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Introduction:Decubitus ulcer is a pressure-induced tissue injury that may affect skin, muscle, connective tissue, cartilage and bone. The present study was designed to find out risk factors of decubitus ulcer in head and spinal cord injured patient admitted to intensive care units (ICU). Materials and Methods: In this cross - seetional analythical study all consecutive craniospinal trauma patients admitted to intensive care unit were included.Upon arrival at the hospital and every 48 hours, all patients were examined for existence of bed sore. Braden scale, age, kind of mattress, site of primary injury and level of consciousness were used to determine risk factors. Data was analyzed using T and Chi square tests and logistic regretion. Results: Among 198 patients (171 male, 27 female with mean age of 31.4=19.8), 166 patients (3.8%) had cranial and 32 (16.2%) patients had spinal trauma. Of samples, 45 (22.7%) patients had 67 sores in 13 different sites. Incidence of bed sore was 22.7% (in cranial and spinal injured patients was 4.54% and 18.18% respectively). The most common sites were intergluteal cleft (33.3%) and sacral regions (28.9%). Bed sores were observed more frequently in immobile patients and those with impaired sensation, the difference were statistically significant (p<0.005 and p<0.005 respectively) hence immobility and impaired sensation are known as risk factors. Patient’s sores were not influenced by age, moisture, activity, nutrition and type of mattress variables. Time of hospital stay in patients with bed sore was significantly more than those without bed sore (P<0.00001). Coma patients (GCS 8) had developed bed sore more frequently than conscious ones (OR=6.1, RR=4.4, P=0.00001). Conclusion: Results show that risk factors of deubitus ulcers in ICU admitted craniospinal trauma patients were decreased sensation, activity and level of conciousness and lenglt of hospital stay.

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Abstract Background: Spinal cord slices culturing from adult mammals could be considered as a suitable in-vitro model for evaluating cellular viability, spinal cord injury and cell death mechanisms. In present study, determining of cell death in motor neurons of cultured spinal cord slices in adult mouse was done. Materials and Methods: In a experimental- laboratory study, thoracic regions of spinal cords from 4 Balb/c mice were cut into 400-µm slices using tissue chopper and incubated in a Co2 incubator at 37˚C for different periods of time. Freshly prepared slices (0h) and cultured slices were fixed and sectioned using cryostat. To study morphological and biochemical features of cell death, fluorescent staining, TUNEL method and agarose gel electrophoresis were used. Results: In freshly prepared slices of motor neurons showed no apoptotic changes. While, 6, 12 and 24h after culturing, this neurons displayed morphological features of apoptosis including cell shrinkage as well as nuclear and chromatin condensation. Also, 6 and 12h after culturing were TUNEL positive. In addition, extracted DNA from cultured slices for 24h were indicated the nucleosomal DNA fragmentation on agarose gel electrophoresis. Conclusion: Results were showed the occurrence of apoptosis in motor neurons of cultured adult mouse spinal cord slices.

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Introduction: Methamphetamine is a powerful psychostimulant that has been significantly abused in recent years. Buprenorphine, a derivative of morphine alkaloids, is effective in treating opioid addiction.
Methods: This experimental study involved eight groups of seven male rats each. It examined the effects of a 5-day intraperitoneal injection of methamphetamine, buprenorphine, their interactions, and methamphetamine withdrawal on the expression of histamine and histamine N-methyltransferase genes in the lumbar spinal cord. The data were analyzed using One-way ANOVA.
Results: The intraperitoneal administration of 10 mg/kg of methamphetamine and 6 or 10 mg/kg of buprenorphine over five days did not change the expression levels of the histamine or histamine N-methyltransferase genes in the lumbar spinal cord of male rats. However, discontinuing methamphetamine led to an increase in the expression of both genes in this area (P < 0.01). Furthermore, when examining the interaction between the two drugs, it was found that the expression of the histamine N-methyltransferase gene was significantly higher in the group receiving methamphetamine plus 10 mg/kg buprenorphine compared to the methamphetamine-only group (P < 0.01).
Conclusions: Based on the results of this study and the mechanisms proposed in previous studies, it seems that methamphetamine withdrawal and/or the use of buprenorphine as a possible therapeutic approach can lead to the stabilization of the physiological balance of the central nervous system by temporarily increasing brain histamine, and thus help reduce the complications of methamphetamine abuse.