Baiyun Liu

Hydrogen-rich water protects against ischemic brain injury in rats by regulating calcium buffering proteins.

Hydrogen-rich water (HRW) has anti-oxidant activities, and it exerts neuroprotective effects during ischemia-reperfusion brain injury. Parvalbumin and hippocalcin are two calcium buffering proteins, which are involved in neuronal differentiation, maturation and apoptosis. The aim of this study was to investigate whether HRW could moderate parvalbumin and hippocalcin expression during ischemic brain injury and glutamate toxicity-induced neuronal cell death. Focal brain ischemia was induced in male Sprague-Dawley rats by middle cerebral artery occlusion (MCAO). Rats were treated with H2O or HRW (6 ml/kg per rat) before and after MCAO, and cerebral cortical tissues were collected 1, 7 and 14 days after MCAO. Based on our results, HRW treatment was able to reduce brain infarct volume and improve neurological function following ischemic brain injury. In addition, HRW prevented the ischemia-induced reduction of parvalbumin and hippocalcin levels in vivo and also reduced the glutamate toxicity-induced death of neurons, including the dose-dependent reduction of glutamate toxicity-associated proteins in vitro. Moreover, HRW attenuated the glutamate toxicity-induced elevate in intracellular Ca(2+) levels. All these results suggest that HRW could protect against ischemic brain injury and that the maintenance of parvalbumin and hippocalcin levels by HRW during ischemic brain injury might contribute to the neuroprotective effects against neuron damage.

Hydrogen-rich water attenuates brain damage and inflammation after traumatic brain injury in rats.

Inflammation and oxidative stress are the two major causes of apoptosis after traumatic brain injury (TBI). Most previous studies of the neuroprotective effects of hydrogen-rich water on TBI primarily focused on antioxidant effects. The present study investigated whether hydrogen-rich water (HRW) could attenuate brain damage and inflammation after traumatic brain injury in rats. A TBI model was induced using a controlled cortical impact injury. HRW or distilled water was injected intraperitoneally daily following surgery. We measured survival rate, brain edema, blood-brain barrier (BBB) breakdown and neurological dysfunction in all animals. Changes in inflammatory cytokines, inflammatory cells and Cho/Cr metabolites in brain tissues were also detected. Our results demonstrated that TBI-challenged rats exhibited significant brain injuries that were characterized by decreased survival rate and increased BBB permeability, brain edema, and neurological dysfunction, while HRW treatment ameliorated the consequences of TBI. HRW treatment also decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β and HMGB1), inflammatory cell number (Iba1) and inflammatory metabolites (Cho) and increased the levels of an anti-inflammatory cytokine (IL-10) in the brain tissues of TBI-challenged rats. In conclusion, HRW could exert a neuroprotective effect against TBI and attenuate inflammation, which suggests HRW as an effective therapeutic strategy for TBI patients.

Neuroprotective efficacy of decompressive craniectomy after controlled cortical impact injury in rats: An MRI study.

Decompressive craniectomy (DC) is one of the therapeutic options for severe traumatic brain injury (TBI), and it has long been used for the treatment of patients with malignant post-traumatic brain edema. However, a lack of definitive evidence prevents physicians from drawing any conclusions about the efficacy of DC for the treatment of TBI. Magnetic resonance imaging (MRI) is widely used to evaluate the effects of TBI in both experimental and clinical studies. Therefore, the aim of the present study was to investigate the MRI assessment of DC post-TBI in rats to provide experimental animal data and radiological evidence to support the clinical application of DC. We used both in vivo MRI and proton magnetic resonance spectroscopy ((1)H-MRS) to evaluate the therapeutic effect of DC on lateral controlled cortical impact (CCI) rat models at 3h, 1 d, 2 d, 3d and 7d after TBI. Our data suggest that DC can reduce brain edema; decrease the apparent diffusion coefficient value, contusion volume and lactate (Lac)/creatine (Cr) ratio; and increase the N-acetylaspartate (NAA)/Cr and choline (Cho)/Cr ratios after TBI. The present results suggest that DC can indeed reduce brain edema formation and exhibits good neuroprotective efficacy after CCI injury in rats.

The characteristics of post-neurosurgical bacterial meningitis in elective neurosurgery in 2012: A single institute study.

OBJECTIVE Most post-neurosurgical meningitis research has been focused on large cohorts with numerous cases followed over several years. However, the characteristics of post-neurosurgical meningitis in an entire single year are still unclear, and knowledge of these characteristics might influence the selection of appropriate antibiotics and therapeutic strategies for the successful management of this disease. Our aim is to obtain a better understanding of post-neurosurgical meningitis over a single entire year. MATERIALS AND METHODS Patients with positive meningitis cultures after neurosurgical operations in our hospital during the entire year of 2012 were included in the analysis. We report demographic characteristics, morbidity during different seasons, clinical and bacteriological profiles, sensitivity to antibiotics and causes of the post-neurosurgical meningitis infections in our cohort. RESULTS Of the 6407 patients who underwent neurosurgical procedures during the study period, 146 developed post-neurosurgical meningitis and the overall incidence of meningitis was 2.28%. The incidence of meningitis was significantly higher in patients who underwent surgery in the autumn and winter than spring or summer (p=0.000). The most common organisms causing meningitis were Gram-positive bacteria, followed by the Klebsiella and Baumannii species. Compound sulfamethoxazole (52.6%) and vancomycin (10.5%) were the most active antibiotics against Gram-positive bacteria strains, whereas meropenem (43.8%) and polymyxin (18.8%) were active against Gram-negative bacillus strains. CONCLUSIONS Post-neurosurgical meningitis usually occurs in the autumn and winter of the year in our hospital. Gram-positive organisms, which are sensitive to compound sulfamethoxazole and vancomycin, are the most common causative pathogens of post-neurosurgical meningitis in the northern mainland of China.

Decompressive craniectomy for severe traumatic brain injury patients with fixed dilated pupils

Objective The outcome of decompressive craniectomy (DC) for severe traumatic brain injury (sTBI) patients with fixed dilated pupils (FDPs) is not clear. The objective of this study was to validate the outcome of DC in sTBI patients with FDPs. Patients We retrospectively collected data from 207 sTBI patients with FDPs during the time period of May 4, 2003–October 22, 2013: DC group (n=166) and conservative care (CC) group (n=41). Measurements Outcomes that were used as indicators in this study were mortality and favorable outcome. The analysis was based on the Glasgow Outcome Scale recorded at 6 months after trauma. Results A total of 49.28% patients died (39.76% [DC group] vs 87.80% [CC group]). The mean increased intracranial pressure values after admission before operation were 36.20±7.55 mmHg in the DC group and 35.59±8.18 mmHg in the CC group. After performing DC, the mean ICP value was 14.38±2.60 mmHg. Approximately, 34.34% sTBI patients with FDPs in the DC group gained favorable scores and none of the patients in the CC group gained favorable scores. Conclusion We found that DC plays a therapeutic role in sTBI patients with FDPs, and it is particularly important to reduce intracranial pressure as soon as possible after trauma. For the patients undergoing DC, favorable outcome and low mortality could be achieved.

Primary Intracranial Alveolar Soft-Part Sarcoma: Report of Two Cases and a Review of the Literature

BACKGROUND Alveolar soft part sarcoma (ASPS), a rare malignant soft-tissue sarcoma affecting mainly adolescents and young children, frequently metastasizes to the brain. Primary intracranial ASPS, however, is extremely rare. We present 2 cases of primary intracranial ASPS without demonstrable systemic lesions. CASE PRESENTATION We report 2 cases of primary intracranial lesions that were surgically treated, and a postoperative diagnosis of ASPS was determined in both of the cases. The tumor in the 28-year-old female patient completely resolved after a treatment course consisting of surgical intervention and radiotherapy. After a follow-up period of 27 months, the patient was tumor-free. The other patient was a 13-year-old boy with a right middle cranial fossa tumor who experienced subtotal surgery, experienced a tumor relapse, and died 2 years after surgery. CONCLUSIONS This is the fifth report about primary intracranial ASPS. We herein present the clinical pathologic characteristics, imaging features, and differential diagnosis of primary ASPS of the brain. Gross total resection is the most effective therapeutic option for primary intracranial ASPS.

Decompressive craniectomy protects against hippocampal edema and behavioral deficits at an early stage of a moderately controlled cortical impact brain injury model in adult male rats

HighlightsDC could attenuate TBI‐induced learning and memory deficits.DC could normalize MMP‐9 expression levels and reduce hippocampus edema formation after TBI.DC could stabilize expression of Synapsin I and potentially maintain hippocampal synaptic function after TBI.The reduction of hippocampus edema formation induced by DC was evidenced by increased ADC values. ABSTRACT A decompressive craniectomy (DC) has been shown to be a life‐saving therapeutic treatment for traumatic brain injury (TBI) patients, which also might result in post‐operative behavioral dysfunction. However, there is still no definite conclusion about whether the behavioral dysfunction already existed at an early stage after the DC operation or is just a long‐term post‐operation complication. Therefore, the aim of the present study was to analyze whether DC treatment was beneficial to behavioral function at an early stage post TBI. In this study, we established a controlled cortical impact injury rat model to evaluate the therapeutic effect of DC treatment on behavioral deficits at 1 d, 2 d, 3 d and 7 d after TBI. Our results showed that rats suffered significant behavioral and mood deficits after TBI compared to the control group, while decompressive craniectomy treatment could normalize MMP‐9 expression levels and reduce hippocampal edema formation, stabilize the expression of Synapsin I, which was a potential indicator of maintaining the hippocampal synaptic function, thus counteracting behavioral but not mood decay in rats subjected to TBI. In conclusion, decompressive craniectomy, excepting for its life‐saving effect, could also play a potential beneficial neuroprotective role on behavioral but not mood deficits at an early stage of moderate traumatic brain injury in rats.

Protective functions of PJ34, a PARP inhibitor, is related to down-regulation of calpain and NF-κB in a mouse model of TBI

OBJECTIVES Poly(ADP-ribose) polymerase (PARP), calpain, and nuclear factor-κB (NF-κB) are reported to participate in inflammatory reactions in pathologic conditions and are involved in traumatic brain injury. The objective of this study was to investigate whether PARP participates in inflammation related to calpain and NF-κB in a mouse model of controlled cortical impact (CCI). METHODS PJ34 (10 mg/kg), a selective PARP inhibitor, was administered intraperitoneally 5 minutes and 8 hours after experimental CCI. We then performed a histopathologic analysis, and we measured calpain activity and protein levels in all animals. The cytosolic, mitochondria, and nuclear fractions were prepared and used to determine the levels of PARP, calpastatin, NF-κB p65, inhibitory-κB-α, tumor necrosis factor-α, interleukin-1β, intracellular adhesion molecule-1, inducible nitric oxide synthase, and cyclooxygenase-2. We then measured blood-brain barrier disruption using electron microscopy at 6 and 24 hours after CCI. RESULTS Treatment with PJ34 markedly reduced the extent of both cerebral contusion and edema, improved neurologic scores, and attenuated blood-brain barrier damage resulting from CCI. Our data showed that the cytosolic and nuclear fractions of calpain and NF-κB were up-regulated in the injured cortex and that these changes were reversed by PJ34. Moreover, PJ34 significantly enhanced the calpastatin and inhibitory-κB levels and decreased the levels of inflammatory mediators. CONCLUSIONS PARP inhibition by PJ34 suppresses the overactivation of calpain and the production of inflammatory factors that are caused by NF-κB activation and attenuates neuronal cell death in a mouse model of CCI.

Effects of cerebral perfusion pressure on regional cerebral blood flow in dogs with acute epidural hematoma: quantitative evaluation with contrast-enhanced ultrasound

To discuss the relationship between the regional cerebral blood flow (rCBF) and cerebral perfusion pressure (CPP) and the effect of CPP on rCBF in different spaces in an experimental animal model. As the ICP increased, the CPP and rCBF (A × β value measured by CEU) decreased to varying degrees. The rCBF1 and rCBF2 were well correlated with the CPP. At the same CPP, rCBF1 decreased significantly than the level of rCBF2 (p < 0.01). Six healthy cross-breed dogs, both males and females, weighing 18.3 ± 1.6 kg, were selected to establish models of increased intracranial pressure (ICP) via the installation of an epidural latex sacculus. The calculated CPP was in accordance with the ICP through the formula CPP = MAP - ICP, and contrast-enhanced ultrasound (CEU) was used to instantly measure the rCBF 1 and 2 cm around the sacculus edge. The relationship between rCBF 1 cm (rCBF1) and 2 cm (rCBF2) around the sacculus edge and the CPP was analyzed. As the ICP increased, the CPP and rCBF both decreased. The rCBF and the CPP had a linear relationship, but the perfusion pressure did not necessarily determine all parts of the rCBF. The rCBF was different in different spaces: the farther away from the injured site, the smaller the effect on the rCBF.

Portable near-infrared rapid detection of intracranial hemorrhage in Chinese population

BACKGROUND Secondary brain injury is the main cause of mortality from traumatic brain injury (TBI). One hallmark of TBI is intracranial hemorrhage, which occurs in 40-50% of severe TBI cases. Early identification of intracranial hematomas in TBI patients allows early surgical evacuation, and can reduce the case-fatality rate of TBI. Since pre-hospital care is the weakest part of Chinese emergency care, there is an urgent need for a capability to detect brain hematomas early. The purpose of this observational study was to evaluate the performance of a near infrared (NIR) based, device to screen for traumatic intracranial hematomas in Chinese population. METHODS Data was collected using the NIR device at the time of a computed tomography (CT) or magnetic resonance imaging (MRI) scan was performed to evaluate a suspected TBI. 85 patients were included in the per protocol population. Of the 85 patients, 45 were determined by CT scan to have intracranial hemorrhage. The CT and MRI scans were read by an independent neuroradiologist who was blinded to the NIR measurements. RESULTS The NIR device demonstrated sensitivity of 95.6% (95% confidence intervals [CI] 83.6-99.2%) and specificity of 92.5% (CI 78.5-98%) in detecting intracranial hematomas larger than 3.5ml in volume, and that were less than 2.5cm from the surface of the brain. CONCLUSION These results confirm in Chinese population the results of previous studies that demonstrated a NIR based device can reliably screen for intracranial hematomas that are likely to be of clinical importance.