Explore the vast range of titles available.

Although 4G (fourth generation) i.e. LTE (long term evolution) systems are now in use world-wide. But today’s 4G systems have some challenges left such as spectrum scarcity and energy efficiency. The prime objectives of near-by-future 5G (fifth generation) wireless communications are reliability, higher data rate, higher bandwidth, high spectrum efficiency, higher energy efficient and that too at lower latency. Channel coding tend to increase the reliability of the wireless communications system by adding extra bits in a controlled fashion and is considered to be most persuasive element of communication system. 4G LTE Turbo Codes have already been replaced by LDPC (low density parity check) Codes in many of the standards including mMTC (massive machine type communication), D2D (device to device communication) and URLLC (ultra-reliable low latency reliable communications). LDPC Codes and Polar Codes are securing much more observation because of their inherent advantages of excellent bit-error-rate performance, fast encoding and decoding procedures; which make them the strong contenders for 5G Channel Codes too. This paper provides the broad survey and comparison of the LDPC and Polar Codes along with their advantages and drawbacks which will aid in further improvement of the next generation wireless networks. In order to enlighten future research possibilities in this direction, issues addressed by distinct researchers have been explored too.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can cause neurological disease in humans, but little is known about the pathogenesis of SARS-CoV-2 infection in the central nervous system (CNS). Herein, using K18-hACE2 mice, we demonstrate that SARS-CoV-2 neuroinvasion and encephalitis is associated with mortality in these mice. Intranasal infection of K18-hACE2 mice with 105 plaque-forming units of SARS-CoV-2 resulted in 100% mortality by day 6 after infection. The highest virus titers in the lungs were observed on day 3 and declined on days 5 and 6 after infection. By contrast, very high levels of infectious virus were uniformly detected in the brains of all the animals on days 5 and 6. Onset of severe disease in infected mice correlated with peak viral levels in the brain. SARS-CoV-2-infected mice exhibited encephalitis hallmarks characterized by production of cytokines and chemokines, leukocyte infiltration, hemorrhage and neuronal cell death. SARS-CoV-2 was also found to productively infect cells within the nasal turbinate, eye and olfactory bulb, suggesting SARS-CoV-2 entry into the brain by this route after intranasal infection. Our data indicate that direct infection of CNS cells together with the induced inflammatory response in the brain resulted in the severe disease observed in SARS-CoV-2-infected K18-hACE2 mice.

microRNAs (miRNAs) are known to play critical roles in the regulation of gene expression during neurodegenerative diseases and neurotropic viral infections. However, their specific contribution to the pathogenesis of Powassan virus (POWV) infection in the brain remains poorly understood. Understanding miRNA dynamics in the brain during POWV infection may reveal novel insights into viral neuropathogenesis and host antiviral responses. Therefore, in the present study, we analyzed miRNA expression profiles in the mouse brain at different time points following a peripheral POWV infection. A total of 599 miRNAs were examined at day 3, 6, and 9 post-infection. Infection with POWV resulted in the modulation of several miRNAs in the brain at all time points. There was a progressive increase in the number of dysregulated miRNAs over the course of infection. This correlated with POWV dissemination into the brain with a progressive increase in viral RNA levels that peaked at day 9 post-infection. There was an early upregulation of miR-1983, miR-19a, and miR-216b that persisted until day 9 post-infection. POWV infection also resulted in the downregulation of miR-500 at all examined time points. Using IPA, we determined the significant canonical pathways affected by miRNA dysregulation. POWV infection modulated the activation of the thyroid hormone receptor and retinoid X receptor (TR/RXR) and the regulation of the phosphatase and tensin homolog (PTEN). Additionally, macrophage classical activation and growth arrest and DNA damage-inducible 45 (GADD45) signaling were activated as early as day 3 post-infection and persisted until day 9 post-infection. Furthermore, our analysis revealed the activation of cell death pathways such as necrosis and apoptosis and the inhibition of cell cycle progression, as well as leukopoiesis. To our knowledge, this is the first study to evaluate the modulation of miRNAs in the brain following POWV infection.

Extraskeletal mesenchymal chondrosarcoma is a rare soft tissue sarcoma arising from soft tissues, mainly of the lower extremities, meninges, and orbits. It usually presents during the second to third decades of life, and has a slight predominance in females. Histologically, it has a typical biphasic pattern comprising small cells and islands of hyaline cartilage. It can pose a diagnostic challenge in small biopsy specimens where 1 of the 2 components can be absent. The prognosis is extremely variable; survival varies depending on the location of the tumor.

SARS-CoV-2 can cause severe lung damage due to uncontrolled viral replication or/and excessive inflammation. New variants of concern (VOCs) have raised additional concerns due to disparate pathogenicity and possible enhanced virulence. Herein, using RNA sequencing, we performed a comparative transcriptomic analysis following infection with major VOCs. We evaluated the transcriptional changes induced in the lungs of K18-hACE2 mice following infection with the ancestral B.1 lineage (Wuhan), B.1.1.7 (Alpha), B.1.351 (Beta), B.1.617.2 (Delta), B.1.1.529 (Omicron) variants or mouse-adapted SARS-CoV-2 (MA10). Our work reveals the molecular basis of pathological hallmarks in the lungs associated with SARS-CoV-2 infection. We report that infection with B.1, pre-Omicron VOCs, and MA10 induce similar molecular fingerprints of excessive lung inflammation and immune activation in K18-hACE2 mice. Analysis of differentially expressed genes revealed both shared and variant-specific responses, with key immune markers such as Cxcl10, Zbp1, Ifit3, Isg15, Rsad2, and Irf7 consistently upregulated across variants. Clustering of highly variable genes across samples revealed two variant groups distinguished by upregulation of antigen presentation and immune-related genes ( e.g. Retnla, Saa3, Plac8, Ly6c2, H2-D1, and H2-K1 ). Delta, Beta, Alpha, and MA10 showed elevated expression, whereas Wuhan and Omicron exhibited attenuated responses. In addition, we show that Z-DNA-binding protein 1 (ZBP1) plays a role in viral clearance in the lungs after SARS-CoV-2 infection. ZBP1 deficiency resulted in reduced expression of cell death-associated markers and virus-induced cell death in the lungs following MA10 infection. Furthermore, the knockout of ZBP1 resulted in an attenuated inflammatory response with reduced production of proinflammatory cytokines and chemokines and decreased macrophage infiltration in the lungs. These results suggest that ZBP1 plays a role in viral clearance and in enhancing the inflammatory response and virus-induced cell death during SARS-CoV-2 infection. Altogether, our study provides insights into the pathogenesis of SARS-CoV-2 infection in mice, facilitating the identification of biomarkers and the development of potential therapeutic targets.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused the current pandemic, resulting in millions of deaths worldwide. Increasingly contagious variants of concern (VoC) have fueled recurring global infection waves. A major question is the relative severity of the disease caused by previous and currently circulating variants of SARS-CoV-2. In this study, we evaluated the pathogenesis of SARS-CoV-2 variants in human ACE-2-expressing (K18-hACE2) mice. Eight-week-old K18-hACE2 mice were inoculated intranasally with a representative virus from the original B.1 lineage or from the emerging B.1.1.7 (alpha), B.1.351 (beta), B.1.617.2 (delta), or B.1.1.529 (omicron) lineages. We also infected a group of mice with the mouse-adapted SARS-CoV-2 (MA10). Our results demonstrate that B.1.1.7, B.1.351 and B.1.617.2 viruses are significantly more lethal than the B.1 strain in K18-hACE2 mice. Infection with the B.1.1.7, B.1.351, and B.1.617.2 variants resulted in significantly higher virus titers in the lungs and brain of mice compared with the B.1 virus. Interestingly, mice infected with the B.1.1.529 variant exhibited less severe clinical signs and a high survival rate. We found that B.1.1.529 replication was significantly lower in the lungs and brain of infected mice in comparison with other VoC. The transcription levels of cytokines and chemokines in the lungs of B.1- and B.1.1.529-infected mice were significantly less when compared with those challenged with other VoC. Together, our data provide insights into the pathogenesis of previous and circulating SARS-CoV-2 VoC in mice.

Zika virus (ZIKV) infections have caused a wide spectrum of neurological diseases, such as Guillain-Barré syndrome, myelitis, meningoencephalitis, and congenital microcephaly. No effective therapies currently exist for treating patients infected with ZIKV. MicroRNAs (miRNAs) are a group of small RNAs involved in the regulation of a wide variety of cellular and physiological processes. In this study, we analyzed digital miRNA and mRNA profiles in ZIKV-infected primary mouse neurons using the nCounter technology. A total of 599 miRNAs and 770 mRNAs were examined. We demonstrate that ZIKV infection causes global downregulation of miRNAs with only few upregulated miRNAs. ZIKV-modulated miRNAs including miR-155, miR-203, miR-29a, and miR-124-3p are known to play critical role in flavivirus infection, anti-viral immunity and brain injury. ZIKV infection also results in downregulation of miRNA processing enzymes. In contrast, ZIKV infection induces dramatic upregulation of anti-viral, inflammatory and apoptotic genes. Furthermore, our data demonstrate an inverse correlation between ZIKV-modulated miRNAs and target host mRNAs induced by ZIKV. Biofunctional analysis revealed that ZIKV-modulated miRNAs and mRNAs regulate the pathways related to neurological development and neuroinflammatory responses. Functional studies targeting specific miRNA are warranted to develop therapeutics for the management of ZIKV neurological disease.

West Nile virus (WNV) and Japanese encephalitis virus (JEV) are major mosquito-borne pathogens that cause severe neurological illnesses in humans, including encephalitis and meningitis. Neurons are the primary target of WNV and JEV infections in the brain. However, the pathogenic mechanisms and host immune response associated with WNV and JEV infections in the primary neurons are not fully characterized. Herein, using high-throughput RNA sequencing (RNA-Seq), we performed a comparative transcriptomic analysis of the primary mouse neurons following infection with WNV and JEV. We identified differentially expressed host genes (DEGs) that were commonly induced in neurons by both viruses, as well as those uniquely regulated in a virus-specific manner. We observed pronounced changes in gene expression profiles that indicate activation of a robust antiviral response accompanied by signatures of neuronal dysfunction. Notably, interferon-stimulated genes such as Irf7 , Isg15 , and Ifnb1 were markedly upregulated in WNV- and JEV-infected neurons. Additionally, we observed the significant upregulation of proinflammatory chemokine and cytokine genes such as Il6 , Cxcl2 and Cxcl10 which was further validated by Luminex assay. Ingenuity Pathway Analysis (IPA) revealed the activation of several cell death pathways including pyroptosis and necroptosis. We also showed the significant dysregulation in pattern recognition receptors and neurotransmitter receptors such as glutamatergic and acetylcholine receptors. This dysregulation extended to the synaptic signaling and reduced synaptogenesis in infected neurons. Quantitative RT-PCR confirmed the upregulation of key cytokines like Il6 and Ifna , further establishing the validity of the RNA-Seq approach. Overall, this study provides insights into the pathological changes in the neurons following WNV and JEV infections.

The global pandemic of prediabetes and diabetes has led to a severe corresponding complication of these disorders. Neuropathy is one of the most prevalent complication of diabetes is, affecting blood supply of the peripheral nervous system that may eventually results into loss of sensations, injuries, diabetic foot and death. The utmost identified risk of diabetic neuropathy is uncontrolled high blood glucose levels. However, aging, body mass index (BMI), oxidative stress, inflammation, increased HbA1c levels and blood pressure are among the other key factors involved in the upsurge of this disease. The so far treatment to deal with diabetic neuropathy is controlling metabolic glucose levels. Apart from this, drugs like reactive oxygen species (ROS) inhibitors, aldose reductase inhibitors, PKC inhibitors, Serotonin-norepinephrine reuptake inhibitors (SNRIs), anticonvulsants, N-methyl-D-aspartate receptor (NMDAR) antagonists, are the other prescribed medications. However, the related side-effects (hallucinations, drowsiness, memory deficits), cost, poor pharmacokinetics and drug resistance brought the trust of patients down and thus herbal renaissance is occurring all over the word as the people have shifted their intentions from synthetic drugs to herbal remedies. Medicinal plants have widely been utilized as herbal remedies against number of ailments in Indian medicinal history. Their bioactive components are very much potent to handle different chronic disorders and complications with lesser-known side effects. Therefore, the current article mainly concludes the etiology and pathophysiology of diabetic neuropathy. Furthermore, it also highlights the important roles of medicinal plants and their naturally occurring bioactive compounds in addressing this disease.Graphical abstract

Since the onset of the COVID-19 pandemic, various severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) variants have emerged. Although the primary site of SARS-CoV-2 infection is the lungs, it can also affect the brain and induce neurological symptoms. However, the specific effects of different variants on the brain remain unclear. In this study, a whole-transcriptome analysis was conducted using the brain tissues of K18-hACE2 mice infected with the ancestral B.1 (Wuhan) variant and with major SARS-CoV-2 variants of concern, including B.1.1.7 (Alpha), B.1.351 (Beta), B.1.617.2 (Delta) and B.1.529 (Omicron). After sequencing, differential gene expression, gene ontology (GO) and genome pathway enrichment analyses were performed. An Immune Cell Abundance Identifier (ImmuCellAI) was used to identify the abundance of different cell populations. Additionally, RT-qPCR was used to validate the RNA-seq data. The viral load and hierarchical clustering analyses divided the samples into two different clusters with notable differences in gene expression at day 6 post-infection for all variants compared to the control group. GO and the Kyoto Encyclopedia of genes and genomes enrichment analyses revealed similar patterns of pathway enrichment for different variants. ImmuCellAI revealed the changes in immune cell populations, including the decrease in CD4+ T and B cell proportions and the increase in CD8+ T and dendritic cell proportions. A co-expression network analysis revealed that some genes, such as STAT1, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), were dysregulated in all variants. A RT-qPCR analysis for IL-6, CXCL10 and IRF7 further validated the RNA-seq analysis. In conclusion, this study provides, for the first time, an extensive transcriptome analysis of a K18-hACE2 mouse brain after infection with major SARS-CoV-2 variants.