Managing COVID-19 Lockdown Impacts: Sustaining GLP Compliance and Man Material Medium (MMM) Strategy for Augmenting Prevention of Workplace Infections.

Good Laboratory Practices (GLP) is a well-established global system that encompass a set of principles or a framework for defining how laboratory studies are planned, performed, monitored, recorded, reported, and stored for future reference. It is important that compliance with the principles of GLP continues to be maintained. Coronavirus disease 2019 (COVID-19) pandemic lockdowns in various countries, including India, have been sudden and over an extended duration. Although every GLP laboratory has Standard Operating Procedure for disaster management, the sudden lockdown due to COVID-19 created specific emergency procedures related to this situation such as travel bans, safe distancing, and work from home notifications. Good Laboratory Practice compliances in the context of animal experimentation during and post lockdown period need effective managerial responses that are not just flexible and innovative but can ensure they are well-calibrated to the challenges of business continuity and maintenance of health directives. On-the-ground realities suggest there may still be practical challenges to compliance, and guidelines may not always be complied with. This article discusses the issues that may be encountered due to COVID-19 that could potentially impact the GLP status of a study and suggests ways to manage them so as to minimize or prevent infection with COVID-19. We propose an MMM (Man, Material, and Medium) strategy to ensure compliance with health directives and guidelines that will help staff to keep themselves and others safe in the workplace while endeavoring to comply with GLP requirements.

Mitochondrial dysfunction - Silent killer in cerebral ischemia.

Mitochondrial dysfunction aggravates ischemic neuronal injury through activation of various pathophysiological and molecular mechanisms. Ischemic neuronal injury is particularly intensified during reperfusion due to impairment of mitochondrial function. Mitochondrial mutilation instigates alterations in calcium homeostasis in neurons, which plays a pivotal role in the maintenance of normal neuronal function. Increase in intracellular calcium level in mitochondria triggers the opening of mitochondrial transition pore and over production of reactive oxygen species (ROS). Several investigations have concluded that ROS not only contribute to lipids and proteins damage, but also transduce apoptotic signals leading to neuronal death. In addition to the above mentioned reasons, endoplasmic reticulum (ER) stress due to excitotoxicity also leads to neuronal death. Recently, some newer proteins have been claimed to induce "mitophagy" by triggering the receptors on autophagic membranes leading to neurodegeneration. This review summarizes the mechanisms underlying neuronal death involving mitochondrial dysfunction and mitophagy.