Neoantigen Identification and Dendritic Cell-Based Vaccines for Lung Cancer Immunotherapy.

Immunotherapies can treat many cancers, including difficult-to-treat cases such as lung cancer. Due to its tolerability, long-lasting therapeutic responses, and efficacy in a wide spectrum of patients, immunotherapy can also help to treat lung cancer, which has few treatment choices. Tumor-specific antigens (TSAs) for cancer vaccinations and T-cell therapies are difficult to discover. Neoantigens (NeoAgs) from genetic mutations, irregular RNA splicing, protein changes, or viral genetic sequences in tumor cells provide a solution. NeoAgs, unlike TSAs, are non-self and can cause an immunological response. Next-generation sequencing (NGS) and bioinformatics can swiftly detect and forecast tumor-specific NeoAgs. Highly immunogenic NeoAgs provide personalized or generalized cancer immunotherapies. Dendritic cells (DCs), which originate and regulate T-cell responses, are widely studied potential immunotherapeutic therapies for lung cancer and other cancers. DC vaccines are stable, reliable, and safe in clinical trials. The purpose of this article is to evaluate the current status, limitations, and prospective clinical applications of DC vaccines, as well as the identification and selection of major histocompatibility complex (MHC) class I and II genes for NeoAgs. Our goal is to explain DC biology and activate DC manipulation to help researchers create extremely potent cancer vaccines for patients.

Thrombolysis vs Anticoagulation: Unveiling the Trade-Offs in Massive Pulmonary Embolism.

Massive pulmonary embolism (MPE) is a severe form of venous thromboembolism (VTE) wherein enormous blood clots block the pulmonary arteries, resulting in substantial illness and death. Even with the progress made in diagnostic methods and treatments, the most effective approach for managing MPE is still a topic of considerable discussion. This study examines the delicate equilibrium between thrombolysis and anticoagulation in managing the problematic clinical situation posed by MPE, elucidating the compromises linked to each strategy. The genesis of MPE lies in the pathophysiology of VTE, when blood clots that originate from deep veins in the lower legs or pelvis move to the pulmonary vasculature, leading to an abrupt blockage. This obstruction leads to a series of hemodynamic alterations, such as elevated pulmonary vascular resistance, strain on the right ventricle, and compromised cardiac output, finally resulting in cardiovascular collapse. The seriousness of MPE is commonly categorized according to hemodynamic stability, with significant cases presenting immediate risks to patient survival. Traditionally, heparin has been the primary approach to managing MPE to prevent the spread of blood clots and their movement to other parts of the body. Nevertheless, there have been ongoing discussions regarding the effectiveness of thrombolysis, which entails the immediate delivery of fibrinolytic drugs to remove the blood clot. The use of thrombolysis in managing MPE is being reconsidered because of concerns over bleeding complications and long-term results despite its capacity to resolve the blocking clot quickly. This review rigorously analyzes the current body of evidence, exploring the intricacies of thrombolysis and anticoagulation in MPE. The focus is on evaluating the risk-benefit balance of each treatment option, considering aspects such as the patient's other medical conditions, hemodynamic stability, and potential long-term consequences. This review aims to clarify the complexities of the thrombolysis versus anticoagulation dilemma. It seeks to provide clinicians, researchers, and policymakers with a thorough understanding of the trade-offs in managing MPE. The goal is to facilitate informed decision-making and enhance patient outcomes.

Paroxysmal atrial fibrillation and hemochromatosis: a narrative review.

Paroxysmal atrial fibrillation (PAF) and hemochromatosis have a complex relationship. This review explores its mechanisms, prevalence, correlations, and clinical manifestations. Hereditary hemochromatosis (HH) involves iron overload due to HFE protein mutations, while atrial fibrillation (AF) is characterized by irregular heart rhythms. Iron overload in hemochromatosis can promote cardiac arrhythmias. AF is prevalent in developed countries and may be linked to cryptogenic strokes. Genetic variations and demographic factors influence the occurrence of both conditions. HH affects multiple organ systems, including the heart, while AF causes palpitations and reduced exercise tolerance. Diagnosis involves iron markers, genotypic testing, and electrocardiogram (ECG) findings. Treatment strategies focus on reducing iron levels in hemochromatosis and managing AF through antithrombotic therapy and rhythm control. Untreated hemochromatosis carries a higher risk of complications, and PAF is associated with increased cardiovascular-related mortality. For better understanding of the mechanisms and to improve management, additional studies are required. Tailored approaches and combined treatments may enhance patient outcomes.

Neuropsychiatric Disorders: Bridging the Gap Between Neurology and Psychiatry.

Given the ongoing difficulties faced by clinicians and researchers in dealing with neuropsychiatric illnesses, it is becoming more and more evident that there is a need to go beyond traditional disciplinary boundaries. This research consolidates existing material, examining changes in history, the fundamental neurobiological aspects, and the shared clinical manifestations between neurology and psychiatry. This inquiry examines the historical development of neuropsychiatry, focusing on the relationship between early understandings of mental illness and the later division of neurology and psychiatry. The focus is on recent advancements in comprehending the common neurobiological pathways and genetic factors that highlight the merging of these fields. The research highlights the complexities of clinical presentations in neuropsychiatric illnesses by analyzing the overlapping cognitive, affective, and behavioral symptoms. The text critiques the diagnostic issues in traditional frameworks, emphasizing the limitations in differentiating between neurological and psychiatric origins. This has ramifications for achieving correct diagnosis and arranging appropriate treatment. The paper explores developing multidisciplinary care approaches, highlighting successful collaborations between neurologists and psychiatrists. This study examines the difficulties in carrying out a plan and the process of identifying obstacles to combining different elements. It also highlights the urgent need for improved instruction and learning for smooth cooperation. The paper examines the therapeutic implications by investigating pharmacological therapies focusing on shared pathways. It also discusses the difficulties involved in managing neurological and psychiatric diseases that occur together. The study also explores non-pharmacological therapies, such as psychotherapy and rehabilitation methods, as part of a comprehensive treatment approach. Anticipating the future, the report identifies areas where the study could be improved and forecasts the influence of technological improvements on the subject. Suggestions are put out to encourage additional exploration, cooperation, and originality to narrow the divide between neurology and psychiatry, ultimately augmenting our comprehension and treatment of neuropsychiatric illnesses. This real-time synthesis adds to the ongoing discussion, providing valuable insights that align with the ever-changing field of contemporary neuropsychiatric research and therapy.

Thyroid and Its Ripple Effect: Impact on Cardiac Structure, Function, and Outcomes.

Thyroid dysfunction is a widespread and complex issue in the field of endocrine disorders. It has a significant impact on multiple physiological systems, particularly on the heart. This review explores the complex interaction between thyroid dysfunction and cardiac dynamics, examining the detailed network of molecular, cellular, and systemic changes that underlie the close connection between these two physiological areas. Thyroid dysfunction, which includes both hyperthyroidism and hypothyroidism, is a common endocrine condition that affects millions of people worldwide. The thyroid hormones thyroxine and triiodothyronine regulate various metabolic activities essential for maintaining cellular balance. Disruptions in thyroid function result in widespread consequences, affecting the cardiovascular system. Thyroid hormones directly impact cardiac muscle cells, controlling their ability to contract, their electrical properties, and their reaction to hypertrophy. Thyroid dysfunction goes beyond the level of individual cells and involves complex interactions among vascular dynamics, neurohormonal control, and endothelial function. These factors all contribute to the development of cardiovascular illness. The impact of thyroid dysfunction on cardiac structure, function, and outcomes is not limited to a one-way pattern. Instead, it involves a dynamic two-way interaction. The manifestations of this condition can vary from minor changes in the electrical activity of the heart to more obvious structural abnormalities, such as an increase in the size of the heart muscle and a decrease in its ability to relax during the filling phase. Furthermore, the correlation between thyroid dysfunction and adverse cardiovascular outcomes, such as heart failure and arrhythmias, highlights the clinical importance of this connection. This review provides a complete overview of the relationship between thyroid dysfunction and cardiac dynamics by analyzing a wide range of research from clinical, molecular, and epidemiological perspectives. This study seeks to enhance our comprehension of the comprehensive effects of thyroid dysfunction on the anatomy and function of the heart by explaining the complex molecular mechanisms and systemic consequences. The goal is to establish a basis for informed clinical treatment and future research efforts.

A crossbar architecture based system (CAS) as hydrogen gas sensing platform.

The development of sensing technologies and miniaturization allows for the development of smart systems with elevated sensing performance. Silicon-based hydrogen sensors have received a lot of attention due to its electrical conductivity and the mechanical endurance. With this motivation, we have proposed a two-terminal silicon-based device in a crossbar architecture as a hydrogen gas sensing platform. In this work, we have adopted a multi-layer modeling approach to analyze the performance of the proposed system. Technology computer-aided design models have been used to capture device performance. A gas sensor model based on hydrogen adsorption on the Palladium surface and a crossbar model has been adopted to understand the Palladium work function variation with gas pressure and the performance of the proposed crossbar system respectively. We have shown the impact of parameters like interconnect resistance and array size on the whole system's performance. Finally, a comprehensive analysis has been provided for the design rule of this architecture. A fabrication process to spur future experimental works has also been added. This work will provide computational insight into the performance of a crossbar hydrogen sensor system, optimized against some critical parameters.

Bioactives Promiscuity of Mucin: Insight from Multi-Spectroscopic, Thermodynamic, and Molecular Dynamic Simulation Analyses.

Mucosal drug delivery plays an increasing role in the clinical setting owing to mucin's advantageous biochemical and pharmacological properties. However, how this transport system recognizes different substrates remains unclear. In this study, we explore the mechanism of bioactive (quercetin and berberine) promiscuity of mucin using various spectroscopic techniques and molecular dynamics simulations. The UV-visible spectroscopy results and the decreased fluorescence intensity of mucin in the presence of the bioactive compounds via a static quenching mechanism confirmed ground-state complex formation between the bioactives and mucin. The binding constants (Kb) were evaluated at different temperatures to afford Kb values of ∼104 Lmol-1, demonstrating the moderate and reasonable affinity of the bioactives for mucin, yielding greater diffusion into the tissues. Thermodynamic analysis and molecular dynamics (MD) simulations demonstrate that mucin-bioactive complex formation occurs primarily because of electrostatic/ionic interactions, while hydrophobic interactions were also crucial in stabilizing the complex. Far-UV circular dichroism spectroscopy showed that bioactive binding induced secondary structural changes in mucin. Sitemap and MD simulation indicated the principal binding site of mucin for the bioactives. This study also provides insight into the bioactives promiscuity of mucin in the presence of a crowded environment, which is relevant to the biological activity of mucin in vivo. An in vitro drug release study revealed that crowding assisted drug release in an enhanced burst manner compared with that in a dilute buffer system. This work thus provides fresh insight into drug absorption and distribution in the native cellular environment and helps direct new drug design and use in pharmaceutical and pharmacological fields.

Role of lymphocytes, macrophages and immune receptors in suppression of tumor immunity.

Cancer is now the leading cause of mortality across the world. Inflammatory immune cells are functionally important in the genesis and progression of tumors, as demonstrated by their presence in human tumors. Numerous research has recently been conducted to determine if the innate and adaptive immune systems' cytotoxic cells can inhibit tumor growth and spread. Majority of cancers, when growing into identifiable tumors use multiple strategies to elude immune monitoring by lowering tumor immunity. Immunological suppression in the tumor microenvironment is achieved through interfering with antigen-presenting cells and effector T cells. Treatment of cancer requires managing both the tumor as well as tumor microenvironment (TME). Most patients will not be able to gain benefits from immunotherapy because of the immunosuppressive tumor microenvironment. The actions of many stromal myeloid and lymphoid cells are regulated to suppress tumor-specific T lymphocytes. These frequently exhibit inducible suppressive processes brought on by the same anti-tumor inflammatory response the immunotherapy aims to produce. Therefore, a deeper comprehensive understanding of how the immunosuppressive environment arises and endures is essential. Here in this chapter, we will talk about how immune cells, particularly macrophages and lymphocytes, and their receptors affect the ability of tumors to mount an immune response.

Acute Ischemic Stroke Among Cannabis Users in the United States and Possible Risk Factors for Mortality.

BACKGROUND: With changes in state laws, cannabis is now more accessible in many parts of the United States. The drug has previously been associated with a higher incidence of acute ischemic stroke (AIS). Our study analyzed the effect of cannabis use on AIS outcomes. METHODS: The 2019 National Inpatient Sample from Healthcare Cost and Utilization Project and Agency for Healthcare Research and Quality was used to evaluate the AIS patients ages 25 and more. Cannabis users were compared with nonusers. Their mortality risks were also assessed. RESULTS: Five hundred thirty-nine thousand eight hundred eighty patients with AIS were in our study and 8850 used cannabis. Among the cannabis users with AIS, 69.8% were males, 50.6% were white, 61.8% were aged 46 to 65, 32.1% used Medicaid, 86.1% were nonobese, 72.0% were nondiabetics, 81.7% had hypertension, 80.7% did not have a history of alcohol abuse, and 77.5% were smokers (nicotine). Only 12.8% of cannabis users reported any cardiac dysrhythmia, whereas 5.4% required mechanical thrombectomy, and 8.0% received intravenous tissue plasminogen activator (tPA).After adjusting the variables, cannabis users covered by Medicare, with diabetes, a history of alcohol abuse, cardiac dysrhythmias, and who underwent mechanical thrombectomy had a higher risk of dying. The overall adjusted odds ratio of dying among cannabis users with AIS was 0.603 (95% CI, 0.504-0.722, P <0.01). CONCLUSIONS: Although the overall mortality risk seems to be lower among cannabis users, those with certain risk factors still present higher mortality risks. Patients with cannabis use should therefore be monitored closely for possible complications and mortality after AIS.

Novel Therapies in Diabetes: A Comprehensive Narrative Review of GLP-1 Receptor Agonists, SGLT2 Inhibitors, and Beyond.

Diabetes mellitus, a widespread metabolic illness with increasing global occurrence, continues to have a significant impact on public health. Diabetes is a condition marked by long-term high blood sugar levels. It is caused by a combination of genetic, environmental, and lifestyle factors, which lead to problems with insulin production and insulin resistance. This dysfunctional state disturbs the delicate balance of glucose regulation, promoting the emergence of problems in both large and small blood vessels that have a substantial impact on illness and death rates. Traditional therapy methods have traditionally given more importance to managing blood sugar levels by using insulin sensitizers, secretagogues, and other medications that lower glucose levels. Advancements in our understanding of the underlying mechanisms of diabetes have led to a significant change in approach, focusing on comprehensive therapies that target not only high blood sugar levels but also the accompanying dangers to the heart and kidneys. This study examines the evolving field of diabetes therapies, explicitly highlighting the significance of GLP-1 receptor agonists and SGLT2 inhibitors. These two types of drugs have become essential components in modern diabetes management. GLP-1 receptor agonists replicate the effects of natural glucagon-like peptide-1, leading to insulin production that is reliant on glucose levels, reducing the release of glucagon, and providing cardiovascular advantages that go beyond controlling blood sugar levels. SGLT2 inhibitors, however, act on the process of renal glucose reabsorption, leading to increased excretion of glucose in the urine and showing significant benefits for cardiovascular and renal protection. This extensive investigation seeks to contribute to the ongoing discourse on diabetes therapies by synthesizing existing research. This review aims to provide clinicians, researchers, and policymakers with a comprehensive understanding of the disease background and the specific pharmacological details of GLP-1 receptor agonists, SGLT2 inhibitors, and other related treatments. The goal is to assist them in developing more effective and personalized strategies to tackle the complex challenges presented by diabetes.

Neurological Manifestations of Infectious Diseases: Insights From Recent Cases.

This narrative review examines the complex connection between infectious diseases and their neurological effects. It provides a detailed analysis of recent instances and insights derived from various pathogens. As we explore the realm of infectious agents, including viruses, bacteria, parasites, and fungi, a thorough and diverse analysis reveals the intricacies of neurological problems. The review begins by examining viral infections, specifically focusing on how viruses invade the neurological system and its subsequent effects. Significant instances from recent widespread disease outbreaks function as instructive benchmarks, highlighting the progressing comprehension of these ever-changing interconnections. The article examines the complex pathophysiology of neurological problems caused by bacterial infections. It presents current cases that illustrate the various ways these complications might manifest and the difficulties faced in their therapeutic management. Parasitic and fungal infections, which are typically overlooked, are being carefully examined to emphasize their distinct role in causing neurological complications. The mentioned cases highlight the importance of being thoroughly aware of these less-explored areas ranging from protozoan parasites to opportunistic fungal infections. In addition to the immediate effects caused by infectious agents, the review investigates autoimmune responses activated by infections. It provides a detailed examination of specific instances that shed light on the complex relationship between viral triggers and future neurological problems. This text elaborates on the intricacy of autoimmune-related neurological issues, highlighting the necessity for a comprehensive approach to diagnosing and treating them. The narrative next redirects its attention to the diagnostic difficulties that arise when interpreting the neurological symptoms of viral disorders. This article provides a thorough examination of existing diagnostic tools, along with an investigation into new technologies that have the potential to improve our capacity to identify and comprehend complex presentations. This debate connects to the following examination of treatment methods, where current cases that showcase successful interventions are carefully examined to extract valuable insights into good clinical management. The discussion focuses on the public health implications of preventive efforts against infectious infections, including their neurological consequences. The story emphasizes the link between infectious diseases and overall societal health, advocating for a proactive strategy to reduce the impact of neurological complications. The abstract concludes by providing a prospective viewpoint, highlighting areas of research that still need to be addressed, and suggesting potential future avenues. This narrative review seeks to provide a comprehensive resource for physicians, researchers, and public health professionals dealing with the complex field of neurological manifestations in infectious diseases. It combines recent examples, synthesizes current information, and offers a holistic perspective.

Lipid Disorders and Cardiovascular Risk: A Comprehensive Analysis of Current Perspectives.

The increasing worldwide prevalence of cardiovascular diseases (CVDs) highlights the need to understand the complex relationships between lipid abnormalities and elevated cardiovascular risk. This review thoroughly investigates the complex terrain of lipid abnormalities, highlighting their crucial significance in developing CVDs. Dyslipidemia, which is closely connected to atherosclerosis, is a significant risk factor for CVDs, including coronary artery disease, myocardial infarction, and stroke. This review thoroughly examines the intricate relationship between lipoproteins, cholesterol metabolism, and the inflammatory cascade, providing a detailed comprehension of the mechanisms that contribute to atherogenic processes. An extensive analysis of the occurrence and distribution of lipid diseases worldwide indicates a concerning high frequency, which calls for a reassessment of public health approaches. Dyslipidemia is caused by a combination of genetic predispositions, lifestyle factors, and metabolic abnormalities, as supported by significant data. Moreover, investigating different types of lipoproteins and their specific functions in the development of atherosclerosis provides insight into the complex causes of CVDs. In addition to conventional lipid profiles, newly identified biomarkers and advanced imaging techniques are being carefully examined for their ability to improve risk classification and treatment strategies' effectiveness. From a critical perspective, the review thoroughly examines the current state of lipid-modifying medicines, specifically statins, fibrates, and new therapeutic approaches. The text discusses the emerging concept of precision medicine, which involves tailoring treatment approaches to individuals based on their genetic and molecular characteristics. This approach has the potential to improve treatment outcomes. In addition, this study critically assesses the effects of lifestyle changes and nutritional interventions on lipid homeostasis, offering a comprehensive view of preventive strategies. This review consolidates current viewpoints on lipid diseases and their complex correlation with cardiovascular risk. This review contributes to the ongoing cardiovascular disease prevention and management dialogue by clarifying the molecular mechanisms, exploring new therapeutic options, and considering broader societal implications.

Insulin Resistance and Coronary Artery Disease: Untangling the Web of Endocrine-Cardiac Connections.

The relationship between insulin resistance and coronary artery disease (CAD) is a crucial study area in understanding the complex connection between metabolic dysregulation and cardiovascular morbidity. This scholarly investigation examines the intricate relationship between insulin resistance, a key characteristic of metabolic syndrome, and CAD development. The goal is to understand the detailed molecular and physiological connections that underlie the dangerous connection between the endocrine and cardiac systems. The recognition of insulin resistance as a key player in cardiovascular disease highlights the need to study the complex relationships between insulin signaling pathways and the development of atherosclerosis. This research analyzes the molecular processes by which insulin resistance leads to disruptions in lipid metabolism, inflammatory reactions, and malfunction of the blood vessel's inner lining. These processes create an environment that promotes the development and advancement of CAD. As we begin this scientific exploration, it becomes clear that insulin resistance acts as a metabolic indicator and a potent mediator of endothelial dysfunction, oxidative stress, and systemic inflammation. The complex interaction between insulin-sensitive tissues and the vascular endothelium plays a crucial role in defining the pathophysiological landscape of CAD. Furthermore, this discussion highlights the mutual interaction between the endocrine and cardiac systems, where CAD produced by myocardial ischemia worsens insulin resistance through complex molecular pathways. Discovering new therapeutic targets that disrupt the harmful cycle between insulin resistance and the development of CAD shows potential for creating specific therapies to reduce cardiovascular risk in people with insulin resistance. This study aims to clarify the complexities of the connection between the endocrine system and the heart, establishing the basis for a thorough comprehension of how insulin resistance contributes to the development and advancement of CAD.

Large-Scale Traveling Atmospheric and Ionospheric Disturbances Observed in GUVI With Multi-Instrument Validations.

This study presents multi-instrument observations of persistent large-scale traveling ionosphere/atmospheric disturbances (LSTIDs/LSTADs) observed during moderately increased auroral electrojet activity and a sudden stratospheric warming in the polar winter hemisphere. The Global Ultraviolet Imager (GUVI), Gravity field and steady-state Ocean Circulation Explorer, Scanning Doppler Imaging Fabry-Perot Interferometers, and the Poker Flat Incoherent Scatter Radar are used to demonstrate the presence of LSTIDs/LSTADs between 19 UT and 5 UT on 18-19 January 2013 over the Alaska region down to lower midlatitudes. This study showcases the first use of GUVI for the study of LSTADs. These novel GUVI observations demonstrate the potential for the GUVI far ultraviolet emissions to be used for global-scale studies of waves and atmospheric disturbances in the thermosphere, a region lacking in long-term global measurements. These observations typify changes in the radiance from around 140 to 180 km, opening a new window into the behavior of the thermosphere.

Cardiac arrhythmias and mortality risk among patients with obstructive sleep apnea following admission for acute myocardial infarction or acute ischemic stroke.

Introduction: Obstructive sleep apnea (OSA) can cause several cardiovascular changes that increase the risk of various complications such as acute myocardial infarction (AMI) and acute ischemic stroke (AIS). Material and methods: We used the 2019 National Inpatient Sample (NIS) from the Healthcare Cost and Utilization Project (HCUP), the Agency for Healthcare Research and Quality (AHRQ), and their many collaborators to study the differences in characteristics and outcomes of OSA patients following AMI or AIS and the presence of several cardiac arrhythmias and their associated mortality risks. Results: A lower mortality rate was seen among OSA patients with AIS (2.5% compared to 3.8% in non-OSA), and AMI (2.8% compared to 4.7% in non-OSA). OSA patients with AIS had a higher risk of dying if they were aged 66 or over, of Hispanic origin, or if they reported ventricular tachycardia, or paroxysmal atrial fibrillation. For those with OSA and admitted for AMI, they were more at risk of dying if they were aged 66 or over, not classified as "White, Black, or Hispanic", with a history of diabetes, reported ventricular tachycardia, or ventricular fibrillation. Lower adjusted odds ratios were noted among OSA patients with hypertension in both AMI and AIS cases. Conclusions: Further studies comparing these characteristics based on the severity of OSA are therefore encouraged.

Mechanism Studies of Madden-Julian Oscillation Coupling Into the Mesosphere/Lower Thermosphere Tides Using SABER, MERRA-2, and SD-WACCMX.

The Madden-Julian Oscillation (MJO), an eastward-moving disturbance near the equator (±30°) that typically recurs every ∼30-90 days in tropical winds and clouds, is the dominant mode of intraseasonal variability in tropical convection and circulation and has been extensively studied due to its importance for medium-range weather forecasting. A previous statistical diagnostic of SABER/TIMED observations and the MJO index showed that the migrating diurnal (DW1) and the important nonmigrating diurnal (DE3) tide modulates on MJO-timescale in the mesosphere/lower thermosphere (MLT) by about 20%-30%, depending on the MJO phase. In this study, we address the physics of the underlying coupling mechanisms using SABER, MERRA-2 reanalysis, and SD-WACCMX. Our emphasis was on the 2008-2010 time period when several strong MJO events occurred. SD-WACCMX and SABER tides show characteristically similar MJO-signal in the MLT region. The tides largely respond to the MJO in the tropospheric tidal forcing and less so to the MJO in tropospheric/stratospheric background winds. We further quantify the MJO response in the MLT region in the SD-WACCMX zonal and meridional momentum forcing by separating the relative contributions of classical (Coriolis force and pressure gradient) and nonclassical forcing (advection and gravity wave drag [GWD]) which transport the MJO-signal into the upper atmosphere. Interestingly, the tidal MJO-response is larger in summer due to larger momentum forcing in the MLT region despite the MJO being most active in winter. We find that tidal advection and GWD forcing in MLT can work together or against each other depending on their phase relationship to the MJO-phases.

Molecular Insight into the Effects of Enhanced Hydrophobicity on Amyloid-like Aggregation.

Generally, hydrophobic amino acids provide hydrophobic interactions during peptide aggregation. However, besides the hydrophobic amino acids, some hydrophilic amino acids, such as glutamine, are also considered to be essential elements in many self-aggregating peptides. For example, huntingtin contains polyglutamine at its N-terminus and the yeast prion Sup35 protein has the GNNQQNY sequence, a peptide well-known for its ability for amyloid fibril formation. However, despite the frequent emergence of glutamine in self-assembling systems, the molecular mechanism of amyloid formation involving this unique amino acid has not been well documented. It is still not clear how this hydrophilic amino acid is responsible for the hydrophobic interaction in the self-association process. Therefore, in this study, we have carried out classical molecular dynamics simulations of the GNNQQNY peptide and its derivatives in pure water. We quantify the propensity for the formation of ß-sheet conformation with an increasing glutamine number in the peptide sequence. In addition, we assess the importance of the hydrophobicity of the dimethanediyl group present in glutamine (as well as in glutamic acid) for the self-association of the peptides through nonpolar solvent medium simulations.

A theory of resistivity in Kondo lattice materials: memory function approach.

We have theoretically analysed DC resistivity (ρ) in the Kondo-lattice materials using the powerful memory function formalism. The complete temperature evolution of ρ is investigated using the Wölfle-Götze expansion of the memory function. The resistivity in this model originates from spin-flip magnetic scattering of conduction s-electron off the quasi-localized d or f electron spins. We find the famous resistivity upturn in lower temperature regime (k B T ≪ µ d ), where µ d is the effective chemical potential of d-electrons. In the high temperature regime (µ d ≪ k B T) we discover that resistivity scales as cube root of T ([Formula: see text]). Our results are in reasonable agreement with the experimental results reported in the literature.