GPR32 surface expression in human monocytes was up-regulated by zymosan and granulocyte-monocyte-colony-stimulating factor. These results indicate that RvD1 specifically interacts with both ALX and GPR32 on phagocytes and suggest that each plays a role in resolving acute inflammation.

Ultra-Wide Band Gap Ga2O3-on-SiC MOSFETs.

Ultra-wide band gap semiconductor devices based on ß-phase gallium oxide (Ga2O3) offer the potential to achieve higher switching performance and efficiency and lower manufacturing cost than that of today's wide band gap power electronics. However, the most critical challenge to the commercialization of Ga2O3 electronics is overheating, which impacts the device performance and reliability. We fabricated a Ga2O3/4H-SiC composite wafer using a fusion-bonding method. A low-temperature (≤600 °C) epitaxy and device processing scheme was developed to fabricate MOSFETs on the composite wafer. The low-temperature-grown epitaxial Ga2O3 devices deliver high thermal performance (56% reduction in channel temperature) and a power figure of merit of (∼300 MW/cm2), which is the highest among heterogeneously integrated Ga2O3 devices reported to date. Simulations calibrated based on thermal characterization results of the Ga2O3-on-SiC MOSFET reveal that a Ga2O3/diamond composite wafer with a reduced Ga2O3 thickness (∼1 µm) and a thinner bonding interlayer (<10 nm) can reduce the device thermal impedance to a level lower than that of today's GaN-on-SiC power switches.

Decoding functional metabolomics with docosahexaenoyl ethanolamide (DHEA) identifies novel bioactive signals.

Neuroinflammation and traumatic brain injury involve activation of inflammatory cells and production of local pro-inflammatory mediators that can amplify tissue damage. Using LC-UV-MS-MS-based lipidomics in tandem with functional screening at the single-cell level in microfluidic chambers, we identified a series of novel bioactive oxygenated docosahexaenoyl ethanolamide- (DHEA) derived products that regulated leukocyte motility. These included 10,17-dihydroxydocosahexaenoyl ethanolamide (10,17-diHDHEA) and 15-hydroxy-16(17)-epoxy-docosapentaenoyl ethanolamide (15-HEDPEA), each of which was an agonist of recombinant CB2 receptors with EC(50) 3.9 × 10(-10) and 1.0 × 10(-10) M. In human whole blood, 10,17-diHDHEA and 15-HEDPEA at concentrations as low as 10 pM each prevented formation of platelet-leukocyte aggregates involving either platelet-monocyte or platelet-polymorphonuclear leukocyte. In vivo, 15-HEDPEA was organ-protective in mouse reperfusion second organ injury. Together these results indicate that DHEA oxidative metabolism produces potent novel molecules with anti-inflammatory and organ-protective properties.

Eicosanoids and other lipid mediators and the tumor hypoxic microenvironment.

Hypoxia is a pathological hallmark feature of solid tumors. Though hypoxia is an adverse physiological state, tumors have evolved to utilize this unsuitable environment to their own advantage by activating key biochemical and cellular pathways that are important in progression, survival, and metastasis. Several studies have emphasized the importance of lipid mediators in regulating key biomolecules in the hypoxic microenvironment, for example hypoxia inducible factor-1 (HIF-1), the master regulator of hypoxia. Lipid mediators have been reported to enhance the levels and activity of HIF-1, which subsequently signal to stimulate angiogenesis and tumor cell survival under hypoxic conditions. There are also reports of hypoxia and HIF-1 enhancing the levels of some lipid mediators mostly by upregulating the levels of the enzymes responsible for their biosynthesis. This review gives a brief overview of these two mechanisms and the role played by bioactive lipid mediators in the regulation of tumor progression and survival under hypoxia.

MicroRNAs in resolution of acute inflammation: identification of novel resolvin D1-miRNA circuits.

Mechanisms controlling resolution of acute inflammation are of wide interest. Here, we investigated microRNAs (miRNAs) in self-limited acute inflammatory exudates and their regulation by resolvin D1 (RvD1). Using real-time PCR analysis, we found in resolving exudates that miR-21, miR-146b, miR-208a, miR-203, miR-142, miR-302d, and miR-219 were selectively regulated (P<0.05) in self-limited murine peritonitis. RvD1 (300 ng/mouse or 15 µg kg(-1)) reduced zymosan-elicited neutrophil infiltration into the peritoneum 25-50% and shortened the resolution interval (R(i)) by ∼4 h. In peritonitis at 12 h, RvD1 up-regulated miR-21, miR-146b, and miR-219 and down-regulated miR-208a in vivo. In human macrophages overexpressing recombinant RvD1 receptors ALX/FPR2 or GPR32, these same miRNAs were significantly regulated (P<0.05) by RvD1 at concentrations as low as 10 nM, recapitulating the in vivo circuit. In addition, RvD1-miRNAs identified herein target cytokines and proteins involved in the immune system, e.g., miR-146b targeted NF-κB signaling, and miR-219 targeted 5-lipoxygenase and reduced leukotriene production. RvD1 also reduced nuclear translocation of NF-κB and SMAD and down-regulated phospho-IκB. Taken together, these results indicate that resolvin-regulated specific miRNAs target genes involved in resolution and establish a novel resolution circuit involving RvD1 receptor-dependent regulation of specific miRNAs.

Optimized Quantum Phase Estimation for Simulating Electronic States in Various Energy Regimes.

While quantum algorithms for simulations exhibit better asymptotic scaling than their classical counterparts, they currently cannot be accurately implemented on real-world devices. Instead, chemists and computer scientists rely on costly classical simulations of these quantum algorithms. In particular, the quantum phase estimation (QPE) algorithm is among several approaches that has attracted much attention in recent years due to its genuine quantum character. However, it is memory-intensive to simulate and intractable for moderate system sizes. This paper discusses the performance and applicability of QPESIM, a new simulation of the QPE algorithm designed to take advantage of modest computational resources. In particular, we demonstrate the versatility of QPESIM in simulating various electronic states by examining the ground and core-level states of H2O. For these states, we also discuss the effect of the active-space size on the quality of the calculated energies. For the high-energy core-level states, we demonstrate that new QPE simulations for active spaces defined by 15 active orbitals significantly reduce the errors in core-level excitation energies compared to earlier QPE simulations using smaller active spaces.

Assessment of Plasmodium falciparum histidine rich protein 2 and /3 (pfhrp 2&/ pfhrp 3) gene deletion or mutation in Plasmodium falciparum positive blood samples in a tertiary care centre in South India.

Rapid diagnostic card tests (RDTs) enable timely and appropriate diagnosis of malaria especially in remote areas. Plasmodium falciparum histidine rich protein 2 (PFHRP2) is the most targeted antigen for the detection of Plasmodium falciparum infections by rapid diagnostic card test. Genetic mutations and gene deletions are important emerging factors for false-negative RDTs, which may delay the provision of life-saving treatment for the patients. Hence, we would like to evaluate for the existence of pfhrp2/3 gene deleted P. falciparum parasites in our health care setting. This study was conducted for a period of 2 years in a tertiary care centre in South India. Blood samples that are microscopically confirmed as P. falciparum but negative by RDT were assessed for the presence of pfhrp2, pfhrp3, and their flanking genes using conventional PCR. Follow up of the clinical outcomes were also done for these patients. Of the 63 positive samples collected (50 /63) 79.4% were P.vivax and (13/63) 20.6% were P.falciparum by PCR. Among the 13 P. falciparum positive samples, 4 samples (4/13), (95% CI -10.36% to 61.11%) were found to be RDT negative but microscopically positive.Pfhrp2,pfhrp3 and their flanking genes were amplified for these 4 samples. All 4 samples were found to be negative for both pfhrp2-2 & pfhrp2-3 exon regions and also varying patterns of flanking gene deletions were also noted.This study provides molecular evidence for the existence of pfhrp2 & pfhrp3 deleted P. falciparum parasites in a tertiary care centre in South India warranting periodic evaluation of pfhrp2 based RDT use. Only pfhrp2/3 RDT based decision on diagnosis of P.falciparum malaria should always be reconsidered especially in remote areas.

Plasmon-Phonon Coupling in Electrostatically Gated ß-Ga2O3 Films with Mobility Exceeding 200 cm2 V-1 s-1.

Monoclinic ß-Ga2O3, an ultra-wide bandgap semiconductor, has seen enormous activity in recent years. However, the fundamental study of the plasmon-phonon coupling that dictates electron transport properties has not been possible due to the difficulty in achieving higher carrier density (without introducing chemical disorder). Here, we report a highly reversible, electrostatic doping of ß-Ga2O3 films with tunable carrier densities using ion-gel-gated electric double-layer transistor configuration. Combining temperature-dependent Hall effect measurements, transport modeling, and comprehensive mobility calculations using ab initio based electron-phonon scattering rates, we demonstrate an increase in the room-temperature mobility to 201 cm2 V-1 s-1 followed by a surprising decrease with an increasing carrier density due to the plasmon-phonon coupling. The modeling and experimental data further reveal an important "antiscreening" (of electron-phonon interaction) effect arising from dynamic screening from the hybrid plasmon-phonon modes. Our calculations show that a significantly higher room-temperature mobility of 300 cm2 V-1 s-1 is possible if high electron densities (>1020 cm-3) with plasmon energies surpassing the highest energy LO mode can be realized. As Ga2O3 and other polar semiconductors play an important role in several device applications, the fundamental understanding of the plasmon-phonon coupling can lead to the enhancement of mobility by harnessing the dynamic screening of the electron-phonon interactions.