The need of natural fiber-reinforced composites is increasing at very fast rate because of their ecofriendly production, decomposition, high specific strength, abundance, good physical and mechanical properties. Available literature reveals that past researchers have done a lot of work for the preparation and characterization of fiber-reinforced composites. While developing natural fiber composites, researchers encountered various problems like hydrophilic nature of natural fibers, incompatibility of natural fibers with matrix materials, thermal instability of natural fibers, and poor interfacial bonding between reinforcing phase and matrix phase. However, some of these problems can be solved to a greater extent by considering surface treatment of natural fibers before they are used in the preparation of fiber-reinforced composites. Thus, there is a need for understanding the effect of several surface treatments on the mechanical properties of fiber-reinforced composites. The aim of this paper is to put forth a comprehensive review on the effects of different surface treatments on the mechanical properties such as tensile strength, flexural strength, and impact strength and also interfacial shear strength of the fiber-reinforced composites.

Background and aims: COVID-19 is a contagious disease caused by a new coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Till now there are no vaccines and explicit medicines available for the treatment of COVID-19 disease, therefore the initiatives like public health and social measures are helpful in limiting the quantity of contaminations and saving lives. Keeping this in view, an attempt has been made in the present work to identify the barriers which hinder the implementation of these public health and social measures Methods: The barriers to implement public health and social measures for preventing transmission of COVID-19 are identified using systematic literature review and these barriers are then categorized using Decision-making trial and evaluation laboratory (DEMATEL) method. Results: Results reveal that among ten identified barriers, Lack of resources for implementing public health and social measures is found to be the most influential barrier to implement public health and social measures for preventing transmission of COVID-19. Conclusions: The successful implementation of public health and social measures depends on the adequate availability of resources which include medical equipment, personnel and financial dealings. The outcome of this research work will benefit and motivate the higher authorities to consider and overcome various challenges to prevent the transmission of COVID-19.

BackgroundElectronic cigarettes (e-cigs) were introduced as electronic nicotine delivery systems, and have become very popular in the USA and globally. There is a paucity of data on systemic injury biomarkers of vaping in e-cig users that can be used as a noninvasive assessment of vaping-associated lung injuries. We hypothesised that characterisation of systemic biomarkers of inflammation, anti-inflammatory, oxidative stress, vascular and lipid mediators, growth factors, and extracellular matrix breakdown may provide information regarding the toxicity of vaping in e-cig users.MethodsWe collected various biological fluids, i.e. plasma, urine, saliva and exhaled breath condensate (EBC), measured pulmonary function and vaping characteristics, and assessed various biomarkers in e-cig users and nonusers.ResultsThe plasma samples of e-cig users showed a significant increase in biomarkers of inflammation (interleukin (IL)-1β, IL-6, IL-8, IL-13, interferon (IFN)-γ, matrix metalloproteinase-9, intercellular cell adhesion molecule-1) and extracellular matrix breakdown (desmosine), and decreased pro-resolving lipid mediators (resolvin D1 and resolvin D2). There was a significant increase in growth factor (endothelial growth factor, vascular endothelial growth factor, β-nerve growth factor, platelet-derived growth factor-AA, stem cell factor, hepatocyte growth factor and placental growth factor) levels in plasma of e-cig users versus nonusers. E-cig users showed a significant increase in levels of inflammatory biomarker IFN-γ, oxidative stress biomarker 8-isoprostane and oxidative DNA damage biomarker 8-oxo-dG in urine samples, and of inflammatory biomarker IL-1β in saliva samples. EBC showed a slight increase in levels of triglycerides and 8-isoprostane in e-cig users compared with normal nonusers.ConclusionE-cig users have increased levels of biomarkers of inflammation and oxidative stress, reduced pro-resolving anti-inflammatory mediators, and endothelial dysfunction, which may act as risk factors for increasing susceptibility to systemic diseases. The identified noninvasive biomarkers can be used for determining e-cig vaping-associated lung injuries, and for regulatory and diagnostic aspects of vaping in humans.

Nicotine inhalation via electronic cigarettes (e‐cigs) is an emerging concern. However, little is known about the acute toxicity in the lungs following inhalation of nicotine‐containing e‐cig aerosols. We hypothesized that acute exposure to aerosolized nicotine causes lung toxicity by eliciting inflammatory and dysregulated repair responses. Adult C57BL/6J mice were exposed 2 hours daily for 3 days to e‐cig aerosols containing propylene glycol (PG) with or without nicotine. Acute exposure to nicotine‐containing e‐cig aerosols induced inflammatory cell influx (neutrophils and CD8a+ T lymphocytes), and release of pro‐inflammatory cytokines in bronchoalveolar lavage fluid in a sex‐dependent manner. Inhalation of e‐cig aerosol containing PG alone significantly augmented the lung levels of various homeostasis/repair mediators (PPARγ, ADRP, ACTA2, CTNNB1, LEF1, β‐catenin, E‐cadherin, and MMP2) in a sex‐dependent manner when compared to air controls. These findings were accompanied by an increase in protein abundance and altered gene expression of lipogenic markers (PPARγ, ADRP) and myogenic markers (fibronectin, α‐smooth muscle actin and β‐catenin), suggesting a dysregulated repair response in mouse lungs. Furthermore, exposure to nicotine‐containing e‐cig aerosols or PG alone differentially affected the release of pro‐inflammatory cytokines in healthy and COPD human 3D EpiAirway tissues. Overall, acute exposure to nicotine‐containing e‐cig aerosols was sufficient to elicit a pro‐inflammatory response and altered mRNA and protein levels of myogenic, lipogenic, and extracellular matrix markers in mouse lung in a sex‐dependent manner. Thus, acute exposure to inhaled nicotine via e‐cig leads to dysregulated repair and inflammatory responses, which may lead to airway remodeling in the lungs.

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