Rabbit Anti-S100B monoclonal antibody, clone TD68-13

Objective: To determine whether serum neurogranin (NRGN), glial fibrillary acidic protein (GFAP), and calcium-binding protein S100 beta (S100B) levels are associated with traumatic intracranial lesions compared to computed tomography (CT) findings of patients with mild traumatic brain injury (mTBI). Patients and Methods: The cross-sectional study cohort included 48 patients who were admitted to the Emergency Department with a complaint of mTBI, a Glasgow Coma Scale score of 14-15, and at least one symptom of head trauma (i.e., post-traumatic amnesia, nausea or vomiting, post-traumatic seizures, persistent headache, and transient loss of consciousness). Blood samples and CT scans were obtained for all patients within 4 h of injury. Age-matched patients without intracranial traumatic pathology (CT-) were recruited as a control group. Blood samples were measured for NRGN, GFAP, and S100B levels. Results: Of 48 patients, 24 were CT + and had significantly higher serum NRGN (5.79 vs. 2.95 ng/mL), GFAP (0.59 vs.0.36 ng/mL), and S100B (1.72 vs.0.73 mu g/L) levels than those who were CT- (p = 0.001, p = 0.026, and p < 0.001, respectively). ROC curves showed that NRGN, GFAP, and S100B levels were sufficient to distinguish traumatic brain injury in patients with mTBI. At the cut-off value for NRGN of 1.87 ng/mL, sensivity was 83.3%, and specificity was 58.3%. At the cut-off value for GFAP of 0.23 ng/mL, sensivity was 75% and specificity was 62.5%. The optimal cut-off value for S100B was 0.47 mu g/L (95.8% sensitivity and 62.5% specificity). Conclusion: This is the first study to evaluate NRGN in human serum after mTBI. We confirmed that NRGN levels were significantly higher in CT + patients than CT- patients in the mTBI patient population. Future studies of larger populations and different age groups (especially pediatric) can help reduce the number of CT scans as a reliable and noninvasive diagnostic tool for evaluating NRGN protein levels in mTBI patients with a low probability of intracranial lesions.

Diabetes mellitus (DM) is a serious public health problem and can cause long-term damage to the brain, resulting in cognitive impairment in these patients. Insulin therapy for type 1 DM (DM1) can achieve overall blood glucose control, but glycemic variations can occur during injection intervals, which may contribute to some complications. Among the additional therapies available for DM1 treatment is the implantation of insulin-producing cells (IPCs) to attenuate hyperglycemia and even reverse diabetes. Here, we studied the strategy of implanting IPCs obtained from mesenchymal stromal cells (MSCs) from adipose tissue, comparing two different IPC implant sites, subcapsular renal (SR) and subcutaneous (SC), to investigate their putative protection against hippocampal damage, induced by STZ, in a rat DM1 model. Both implants improved hyperglycemia and reduced the serum content of advanced-glycated end products in diabetic rats, but serum insulin was not observed in the SC group. The SC-implanted group demonstrated ameliorated cognitive impairment (evaluated by novel object recognition) and modulation of hippocampal astroglial reactivity (evaluated by S100B and GFAP). Using GFP + cell implants, the survival of cells at the implant sites was confirmed, as well as their migration to the pancreas and hippocampus. The presence of undifferentiated MSCs in our IPC preparation may explain the peripheral reduction in AGEs and subsequent cognitive impairment recovery, mediated by autophagic depuration and immunomodulation at the hippocampus, respectively. Together, these data reinforce the importance of MSCs for use in neuroprotective strategies, and highlight the logistic importance of the subcutaneous route for their administration.