ABSTRACT
Anatomy in the context of medical or health science often requires dissection. Anatomical dissection is the purposeful and procedural exploration of the human tissues and organs by physically cutting through defined body planes, regions, and organs to access, define and explore the structures in a manner that facilitates learning. Anatomical dissection is a basic requirement for anatomical and medical education. It is a requirement in certain other fields of health sciences as well. Unfortunately, in many instances, the prosector and dissector in the anatomy laboratories are not considered for the hazards to which they are exposed whether in their health plans or remuneration package. Dissectors, unlike conventional hospital laboratory workers are often considered routine workers or teaching assistants. This is the case, for example, in many African medical institutions. Administrators possibly presume that hazards are only associated with service laboratories in the hospital or teaching hospital departments. It would therefore serve the purpose of advocacy, education, and orientation to highlight the hazards that these individuals who serve as dissectors, prosectors and laboratory staff members are exposed to. This commentary highlights the nature and sources of risks that anatomists who dissect, prosect and work in anatomical laboratories are exposed to. It also highlights how the rights and health of anatomists who dissect can be protected with specific recommendations. Hence, the recommendations speak to policies and practices that are required to serve this purpose. After highlighting the major risks that anatomists who dissect might face, and the major causes of the risks, we wish to propose ways by which these could be addressed based on these key considerations: protect, prevent, and compensate. This is what we have also termed the PPC principle for protecting the health and professional rights of anatomists who dissect and work in anatomical laboratories.
ABSTRACT
Exposure to lead (Pb) has been shown to alter the function of central nervous system and affect cholinergic neurons of the visual cortex in animal models. This study sought to investigate the withdrawal symptoms and oxidative stress on the visual cortex after lead exposure. A total of 20 healthy male Wistar rats were randomly divided into two groups (n=10): group A, control, received 10 ml/kg of distilled water for 30 days orally; group B, lead treated group, received 10 mg/kg of lead nitrate solution for 30 days orally. Group B was divided into two subgroups, group B1 serves as non-recovery while B2 serves as recovery (withdrawal). Five rats from each group were sacrificed under ether anesthesia 24 hours after the last oral administration of lead, while the remaining 5 rats (withdrawal subgroup) were sacrificed 30 days after the last oral administration of lead. The visual cortex was grossed from the brain tissue and processed for histology. Blood/serum samples were obtained and markers of oxidative stress (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPX]), and lipid peroxidation (malondialdehyde [MDA]) were analyzed. Lead-exposed rats display a significant reduction in the SOD, CAT, and GPX level as well as increased in MDA level. However, following a recovery period, a non-significant improvement was seen in the histoarchitecture of the visual cortex.