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Purpose of Review: Although the respiratory system is the main target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), it is evident from recent data that other systems, especially cardiovascular and hematological, are also significantly affected. In fact, in severe form, COVID-19 causes a systemic illness with widespread inflammation and cytokine flood, resulting in severe cardiovascular injury. Therefore, we reviewed cardiac injury biomarkers' role in various cardiovascular complications of COVID 19 in recent studies., Recent Findings: Cardiac injury biomarkers were elevated in most of the complicated cases of COVID-19, and their elevation is directly proportional to the worst outcome. Evaluation of cardiac biomarkers with markers of other organ damage gives a more reliable tool for case fatalities and future outcome., Summary: Significant association of cardiac biomarkers in COVID-19 cases helps disease management and prognosis, especially in severely ill patients., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Vancomycin, an antibiotic used occasionally as a last line of treatment for methicillin-resistant Staphylococcus aureus , is reportedly associated with nephrotoxicity. This study aimed at evaluating the protective effects of lutein against vancomycin-induced acute renal injury. Peroxisome proliferator-activated receptor gamma (PPARγ) and its associated role in renoprotection by lutein was also examined. Male BALB/c mice were divided into six treatment groups: control with normal saline, lutein (200 mg/kg), vancomycin (250 mg/kg), vancomycin (500 mg/kg), vancomycin (250 mg/kg) with lutein, and vancomycin (500 mg/kg) with lutein groups; they were euthanized after 7 days of treatment. Thereafter, samples of blood, urine, and kidney tissue of the mice were analyzed, followed by the determination of levels of N-acetyl-β-D-glucosaminidase (NAG) in the urine, renal creatine kinase; protein carbonyl, malondialdehyde, and caspase-3 in the kidney; and the expression of PPARγ, nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappaB (NF-κB) in renal tissue. Results showed that the levels of protein carbonyl and malondialdehyde, and the activity of NAG, creatine kinase and caspase-3, were significantly increased in the vancomycin-treatment groups. Moreover, the levels of Nrf2 significantly decreased, while NF-κB expression increased. Lutein ameliorated these effects, and significantly increased PPARγ expression. Furthermore, it attenuated vancomycin-induced histological alterations such as, tissue necrosis and hypertrophy. Therefore, we conclude that lutein protects against vancomycin-induced renal injury by potentially upregulating PPARγ/Nrf2 expression in the renal tissues, and consequently downregulating the pathways: inflammation by NF-κB and apoptosis by caspase-3.

Severe Acute Respiratory Syndrome Coronavirus-2 is a zoonotic virus with a possible origin in bats and potential transmission to humans through an intermediate host. When zoonotic viruses jump to a new host, they undergo both mutational and natural selective pressures that result in non-synonymous and synonymous adaptive changes, necessary for efficient replication and rapid spread of diseases in new host species. The nucleotide composition and codon usage pattern of SARS-CoV-2 indicate the presence of a highly conserved, gene-specific codon usage bias. The codon usage pattern of SARS-CoV-2 is mostly antagonistic to human and bat codon usage. SARS-CoV-2 codon usage bias is mainly shaped by the natural selection, while mutational pressure plays a minor role. The time-series analysis of SARS-CoV-2 genome indicates that the virus is slowly evolving. Virus isolates from later stages of the outbreak have more biased codon usage and nucleotide composition than virus isolates from early stages of the outbreak.

Biomarkers are increasingly recognized to have significant clinical value in early identification and progression of various cardiovascular diseases. There are many heart conditions, such as congestive heart failure (CHF), ischemic heart diseases (IHD), and diabetic cardiomyopathy (DCM), and cardiac remodeling, in which the severity of the cardiac pathology can be mirrored through these cardiac biomarkers. From the emergency department (ED) evaluation of acute coronary syndromes (ACS) or suspected acute myocardial infarction (AMI) with cardiac marker Troponin to the diagnosis of chronic conditions like Heart Failure (HF) with natriuretic peptides, like B-type natriuretic peptide (BNP), N-terminal pro-B- type natriuretic peptide (Nt-proBNP) and mid regional pro-atrial natriuretic peptide (MR- proANP), their use is continuously increasing. Their clinical importance has led to the discovery of newer biomarkers, such as the soluble source of tumorigenicity 2 (sST2), galectin-3 (Gal-3), growth differentiation factor-15 (GDF-15), and various micro ribonucleic acids (miRNAs). Since cardiac pathophysiology involves a complex interplay between inflammatory, genetic, neurohormonal, and biochemical levels, these biomarkers could be enzymes, hormones, and biologic substances showing cardiac injury, stress, and malfunction. Therefore, multi-marker approaches with different combinations of novel cardiac biomarkers, and continual assessment of cardiac biomarkers are likely to improve cardiac risk prediction, stratification, and overall patient wellbeing. On the other hand, these biomarkers may reflect coexisting or isolated disease processes in different organ systems other than the cardiovascular system. Therefore, knowledge of cardiac biomarkers is imperative. In this article, we have reviewed the role of cardiac biomarkers and their use in the diagnosis and prognosis of various cardiovascular diseases from different investigations conducted in recent years., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Turmeric, the golden Indian spice, and the edible oil of sesame seeds are the essential ingredients of Indian food created by ancestors and established the belief of the curative effect of food for many generations. Considering the anti-inflammatory effects of turmeric, we formulated a nano-emulsion of turmeric infused in edible sesame oil, with a globule size of 200-250 nm using high-energy microfluidization. The product with a zeta potential of -11.5 mV showed spherical globules when imaged for scanning and transmission electron microscopy. We explored the anti-inflammatory potential of this edible nano-emulsion in lung inflammation. The lungs are the internal organ most vulnerable to infection, injury, and rapid inflammation from the external environment because of their constant exposure to pollutants, pathogenic microorganisms, and viruses. We evaluated the nano-emulsion for efficacy in ovalbumin-induced lung injury in mice with an oral treatment for two weeks. The therapeutic effect of nano-emulsion of the sesame oil-extract of turmeric was evident from biochemical analysis of bronchoalveolar lavage fluid, lung histopathology, and flow cytometric analysis. The developed nano-emulsion significantly reduced the inflammation and damage to the alveolar network in ovalbumin-injured mice. Significant reduction in the levels of neutrophils and inflammatory cytokines like IL-4, IL-6, and IL-13 in bronchoalveolar lavage fluid was observed in the nano-emulsion-treated group. Leukotriene B4 and IgE were also significantly altered in the treated group, thus suggesting the suitability of the formulation for the treatment of allergy and other inflammatory conditions. The nano-emulsification process potentiated the immunoregulatory effect of turmeric, as observed from the elevated levels of the natural anti-inflammatory cytokine, IL-10. The dietary constituents-based nano-emulsion of spice turmeric helped in scavenging the free radicals in the injured lungs, thus modulating the inflammation pathway. This easily scalable formulation technology approach can therefore serve as a potential noninvasive and safe treatment modality for reducing lung inflammation in lung injury cases.

Genetic context of extended spectrum β-Lactamase (ESBL) producing Enterobacterales and its association with plasmid mediated quinolone resistance (PMQR), aminoglycoside modifying enzymes (AME) and Trimethoprim/Sulfamethoxazole (TMP-SMX) resistance is little known from North India. Therefore, the current study was aimed to investigate the frequency of Non-β-Lactam antibiotic resistance associated genes in extended spectrum β-Lactamase producing Enterobacterales . For this study, Non-Duplicate phenotypically confirmed ESBL producing Enterobacterales isolates (N = 186) were analyzed for ESBLs, PMQRs, AMEs and TMP-SMX resistance genes using polymerase chain reaction (PCR). PCR detected presence of PMQR genes in 81.29% (N = 139) of ESBL isolates (N = 171), AME genes in 60.82% and TMP-SMX resistance genes in 63.74% of the isolates. Molecular characterization of ESBL producing Enterobacterales showed 84.79% bla TEM followed by 73.68% bla CTX-M , 43.86% bla SHV , 19.88% bla PER and 9.94% bla VEB , respectively. Analysis of PMQR genes revealed 77.7% aac(6')-lb-cr the most commonly detected gene followed by 67.63% oqxB , 62.59% oqxA, 43.17% qnrB , 19.42% qnrD, 18.7% qnrS , 9.35% qnrA , 3.6% qepA and 2.88% qnrC , respectively. Analysis of AMEs gene profile demonstrated 81.73% aac(6')-Ib , the most frequently encountered gene followed by 46.15% aph(3')-Ia, 44.23% ant(3")-Ia, respectively. A 100% prevalence of sul1, followed by dfrA (54.63%) and sul2 (15.74%) was observed. In summary, prevalence of ESBL-Producing genes (particularly bla TEM and bla CTX-M ) along with PMQR, AMEs, and TMP-SMX resistant genes may potentially aid in the transfer of antimicrobial resistance among these strains.

Introduction: Patient counseling can be helpful in improving the outcome of disease management, particularly chronic diseases such as diabetes mellitus, which is common in Saudi Arabia. The present study looks to investigate the levels of counseling and satisfaction among patients attending diabetic clinics in outpatient hospital pharmacy in Al Ahsa, Saudi Arabia., Method: This is a cross-sectional investigation, carried out by using interview-structured questionnaire, targeting diabetes mellitus patients with or without comorbid states. The questionnaire was divided into 3 parts comprising of demographics, counseling types given while collecting prescription, and satisfaction rating of services provided., Result: More males than females participated; most of whom were college graduates older than 51 years. Sixty-three percent of the entire participants are type 1 diabetic patients, while 37% are type 2 diabetes mellitus patients. Coexistence of hypercholesterolemia was higher among type 1 diabetes patients with 51.9%, while hypertension was more common among type 2 diabetic patients representing 68.2%. Findings also showed that counseling was provided for medication use among type 1 diabetic patients but was deficient in the case of type 2 diabetic patients. Patients received low level of counseling on side effects and healthy lifestyle living. Satisfaction level was only 11.1%, indicating that counseling services might be deficient., Conclusion: This study has revealed poor counseling practices and low satisfaction levels in services provided by outpatient hospital pharmacies to diabetic patients. In the face of increasing prevalence of diabetes and comorbidity, counseling of diabetic patients is critical., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2019.)

The Middle East Respiratory Syndrome (MERS) is an emerging disease caused by a recently identified human coronavirus (CoV). Over 2494 laboratory-confirmed cases and 858 MERS-related deaths have been reported from 27 countries. MERS-CoV has been associated with a high case fatality rate, especially in patients with pre-existing conditions. Despite the fatal nature of MERS-CoV infection, a comprehensive study to explore its evolution and adaptation in different hosts is lacking. We performed codon usage analyses on 4751 MERS-CoV genes and determined underlying forces that affect the codon usage bias in the MERS-CoV genome. The current analyses revealed a low but highly conserved, gene-specific codon usage bias in the MERS-CoV genome. The codon usage bias is mainly shaped by natural selection, while mutational pressure emerged as a minor factor affecting codon usage in some genes. Other contributory factors included CpG dinucleotide bias, physical and chemical properties of encoded proteins and gene length. Results reported in this study provide considerable insights into the molecular evaluation of MERS-CoV and could serve as a theoretical basis for optimizing MERS-CoV gene expression to study the functional relevance of various MERS-CoV proteins. Alternatively, an attenuated vaccine strain containing hundreds of silent mutations could be engineered. Codon de-optimization will not affect the amino acid sequence or antigenicity of a vaccine strain, but the sheer number of mutations would make viral reversion to a virulent phenotype extremely unlikely., Competing Interests: Declaration of conflicting interests:The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2020.)

Human bocavirus (HBoV) is a recently discovered parvovirus associated with respiratory and gastroenteric infections in children. To date, four distinct subtypes have been identified worldwide. HBoV1 is the most frequently detected bocavirus in clinical samples derived from the respiratory tract. HBoV has a single-stranded DNA genome, which encodes two nonstructural proteins, NS1 and NP1, and two structural proteins, VP1 and VP2. Despite a large number of available HBoV sequences, the molecular evolution of this virus remains enigmatic. Here, we applied bioinformatic methods to measure the codon usage bias in 156 HBoV genomes and analyzed the factors responsible for preferential use of various synonymous codons. The effective number of codons (ENC) indicates a highly conserved, gene-specific codon usage bias in the HBoV genome. The structural genes exhibit a higher degree of codon usage bias than the non-structural genes. Natural selection emerged as dominant factor influencing the codon usage bias in the HBoV genome. Other factors that influence the codon usage include mutational pressure, gene length, protein properties, and the relative abundance of dinucleotides. The results presented in this study provide important insight into the molecular evolution of HBoV and may serve as a primer for HBoV gene expression studies and development of safe and effective vaccines to prevent infection.

Zika virus is a zoonotic pathogen, which have made frequent incursion into the human population in Africa and South East Asia over the course of several decades but never reached to the pandemic proportions until the most recent outbreak. Viruses are solely dependent on host synthetic machinery for their replication cycle; therefore, replication and persistence in a host species of different genetic background requires certain degree of adaptation. These adaptations are necessary to avoid detection from host immune surveillance and maximize the utilization of available resources for efficient viral replication. Study of genomic composition and codon usage pattern not only offer an insight into the adaptation of viruses to their new host, but may also provide some information about pathogenesis and spread of the virus. To elucidate the genetic features and synonymous codon usage bias in ZIKV genome, a comprehensive analysis was performed on 80 full-length ZIKV sequences. Our analyses shows that the overall extent of codon usage bias in ZIKV genome is low and affected by nucleotide composition, protein properties, natural selection, and gene expression level., (Copyright © 2017. Published by Elsevier B.V.)

The current study aims to assess the effectiveness of different teaching methods adopted for the practical session of Cardio-Pulmonary Resuscitation (CPR). CPR training is one of the compulsory modules of the Public Health Pharmacy (PHP) course at Universiti Sains Malaysia. CPR training comprises of 10% of total marks of the PHP course. To test the effectiveness of the different teaching strategies, three groups were defined using a two-stage cohort distribution-i.e. based on grade point average (GPA) and different teaching modalities. Group One was instructed using images and PowerPoint lecture slides. Group Two was instructed using videos and PowerPoint lecture slides. Group Three was instructed using PowerPoint slides with white boards and videos. Students in Group Three were not provided with a hard/soft copy of the PowerPoint slides and were encouraged to write down all the information on their personal notebooks. A 20-item questionnaire was used to assess the students' understanding toward the CPR session. Data were analyzed using the Statistical Package for Social Science Students, SPSS version 13®. Based on the response attained, the comparison of the final score among the groups was undertaken using one way ANOVA. Twenty-seven students have participated in this study. Final evaluation using the questionnaire revealed that student's in Group Three had a better understanding of CPR (18.1 ± 1.5, p <0.001) than the other two. Students' note taking during the lecture and use of traditional chalkboard teaching were found significant to improve the students' understanding and learning in the CPR session.

The immune system plays important roles in determining the outcomes of hepatitis B virus (HBV) infection. Interleukin-27 (IL-27) is a recently identified pro-inflammatory cytokine produced by macrophages, dendritic cells, and epithelial cells. To determine the correlation between HBV infection and IL-27 expression, we investigated the serum IL-27 levels in patients with HBV infection and in healthy individuals. Results showed that IL-27 was significantly elevated in patients as compared to healthy individuals (P<0.001). IL-27 was also detected at higher levels in patients with liver cirrhosis or hepatocellular carcinoma than those with acute hepatitis B or chronic hepatitis B (P<0.05). We also found that IL-27 expression was influenced by HBV e antigen. In addition, our in vitro studies demonstrated that IL-27 promoter activity, mRNA and protein expression were all stimulated in cells transfected with infectious HBV clone.

Influenza A virus is responsible for influenza epidemics in avian and human populations and poses a great threat to human health. Many researches have been focused on the prevention and treatment of influenza A virus infection. The nucleoprotein (NP) of the virus is an important protein due to its ability to interact with a variety of viral and cellular factors and its role in the viral RNA synthesis. In this study, we have used the influenza A virus nucleoprotein as target for anti-viral therapy through a new approach. By screening a human single-chain intracellular antibody (intrabody) cDNA library using nucleoprotein as bait in a yeast antigen-antibody two-hybrid system, we have identified several intrabodies that specifically interact with the viral nucleoprotein. Interaction between nucleoprotein and anti-nucleoprotein intrabodies was further confirmed by mammalian two-hybrid analysis. Results showed that anti-nucleoprotein intrabodies changed their cellular distribution in association with the viral nucleoprotein. Further studies indicated that anti-nucleoprotein intrabodies abolished the accumulation of not only the complementary RNA and virion RNA but also messenger RNA of influenza virus. In addition, anti-nucleoprotein intrabodies significantly inhibited influenza A virus transcription and replication through blocking the interaction of nucleoprotein with the viral polymerase proteins, polymerase basic protein 1 and polymerase basic protein 2. Thus, this study not only provides a powerful tool for the study of viral protein's functions, but also opens a new potential avenue for the prevention and treatment of influenza virus infections.

Interleukin-32 was recently identified as a pro-inflammatory cytokine produced by T-lymphocytes, natural killer cells, epithelial cells, and blood monocytes. IL-32 is induced by IFN-gamma in a time-dependent manner suggesting a role for IL-32 in innate and adaptive immune responses. In this study we present evidence that Human immunodeficiency virus promotes interleukin-32 production at both mRNA and protein levels. Our results showed that there is a 74% increase in the serum levels of IL-32 among HIV patients as compared to healthy individuals. There was a three-fold increase in the promoter activity of the IL-32 in the present infections HIV clone. This increase in IL-32 promoter activity was substantiated by increased IL-32 mRNA and protein levels. We have also demonstrated that IL-32 suppresses HIV replication. Our results show that HIV LTR activity was increased by more than six-folds when endogenous IL-32 was knocked down by IL-32-specific siRNA whereas it decreased by one-fold when IL-32 was over expressed in the cells. Similarly a more than two-fold increase and a 50% decrease in HIV p24 values were noted when IL-32 was knocked down and when IL-32 was over expressed in the cells, respectively. Our present work shows that raised IL-32 levels in HIV infection may in turn hamper HIV replication; one of the protective mechanisms of nature.

Background: Interleukin (IL)-32 is a recently described pro-inflammatory cytokine that has been reported to be induced by bacteria treatment in culture cells. Little is known about IL-32 production by exogenous pathogens infection in human individuals., Methods and Findings: In this study, we found that IL-32 level was increased by 58.2% in the serum samples from a cohort of 108 patients infected by influenza A virus comparing to that of 115 healthy individuals. Another pro-inflammatory factor cyclooxygenase (COX)-2-associated prostaglandin E2 was also upregulated by 2.7-fold. Expression of IL-32 in influenza A virus infected A549 human lung epithelial cells was blocked by either selective COX-2 inhibitor NS398 or Aspirin, a known anti-inflammatory drug, indicating IL-32 was induced through COX-2 in the inflammatory cascade. Interestingly, we found that COX-2-associate PGE(2) production activated by influenza virus infection was significantly suppressed by over-expression of IL-32 but increased by IL-32-specific siRNA, suggesting there was a feedback mechanism between IL-32 and COX-2., Conclusions: IL-32 is induced by influenza A virus infection via COX-2 in the inflammatory cascade. Our results provide that IL-32 is a potential target for anti-inflammatory medicine screening.

Genetic analysis of all eight genes of two Nanchang avian influenza viruses, A/Duck/Nanchang/1681/92 (H3N8-1681) and A/Duck/Nanchang/1904/92 (H7N1-1904), isolated from Jiangxi province, China, in 1992, showed that six internal genes of H3N8-1681 virus and five internal (except NS gene) genes of H7N1-1904 virus were closely similar to A/Goose/Guangdong/1/96 (H5N1) virus, the first highly pathogenic avian influenza (HPAI) virus of subtype H5N1 isolated in Asia. The neuraminidase (NA) gene of Gs/Gd/1/96 had the highest genetic similarity with A/Duck/Hokkaido/55/96 (H1N1-55) virus. The haemagglutinin (HA) gene of Gs/Gd/1/96 virus might have originated as a result of mutation of H5 HA gene from A/Swan/Hokkaido/51/96 (H5N3-51)-like viruses. The PA gene of H5N3-51 virus had the highest similarity with Gs/Gd/1/96. This study explains the origin of first Asian HPAI H5N1 virus in Guangdong by the reassortment of Nanchang (close to Guangdong) and Hokkaido (Japan) (H1N1-55 and H5N3-51) viruses. Genetic characteristics of donor and recipient viruses were also studied.