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Background: Intracerebral hemorrhage (ICH) is a major cause of death and disability globally. As a type of secondary injury after ICH, treatment for cell death can promote the recovery of neurological function. Methods: Among all the cell death, neuronal necroptosis has recently been demonstrated of significance in the pathogenesis of ICH. However, the administration of drugs against necroptosis has many limitations. Results: In the present study, we found that metformin, a first-line medication for the treatment of type 2 diabetes, can effectively inhibit neuronal necroptosis after ICH by activating the AMPK related pathway, thereby significantly improving neurological function scores and reducing brain edema. Conclusion: These results will provide a new perspective for future research in necroptosis.

One of the most important and useful pieces of information in the preoperative evaluation of a large petroclival meningioma is the running course of the abducens nerve. The abducens nerve is small and has a long intracranial course, making it prone to compression by the tumor at various anatomical points. In relatively large tumors, it is difficult to confirm the entire course of the abducens nerve, even by heavy T2-thin slice imaging. We report a case of successful preoperative estimation of the course of the abducens nerve that aided in its complete preservation during the resection of a large petroclival tumor.

Cellular therapies represent a new frontier in the treatment of neurological diseases. Accumulating evidence from preclinical studies of animal models suggests that mesenchymal stromal cells (MSCs), also known as mesenchymal stem cells, are an effective therapy for neurological diseases. In this study, we established human MSC lines from both cranial bone marrow (cBMMSCs) and iliac crest bone marrow (iBMMSCs) from the same donors and found that cBMMSCs show higher expression of neural crest-associated genes than iBMMSCs. Moreover, as observed in both mRNA and protein assays, neurogenic-induced cells from cBMMSCs expressed significantly higher levels of neural markers, such as NESTIN, SLUG, SOX9, and TWIST, than those from iBMMSCs. Thus, cBMMSCs showed a greater tendency than iBMMSCs to differentiate into neuron-like cells.

Rationale: Klebsiella pneumonia (K. pneumonia), primarily a hospital-acquired pathogen, can cause a variety of deep-seated infections with significant morbidities. However, in the current scenario of global rise in antibiotic abuse, unexpected infection could be caused by K. pneumoniae. Patient concerns: A 56-year-old male who presented with intermittent headache and low fever was admitted, he had transsphenoidal surgery for pituitary adenoma 3 years ago. Routine laboratory tests revealed an elevated WBC count of 10.12 × 109/L and C-reactive protein (CRP) 12.9 mg/L. computed tomography (CT) revealed the sellar region with suspicious hemorrhage. Diagnoses: The patient was initially diagnosed with acute residual tumor hemorrhage. But the consequent diagnose of Klebsiella pneumoniae purulent meningitis was made based on the cerebrospinal fluid lab test and cerebrospinal fluid (CSF) and blood culture, and CT scan. Interventions: Lumbar puncture examination was made and the antibiotics were adjusted to meropenem and vancomycin according to the antibiotic sensitivity test. But because of the patient's unstable vital signs, his family refuse further lateral ventricular drainage. Outcomes: The infection was out of control and the patient died of spontaneous breath and heartbeat arrest. Lessons: Through this case, we could learn that any clue of suspicious intracranial infection should be carefully considered in the current scenario of global rise in antibiotic abuse. The manifestation of intermittent headache and mild fever could be potential signs of fatal infection, and prompt appropriate measures should be taken timely.

Tenascin-C, a matricellular protein, is involved in brain injury. However, change of tenascin-C concentrations in peripheral blood remains unknown after traumatic brain injury (TBI).Serum tenascin-C concentrations were measured in 100 healthy controls, 108 severe TBI patients, 79 moderate TBI patients and 32 mild TBI patients.Serum tenascin-C concentrations of patients were significantly higher than those of controls. Tenascin-C concentrations negatively correlated with Glasgow Coma Scale (GCS) scores in all patients (r=-0.658, P0.001). In severe TBI patients, tenascin-C in serum significantly discriminated patients at risk of 6-month mortality (area under curve, 0.821; 95% confidence interval, 0.735-0.888) and poor outcome (Glasgow Outcome Scale score of 1-3) (area under curve, 0.833; 95% confidence interval, 0.749-0.898) and emerged as an independent predictor for 6-month mortality (odds ratio, 1.114; 95% confidence interval, 1.008-1.233; P=0.005), overall survival (hazard ratio, 1.085; 95% confidence interval, 1.010-1.166; P=0.003) and unfavorable outcome (odds ratio, 1.049; 95% confidence interval, 1.014-1.076; P=0.001). By receiver-operating characteristic analysis, serum tenascin-C concentrations had similar prognostic value compared with GCS scores.Enhanced serum tenascin-C concentrations are closely related to trauma severity and clinical outcomes, substantializing tenascin-C as a potential prognostic biomarker after TBI.