Change of Levels of NGF, ACTH, and AVP in the Cerebrospinal Fluid after Decompressive Craniectomy of Craniocerebral Injury and Their Relationship with Communicating Hydrocephalus.

In recent years, the incidence of craniocerebral trauma has increased, making it one of the important causes of death and disability in neurosurgery patients. The decompressive craniectomy (DC) after severe craniocerebral injury has become the preferred treatment for patients with severe craniocerebral injury, but the incidence of postoperative hydrocephalus has become a difficult problem in clinical treatment. This study observed the changes of nerve growth factor (NGF), adrenocorticotropic hormone (ACTH), and arginine vasopressin (AVP) levels in the CSF after DC in patients with craniocerebral injury and analyzed the relationship between the three indicators and communicating hydrocephalus. The results showed that the levels of NGF, ACTH, and AVP in patients with cranial injury after DC were significantly higher than those in healthy subjects, and subdural effusion, traumatic subarachnoid hemorrhage (tSAH), and the levels of NGF, ACTH, and AVP in the CSF were independent risk factors for communicating hydrocephalus. Monitoring the levels of NGF, ACTH, and AVP is of great significance for clinicians to judge the occurrence of traffic hydrocephalus, evaluate the prognosis of patients with craniocerebral injury after DC, and guide clinical treatment.

SMBA1, a Bax Activator, Induces Cell Cycle Arrest and Apoptosis in Malignant Glioma Cells.

SMBA1 (small-molecule Bax agonists 1), a small molecular activator of Bax, is a potential anti-tumour agent. In the present study, we investigated the biological effects of SMBA1 on glioblastoma (GBM) cells. SMBA1 reduced the viabilities of U87MG, U251 and T98G cells in a time- and dose-dependent manner. Moreover, treatment with SMBA1 induced cell cycle arrest at the G2/M phase transition, accompanied by the downregulation of Cdc25c and cyclin B1 and the upregulation of p21. SMBA1 also induced apoptosis of GBM cells in a dose-dependent manner. Mechanistically, SMBA1 induced apoptosis via the intrinsic pathway. Silencing of Bax or ectopic expression of Bcl-2 significantly inhibited SMBA1-induced apoptosis. Moreover, SMBA1 inhibited the growth of U87MG xenograft tumours in vivo. Overall, SMBA1 shows anti-proliferative effects against GBM cells through activation of the intrinsic apoptosis pathway.

MANF attenuates neuronal apoptosis and promotes behavioral recovery via Akt/MDM-2/p53 pathway after traumatic spinal cord injury in rats.

The aim of this study was to investigate the potential effect and mechanism of action of MANF in attenuating neuronal apoptosis following t-SCI. A clip compressive model was used to induce a crush injury of the spinal cord in a total of 230 rats. The Basso, Beattie, and Bresnahan (BBB) score, spinal cord water content, and blood spinal cord barrier (BSCB) permeability were evaluated. The expression levels of MANF and its downstream proteins were examined by western blotting. Immunofluorescence staining of MANF, NeuN, GFAP, Iba-1, cleaved caspase-3, and TUNEL staining were also performed. Cells were counted in six randomly selected fields in the gray matter regions of the sections from two spinal cord sites (2 mm rostral and caudal to the epicenter of the injury) per sample. A cell-based mechanical injury model was also conducted using SH-SY5Y cells. Cell apoptosis and viability were assessed by flow cytometry, an MTT assay, and trypan blue staining. Subcellular structures were observed by transmission electron microscopy. MANF was mainly expressed in neurons. The expression levels of MANF, and its downstream target, p-Akt, were gradually increased and after t-SCI. Treatment with MANF increased Bcl-2 and decreased Bax and CC-3 levels; these effects were reversed on treatment with MK2206. The BBB score, spinal cord water content, and BSCB destruction were also ameliorated by MANF treatment. MANF decreases neuronal apoptosis and improves neurological function through Akt/MDM-2/p53 pathway after t-SCI. Therefore, MANF might be a potential treatment for patients with t-SCI.© 2018 BioFactors, 2018.

The potential long-term neurological improvement of early hyperbaric oxygen therapy on hemorrhagic stroke in the diabetics.

AIMS: Although Hyperbaric oxygen therapy (HyperBOT) attract our attention successfully these days, it is still full of controversy on the treatment of acute stroke. The aim of this study is to assess the potential long-term neurological consequences and safety of using HyperBOT on intracerebral hemorrhage (ICH) in the diabetics. METHODS: In this prospective, randomized controlled trial, 79 diabetes patients suffering from acute ICH were randomized to treat for 60 min in a monoplace hyperbaric chamber pressurized with pure oxygen to 2.5-atm absolute (ATA) in the HyperBOT group or 1.5 ATA in the normobaric oxygen therapy (NormBOT) group, which was performed as control. Both short-term and long-term neurological consequences were studied and compared in each group on National Institutes of Health Stroke Scale [NIHSS], Barthel Index, modified Rankin Scale [mRS] and Glasgow Outcome Scale [GOS]. The related complications or side-events of all patients were recorded as well at the final follow-up of six months after onset. RESULTS: No distinct difference was observed between each group at one month follow-up. However, in the long-term follow-up of six months, a higher frequency of patients in the HyperBOT group resulted into good outcome with a relative high neurological consequence compared with the NormBOT group (Barthel Index: 85.1% versus 65.6%, P = 0.080; mRS: 89.4% versus 68.8%, P = 0.045; GOS: 83.0% versus 62.5%, P = 0.073; NIHSS: 80.9% versus 56.2%, P = 0.035). CONCLUSIONS: Early HyperBOT was found to be safe and effective with regards to the long-term neurological outcome of diabetic patients suffering from ICH.

Repetitive hyperbaric oxygen treatment increases insulin sensitivity in diabetes patients with acute intracerebral hemorrhage.

AIM: The role of hyperbaric oxygen therapy (HBOT) in the treatment of acute ischemic stroke is controversial. This study aims to investigate whether the peripheral insulin sensitivity of type 2 diabetes patients suffering from intracerebral hemorrhage can be increased after HBOT. METHODS: Fifty-two type 2 diabetes participants were recruited after being diagnosed with intracerebral hemorrhage in our hospital. Insulin sensitivity was measured by the glucose infusion rate during a hyperinsulinemic euglycemic clamp (80 mU m-2 min-1) at baseline and 10 and 30 days after HBOT sessions. Serum insulin, fasting glucose, and hemoglobin A1C were measured in fasting serum at baseline and after HBOT sessions. In addition, early (∼10 days after onset) and late (1 month after onset) outcomes (National Institutes of Health Stroke Scale, NIHSS scores) and efficacy (changes of NIHSS scores) of HBOT were evaluated. RESULTS: In response to HBOT, the glucose infusion rate was increased by 37.8%±5.76% at 1 month after onset compared with baseline. Reduced serum insulin, fasting glucose, and hemoglobin A1C were observed after HBOT. Both early and late outcomes of the HBOT group were improved compared with baseline (P<0.001). In the control group, there was significant difference only in the late outcome (P<0.05). In the assessment of efficacy, there were statistically significant differences between the groups when comparing changes in NIHSS scores at 10 days and 1 month after onset (P<0.05). CONCLUSION: Peripheral insulin sensitivity was increased following HBOT in type 2 diabetes patients with intracerebral hemorrhage. The HBOT used in this study may be effective for diabetes patients with acute stroke and is a safe and harmless adjunctive treatment.

RETRACTED: Early hyperbaric oxygen therapy may improve the long term neurological consequences of diabetic patients suffering from hemorrhagic stroke.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of Neuroscience Letters has learned that text throughout this paper duplicates, or nearly duplicates, text in an earlier paper by others (Rusyniak DE, Kirk MA, May JD, Kao LW, Brizendine EJ, Welch JL, Cordell WH, Alonso RJ; Hyperbaric Oxygen in Acute Ischemic Stroke Trial Pilot Study, Stroke. 2003 Feb;34(2):571-4).