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Simple Summary: Sea turtles are considered an endangered species, largely due to anthropogenic activities. Severe trauma in these species mainly involves the carapace and head. Studies on the incidence of head trauma in sea turtles and analysis of the survival rate after hospitalization performed on many subjects examined over a long period of time were missing in the scientific literature. In this retrospective study, we evaluated 1877 Caretta caretta, 29 of which showed head trauma. The severity of head injuries was assessed clinically and by neurological examination. CT examination was essential to evaluate the impaired central nervous system and sense organs. According to our scoring classification, most head traumatized turtles had severe injuries but in most cases, the animals showed no alteration in mentation state. Only 28% (8/29) of the turtles showed head damage related to severe neurological deficits. Indeed, 21 out of 29 sea turtles were released after a time ranging from a few days to 8 months. To the best of our knowledge, the literature lacks specific data on the incidence, correlations with neurological deficits, complications, and survival rate of traumatic head injuries in loggerhead sea turtles. Sea turtles are considered endangered species, largely due to anthropogenic activities. Much of the trauma in these species involves the carapace and skull, resulting in several degrees of damage to the pulmonary and nervous systems. Among traumatic injuries, those involving the skull can be complicated by brain exposure, and turtles with severe skull injuries that have nervous system impairment, emaciation, and dehydration can often die. Between July 2014 and February 2022, a total of 1877 loggerhead sea turtles (Caretta caretta) were referred for clinical evaluation at the Sea Turtle Clinic (STC) of the Department of Veterinary Medicine of the University of Bari. A retrospective study of 29 consecutive cases of loggerhead sea turtles (Caretta caretta) with skull lesions of different degrees of severity is reported. On admission, physical and neurological evaluations were performed to assess and grade the lesions and neurological deficits. In 20 of the 29 sea turtles with more serious head trauma, computed tomography (CT) findings in combination with physical and neurological assessment enabled the evaluation of the potential correlation between deficits and the extent of head injuries. All sea turtles underwent curettage of the skull wounds, and the treatment protocol included the use of the plant-derived dressing 1 Primary Wound Dressing® (Phytoceutical AG, Endospin Italia) applied on the wound surface as a primary dressing. Out of 29 sea turtles, 21 were released after a time ranging from a few days to 8 months. To the best of our knowledge, the literature lacks specific data on the incidence, correlations with neurological deficits, complications, and survival rate of loggerhead sea turtles with traumatic head injuries. [ABSTRACT FROM AUTHOR]

Introduction: TBI is one of the main causes of deaths and chronic disability worldwide. Overall, TBI (traumatic brain injury) is a growing epidemy in 3rd -world nations and developing countries, which use road transportation and motor vehicles more. The intention of this research is studying the impacts of Neuroprotective Coenzyme Q10, which is a part of mitochondrial electron chain, an effective antioxidant, which plays a role in membrane consolidation. The studies have shown that Co Q10 is effective in treatment of ischemia injury and blood recirculation. The research has been done on neurological scores, health of blood-brain barrier, and brain edema as a result of brain trauma in male rats on a behavioral, biochemical and histological basis. Methods and Materials: In this study, 56 of white male rats’ heads, each weighing 250-330 g, and 6 to 8 heads are used in each group. Before the operation, the animals get anesthesia by the use of Ketamine (50- mg/kg) and Xylazine (10 mg/kg). Also, they get Analgesia by the use of Cocktail Midazolam (intra-dermal, 2mg/kg) and Medetomidine (1mg/kg). Then, the heads are fixed in Stereotaxic in order to find out the yes/no outcome.A few minutes later, various doses of Co-enzyme Q10 are intraperitoneally injected. Results: Neurological scores were measured before, at the time and first, second and third day after the injury. Analyze of statistics and two-way AVONA test show that Co-enzyme doses of 10, 20 and 40 mg/kg have caused the decrease of neurological scores. However, intra peritoneal prescription of doses of 10 and 20 mg/kg has caused an increase in neurological scores of the specific groups. The scores did not change in the dose of 40 mg/kg.Times before the injury, the time of consciousness after the injury and 24, 48 and 72 hours after the injury and also, Beam walk and Beam balance are administered. After 72 hours, Elisa test is done with the CSF. Then, 200 microliter of CSF Fluid from Cisterna Magna is taken and the color of CSF fluid can be observed. Conclution: Prescription of 10 mg and 20 mg doses of Co-enzyme Q10 causes improvement in neurological statistics and balance factors. Also, prescription of 25 mg dose reduces stress, mental dysfunction and also, reduces the drivers of brain inflammation and restructures morphological changes in dead neurons. As a result, this medication can have protective impacts on neuronal cells and TBI which is caused by injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study was aimed to assess the effect of unilateral common carotid artery occlusion on brain pathophysiology in rats pretreated with subchronic hypoxia. MATERIALS AND METHODS: Rats (200 ± 20 g) were randomized into three groups: Group 1 served as sham, Group 2 were normoxic (21% O2 and 79% N2), and Group 3 were hypoxia preconditioned (10% O2 and 90% N2) for 21 days before left common carotid artery occlusion (LCCAO). The LCCAO was done for 75 min followed by reperfusion for 12 h. Neurological scores were recorded. Serum malondialdehyde (MDA) and nitric oxide (NO) levels at pre- and 12 h post-LCCAO were measured. Brain histopathological assessments were also done. RESULTS: Higher neurological deficits scores in Group 2 as compared to Group 3 rats were noticed. Serum MDA and NO levels at 12 h post-LCCAO in Group 2 rats showed significant elevation as compared to preocclusion levels. Group 3 rats did not show such elevations. On histopathology of left and right cerebral hemispheres of Group 1 (sham) did not show any specific changes. In Group 2 rats, the right cerebral hemisphere (nonoccluded) showed no areas of ischemia-induced brain changes, but in the left side (occlusive), there were features of ischemic brain damage including cerebral edema. In the case of Group 3 rats, there were less ischemic damages in the left occluded side as compared to the left side of the Group 2 rats. CONCLUSION: This study clearly demonstrates that subchronic hypoxia pretreatment can reduce ischemic brain injury by unilateral common carotid artery occlusion in rats. [ABSTRACT FROM AUTHOR]