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1.
Clin Ter ; 175(Suppl 1(4)): 10-15, 2024.
Article in English | MEDLINE | ID: mdl-39054972

ABSTRACT

Background: Investigating deaths related to chronic cocaine abuse can be a difficult task, particularly when they occur suddenly and without explanation. Cocaine abuse can trigger biological effects similar to physiological stressors, causing the body to produce heat-shock proteins (HSPs). However, there is still limited information on the specific levels of each HSP type. This systematic review aims to comprehensively collect and analyze all existing literature data regar-ding the relationship between HSPs and cocaine abuse to investigate whether HSPs can be utilized as forensic markers for accurately dia-gnosing cocaine-related deaths. Materials and Methods: The Authors conducted the literature search using PubMed and Scopus databases, searching for articles published between 1 January 1992 and 1 April 2024 using the text string: "heat shock protein" AND "cocaine". Conclusion: Twenty articles were collected, but only nine were included in the systematic review. The data gathered pertained to both human and murine species. The majority of the analyzed articles revealed an elevation in HSP25, HSP27, HSP60, HSP70, HSP72, and HSP73 levels in the brain, cerebellum, and liver, indicating cocaine-induced stress. The relationship between HSP and cocaine has been unclear over time. However, recent studies have shown that cocaine consumption leads to an increase in HSP levels, particularly in the central nervous system. This correlation can also be observed in certain types of liver cells that are capable of binding cocaine metabolites. In conclusion, HSP brain levels, along with other biomarkers, may be used to diagnose sudden, unexpected death related to cocaine abuse.


Subject(s)
Cocaine-Related Disorders , Heat-Shock Proteins , Humans , Cocaine-Related Disorders/complications , Heat-Shock Proteins/metabolism , Animals , Cocaine/adverse effects , Mice , Biomarkers/metabolism
2.
Clin Ter ; 175(Suppl 1(4)): 70-74, 2024.
Article in English | MEDLINE | ID: mdl-39054986

ABSTRACT

Background: The role of forensic pathologists is pivotal in definitively diagnosing drowning cases. Further differentiation becomes essential for distinguishing between freshwater drowning (FWD) and saltwater drowning (SWD). Aquaporins are small integral membrane proteins that serve as major water transport pathways in various cell types. AQP4 appears to be involved in mechanisms related to cerebral volume regulation. Our study aims to examine the expression of AQP4 in the brain as a potential marker for differentiating between FWD and SWD relating to autopsy-performing timing. Materials and Methods: A total of 23 cases were classified into three groups: FWD, SWD, and controls. All samples were classified upon autopsy-performing timing into two subgroups: within and after 72 hours of death. The samples were then processed for histological and immunohistochemical investigations. Conclusion: For autopsies performed within 72 hours of death, we found a significantly higher value of AQP4-positive astrocytes in cases of FWD compared to SWD and control groups. We also found a significantly lower AQP4 expression in SWD cases compared to the control group. For autopsies conducted after 72 hours, the immunohistochemical staining does not reveal the peripheral terminations of astrocytes, which appear blurred and only recognizable as halos. In conclusion, the data aligns with existing literature about autopsies performed within 72 hours. However, in autopsies conducted after 72 hours, uncertain and even opposed results are observed. The difference can be ascribed to the post-mortem transformative processes that take place upon the cessation of vital functions.


Subject(s)
Aquaporin 4 , Autopsy , Drowning , Immunohistochemistry , Humans , Aquaporin 4/analysis , Drowning/diagnosis , Male , Diagnosis, Differential , Female , Adult , Middle Aged , Time Factors , Fresh Water , Aged , Brain/pathology , Brain/metabolism , Young Adult , Seawater , Adolescent , Astrocytes/metabolism , Astrocytes/pathology
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