Project description:RNA samples of each group, extracted from PBMCs (Peripheral blood mononuclear cell) , were hybridized on two dye array. Within groups and between groups analyses to identify canonical pathways and enriched biological annotations were conducted.
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans. Heat-induced physiological and biochemical changes were assessed to determine heat tolerance levels in mice. We performed mRNA and microRNA expression profiling on mouse gastrocnemius muscle tissue samples to determine novel biological pathways associated with heat tolerance.
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans. Heat-induced physiological and biochemical changes were assessed to determine heat tolerance levels in mice. We performed mRNA and microRNA expression profiling on mouse gastrocnemius muscle tissue samples to determine novel biological pathways associated with heat tolerance.
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans.
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans.
Project description:Heat stroke is a life-threatening condition characterized by loss of thermoregulation and severe elevation of core body temperature, which can cause organ failure and damage to the central nervous system. While no definitive test exists to measure heat stroke severity, immune challenge is known to increase heat stroke risk, although the mechanism of this increased risk is unclear. In this study, we used a mouse model of classic heat stroke to test the effect of immune challenge on pathology. Employing multivariate supervised machine learning to identify patterns of molecular and cellular markers associated with heat stroke, we found that prior viral infection simulated with poly I:C injection resulted in heat stroke presenting with high levels of factors indicating coagulopathy. Despite a decreased number of platelets in the blood, platelets are large and non-uniform in size, suggesting younger, more active platelets. Levels of D-dimer and soluble thrombomodulin were increased in more severe heat stroke, and in cases presenting with the highest level of organ damage markers D-dimer levels dropped, indicating potential fibrinolysis-resistant thrombosis. Genes corresponding to immune response, coagulation, hypoxia, and vessel repair were up-regulated in kidneys of heat-challenged animals, and these increases correlated with both viral treatment and distal organ damage while appearing before discernible tissue damage to the kidney itself. We conclude that heat stroke-induced coagulopathy may be a driving mechanistic force in heat stroke pathology, especially when exacerbated by prior infection, and that coagulation markers may serve as an accessible biomarker for heat stroke severity and therapeutic strategies.