ORCID Profile
0000-0002-3380-7092
Current Organisation
King Faisal Specialist Hospital and Research Centre - Jeddah
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Publisher: Cambridge University Press (CUP)
Date: 15-07-2021
DOI: 10.1017/S1049023X21000662
Abstract: Mass-gathering events (MGEs) occur regularly throughout the world. As people congregate at MGEs, there is an increased risk of transmission of communicable diseases. Novel respiratory viruses, such as Severe Acute Respiratory Syndrome Coronavirus-1 (SARS-CoV-1), Influenza A Virus Subtype H1N1 Strain 2009 (H1N1pdm09), Middle East Respiratory Syndrome Coronavirus (MERS-CoV), and Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), or Coronavirus Disease 2019 (COVID-19), may require specific infection prevention and control strategies to minimize the risk of transmission when planning MGEs. This literature review aimed to identify and analyze papers relating to novel respiratory viruses with pandemic potential and to inform MGE planning. This paper used a systematic literature review method. Various health care databases were searched using keywords relating to MGEs and novel respiratory viruses. Information was extracted from identified papers into various tables for analysis. The analysis identified infection prevention and control strategies used at MGEs to inform planning before, during, and following events. In total, 27 papers met the criteria for inclusion. No papers were identified regarding SARS-CoV-1, while the remainder reported on H1N1pdm09 (n = 9), MERS-CoV (n = 15), and SARS-CoV-2 (n = 3). Various before, during, and after event mitigation strategies were identified that can be implemented for future events. This literature review provided an overview of the novel respiratory virus epidemiology at MGEs alongside related public health mitigation strategies that have been implemented at these events. This paper also discusses the health security of event participants and host communities in the context of cancelling, postponing, and modifying events due to a novel respiratory virus. In particular, ways to recommence events incorporating various mitigation strategies are outlined.
Publisher: World Health Organization Regional Office for the Eastern Mediterranean (WHO/EMRO)
Date: 27-05-2020
DOI: 10.26719/EMHJ.20.016
Publisher: Elsevier BV
Date: 2015
DOI: 10.1016/J.JHIN.2014.09.008
Abstract: Microbes tend to attach to available surfaces and readily form biofilms, which is problematic in healthcare settings. Biofilms are traditionally associated with wet or d surfaces such as indwelling medical devices and tubing on medical equipment. However, microbes can survive for extended periods in a desiccated state on dry hospital surfaces, and biofilms have recently been discovered on dry hospital surfaces. Microbes attached to surfaces and in biofilms are less susceptible to biocides, antibiotics and physical stress. Thus, surface attachment and/or biofilm formation may explain how vegetative bacteria can survive on surfaces for weeks to months (or more), interfere with attempts to recover microbes through environmental s ling, and provide a mixed bacterial population for the horizontal transfer of resistance genes. The capacity of existing detergent formulations and disinfectants to disrupt biofilms may have an important and previously unrecognized role in determining their effectiveness in the field, which should be reflected in testing standards. There is a need for further research to elucidate the nature and physiology of microbes on dry hospital surfaces, specifically the prevalence and composition of biofilms. This will inform new approaches to hospital cleaning and disinfection, including novel surfaces that reduce microbial attachment and improve microbial detachment, and methods to augment the activity of biocides against surface-attached microbes such as bacteriophages and antimicrobial peptides. Future strategies to address environmental contamination on hospital surfaces should consider the presence of microbes attached to surfaces, including biofilms.
Publisher: Wiley
Date: 05-04-2023
DOI: 10.1113/JP284031
Abstract: An evolutionary heat shock response (HSR) protects most living species, including humans, from heat‐induced macromolecular damage. However, its role in the pathogenesis of heat stroke is unknown. We examined the whole genome transcriptome in peripheral blood mononuclear cells of a cohort of subjects exposed to the same high environmental heat conditions, who developed heat stroke ( n = 19) versus those who did not ( n = 19). Patients with heat stroke had a mean rectal temperature at admission of 41.7 ± 0.8°C, and eight were in deep coma (Glasgow Coma Score = 3). The transcriptome showed that genes involved in more than half of the entire chaperome were differentially expressed relative to heat stress control. These include the heat shock protein, cochaperone, and chaperonin genes, indicating a robust HSR. Differentially expressed genes also encoded proteins related to unfolded protein response, DNA repair, energy metabolism, oxidative stress, and immunity. The analysis predicted perturbations of the proteome network and energy production. Cooling therapy attenuated these alterations without complete restoration of homeostasis. We validated the significantly expressed genes by a real‐time polymerase chain reaction. The findings reveal the molecular signature of heat stroke. They also suggested that a powerful HSR may not be sufficient to protect against heat injury. The overwhelming proteotoxicity and energy failure could play a pathogenic role. image Most living species, including humans, have inherent heat stress response (HSR) that shields them against heat‐induced macromolecular damage. The role of the HSR in subjects exposed to environmental heat who progressed to heat stroke versus those that did not is unknown. Our findings suggest that heat stroke induces a broad and robust HSR of nearly half of the total heat shock proteins, cochaperones, and chaperonin genes. Heat stroke patients exhibited inhibition of genes involved in energy production, including oxidative phosphorylation and ATP production. Significant enrichment of neurodegenerative pathways, including amyloid processing signalling, the Huntington's and Parkinson's disease signalling suggestive of brain proteotoxicity was noted. The data suggests that more than a powerful HSR may be required to protect against heat stroke. Overwhelming proteotoxicity and energy failure might contribute to its pathogenesis.
Location: United Kingdom of Great Britain and Northern Ireland
Location: Saudi Arabia
Location: Saudi Arabia
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Saber Yezli.