Background: This experimental study was performed to investigate the neuroprotective effects of progesterone on spinal cord ischemia in rabbits.
Methods: Eighteen female New Zealand white rabbits were used in this study. Rabbits were randomized into 3 groups. Spinal cord ischemia was induced by clamping the abdominal aorta from a point just inferior to the left renal artery to the aortic bifurcation for a period of 30 minutes. Group 1 served as the control group, and groups 2 and 3 received intraperitoneal progesterone immediately after the onset of reperfusion, at a dose of 8 mg/kg. Two hours after reperfusion, the animals in group 1 were killed. Four hours after reperfusion, the animals in group 2 were killed, and 6 hours after reperfusion, the group 3 rabbits were killed. Spinal cords were removed and fixed in 10% formalin in a phosphate buffer. Neuronal injury was evaluated by a pathologist who was blinded to the treatment groups, and 5 sections per animal were evaluated. The number of intact large motor neuron cells in the ventral grey matter region was counted.
Results: The analysis revealed that the average mean arterial pressure for group 1 was significantly higher than that for group 2, and the mean sacrificed pressure value for group 1 was significantly higher than that for group 3 (P < .05). The number of intact neurons in group 1 was significantly lower than the number of intact neurons found in both groups 2 and 3 (P < .05). No other statistically significant differences were found between the groups.
Conclusion: The findings from the present study indicate that progesterone effectively protects the spinal cord tissues against ischemic damage in the setting of decreased perfusion.
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http://dx.doi.org/10.1016/j.ajem.2012.09.025 | DOI Listing |
Mol Neurobiol
January 2025
Department of Orthopedics, The Fourth Medical Center, Chinese PLA General Hospital, Beijing, 100048, China.
Spinal cord injury (SCI) is a severe central nervous system injury without effective therapies. PANoptosis is involved in the development of many diseases, including brain and spinal cord injuries. However, the biological functions and molecular mechanisms of PANoptosis-related genes in spinal cord injury remain unclear.
View Article and Find Full Text PDFNeurosurg Rev
January 2025
Lab in Biotechnology and Biosignal Transduction, Department of Orthodontics, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University, Chennai, 77, Tamil Nadu, India.
Pediatr Dermatol
January 2025
Division of Dermatology, Children's Mercy Kansas City, Kansas City, Missouri, USA.
LUMBAR syndrome is characterized by lower body segmental infantile hemangiomas, urogenital abnormalities/hemangioma ulceration, spinal cord malformations, bony deformities, anorectal malformations/arterial anomalies, and/or renal anomalies. Here we present an infant girl with LUMBAR syndrome who was also discovered to have Müllerian agenesis, defined as absent uterus or nonfunctional uterine remnants. While vaginal and uterine duplications are included among the diagnostic criteria for LUMBAR syndrome, this is the first case of associated Mullerian agenesis.
View Article and Find Full Text PDFActa Anaesthesiol Scand
March 2025
Department of Clinical Epidemiology and Biostatistics, Biostatistics Unit, St. Joseph's Healthcare Hamilton, Hamilton, Ontario, Canada.
Background: Classic teaching is that spinal anesthesia is safe at or below the L2-L3 interspace. To evaluate this, we sought to determine the percentage of individuals with a conus medullaris termination (CMT) level at or below the L1-L2 interspace. Further, the relationship of CMT level to age, sex, body mass index (BMI), and spinal pathology was examined, as was the reliability of using Tuffier's line (TL) as an anatomical landmark.
View Article and Find Full Text PDFFEBS J
January 2025
From the Department of Biological Sciences, Delaware State University, Dover, DE, USA.
Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease that affects neurons in the brain and spinal cord, causing loss of muscle control, and eventually leads to death. Phosphorylated transactive response DNA binding protein-43 (TDP-43) is the major pathological protein in both sporadic and familial ALS, forming cytoplasmic aggregates in over 95% of cases. Of the 10-15% of ALS cases that are familial, mutations in TDP-43 represent about 5% of those with a family history.
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