ABSTRACT
OBJECTIVES@#To establish a method for the simultaneous quantitative analysis of etomidate and its metabolite etomidate acid in blood, and to discuss its application value in actual cases.@*METHODS@#Acetonitrile precipitate protein method was used, and C18 column was selected. Gradient elution was performed with acetonitrile and 5 mmol/L ammonium acetate within 6 min. Electrospray ionization source in positive ion mode was used. The internal standard etomidate acid-d5 was obtained by etomidate-d5 alkaline hydrolysis reaction. Ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was used for quantitative analysis. The methodological verification was conducted.@*RESULTS@#Etomidate and etomidate acid in blood showed good linear relationship in the quantitative linear range (r>0.999), with the lower limit of quantification was 2.5 ng/mL and 7.5 ng/mL, respectively. The accuracy, precision, recovery rate, and matrix effect of the method met the professional verification standards. The practical application results showed that etomidate and etomidate acid could be detected in the blood of the abusers, and their mass concentrations ranged from 17.24 to 379.93 ng/mL.@*CONCLUSIONS@#The method established in this study can simultaneously quantify etomidate and etomidate acid in blood, which is simple and convenient to operate with accuracy. It can meet the detection needs of actual cases and provide technical support for law enforcement to crack down on etomidate abuse.
Subject(s)
Chromatography, High Pressure Liquid/methods , Chromatography, Liquid , Etomidate , Tandem Mass Spectrometry/methods , Liquid Chromatography-Mass Spectrometry , AcetonitrilesABSTRACT
<p><b>BACKGROUND</b>High expressions of galectin-3 were identified recently in the end stage of amyotrophic lateral sclerosis (ALS) patients, which suggested that immune reactivity and inflammatory mechanisms might play an important role in the pathogenesis of ALS. The purpose of this study was to investigate plasma galectin-3 levels in different groups and stages of ALS patients and the association with related clinical characteristics.</p><p><b>METHODS</b>A total of 51 patients with ALS and 60 normal controls (NCs) were recruited in this study. Plasma galectin-3 levels were determined using the enzyme-linked immunosorbent assay. Patients with ALS were divided into several groups according to their clinical characteristics: gender, type of disease onset, duration of disease, and clinical conditions of disease. Statistical analyses of the differences of galectin-3 levels between groups and the association with the clinical characteristics of disease were performed.</p><p><b>RESULTS</b>As compared with the NCs (201.64 [22.35-401.63] ng/ml), plasma galectin-3 levels were significantly elevated in the patients with duration >12 months (341.17 [69.12-859.22] ng/ml, P< 0.05), and the patients with limb onset of disease (254.14 [69.12-859.22] ng/ml, P< 0.05); however, no difference was found in the patients with duration ≤12 months (250.62 [109.77-334.92] ng/ml, P > 0.05), and the patients with bulbar onset of disease (251.79 [109.20-404.76] ng/ml, P > 0.05). In addition, galectin-3 levels were significantly increased in the female patients (263.27 [123.32-859.22] ng/ml, P< 0.05) while no difference was found in the male patients (220.39 [69.12-748.73] ng/ml, P > 0.05). The further statistical analyses showed that plasma galectin-3 levels were positively correlated with the duration of disease (r = 0.293, P = 0.037).</p><p><b>CONCLUSIONS</b>Plasma galectin-3 levels were significantly increased in ALS patients with limb onset of disease, especially in ALS female patients, and positively correlated with the duration of disease, which suggested that plasma galectin-3 might be an interesting and useful factor associated with ALS.</p>
Subject(s)
Female , Humans , Male , Middle Aged , Amyotrophic Lateral Sclerosis , Blood , Allergy and Immunology , Pathology , Enzyme-Linked Immunosorbent Assay , Galectin 3 , Blood , Sex Factors , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To investigate the prevalence of male sexual dysfunction in males with Parkinson's disease and the pathogenesis and related factors of the problem.</p><p><b>METHODS</b>We evaluated the sexual function of 140 men with Parkinson's disease using Mini-mental State Examination (MMSE), Unified Parkinson's Disease Rating Scale (Part III) (UPDRS III), Hoenhn-Yahr Staging (HYS), Hamilton Depression Scale (HAMD) and Sexual Dysfunction Standard of ICD-10. We calculated the Levodopa equivalent doses (LED) for all the patients.</p><p><b>RESULTS</b>Sexual dysfunction was found in 58 (41.43%) of the patients with Parkinson's disease. There were no significant differences in age, education, age of onset, course of disease and scores on UPDRS III, HYS and LED between the sexual dysfunction and normal sexual function groups. The HAMD score was 14.95 +/- 9.12 in the sexual dysfunction group, significantly higher than 10.96 +/- 9.82 in the normal sexual function group (P < 0.05), and it was positively correlated with the inci- dence of male sexual dysfunction (P < 0.05).</p><p><b>CONCLUSION</b>Sexual dysfunction is a common symptom in males with Parkinson's disease, and is correlated with the high HAMD score of Parkinson's disease patients.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Humans , Male , Middle Aged , Parkinson Disease , Psychiatric Status Rating Scales , Sexual Dysfunction, PhysiologicalABSTRACT
<p><b>OBJECTIVE</b>To study the influence and mechanism of acute ethanol intoxication (AEI) on rat neuronal apoptosis after severe traumatic brain injury (TBI).</p><p><b>METHODS</b>Ninety-six Sprague-Dawley rats were randomly divided into four groups: normal control, AEI-only, TBI-only and TBI+AEI (n equal to 24 for each). Severe TBI model was developed according to Feeney's method. Rats in TBI+AEI group were firstly subjected to AEI, and then suffered head trauma. In each group, animals were sacrificed at 6 h, 24 h, 72 h, and 168 h after TBI. The level of neuronal apoptosis and the expression of Bcl-2 protein were determined by TUNEL assay and immunohistochemical method, respectively.</p><p><b>RESULTS</b>Apoptotic cells mainly distributed in the cortex and white matter around the damaged area. Neuronal apoptosis significantly increased at 6 h after trauma and peaked at 72 h. Both the level of neuronal apoptosis and expression of Bcl-2 protein in TBI-only group and TBI+AEI group were higher than those in control group (P less than 0.05). Compared with TBI-only group, the two indexes were much higher in TBI+AEI group at all time points (P less than 0.05).</p><p><b>CONCLUSION</b>Our findings suggest that AEI can increase neuronal apoptosis after severe TBI.</p>
Subject(s)
Animals , Male , Rats , Apoptosis , Brain Injuries , Cerebral Cortex , Cell Biology , Disease Models, Animal , Ethanol , Poisoning , Immunohistochemistry , In Situ Nick-End Labeling , Neurons , Physiology , Prosencephalon , Cell Biology , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To verify the efficacy on Parkinson's disease combined with depression treated with electroacupuncture and medication and to explore the therapeutic mechanism.</p><p><b>METHODS</b>Sixty cases of Parkinson's disease combined with depression were randomized into an acupuncture + medication group and a medication group, 30 cases in each one. The conventional therapeutic program of oral administration of madopar and fluoxetine was applied in both groups. In the acupuncture + medication group, on the basic treatment as the above, electroacupuncture was applied to Baihui (GV 20), Yintang (EX-HN 3), Sishencong (EX-HN 1), Taichong (LR 3) and Sanyinjiao (SP 6), etc. The level of the serum brain-derived neurotrophic factor (BDNF) and the score of Hamilton depression scale (HAMD) were observed and compared before treatment and after 3 months of treatment. The efficacy was assessed in two groups.</p><p><b>RESULTS</b>The level of BDFN was improved significantly after treatment as compared with that before treatment in two groups (both P < 0.05) and the result in the acupuncture + medication group was superior to the medication group (P < 0.05). HAMD scores were reduced significantly after treatment as compared with those before treatment in two groups (both P < 0.05) and the result in the acupuncture + medication group was superior to the medication group (P < 0.05). The total effective rate was 90.0% (27/30) in the acupuncture + medication group, which was better than 83.3% (25/30) in the medication group (P < 0.05).</p><p><b>CONCLUSION</b>The combined therapy of electroacupuncture and medication achieves the significant efficacy on Parkinson's disease combined with depression. This therapy regulates effectively serum BDNF level, relieves depression symptoms of the patients. The efficacy of electroacupuncture combined with medication is superior to the simple medication.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Acupuncture Points , Brain-Derived Neurotrophic Factor , Blood , Depression , Blood , Therapeutics , Electroacupuncture , Parkinson Disease , Blood , TherapeuticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of large decompressive craniectomy (LDC) in the management of severe and very severe traumatic brain injury (TBI) and compare it with routine decompressive craniectomy (RDC).</p><p><b>METHODS</b>The clinical data of 263 patients with severe TBI (GCS < or = 8) treated by either LDC or RDC in our department were studied retrospectively in this article. One hundred and thirty-five patients with severe TBI, including 54 patients with very severe TBI (GCS < or = 5), underwent LDC (LDC group). The other 128 patients with severe TBI, including 49 patients with very severe TBI, underwent RDC (RDC group). The treatment outcome and postoperative complications of the two treatment methods were compared and analyzed in a 6-month follow-up period.</p><p><b>RESULTS</b>Ninety-six patients (71.7 %) obtained satisfactory treatment outcome in the LDC group, while only 75 cases (58.6 %) obtained satisfactory outcome in the RDC group (P < 0.05). Moreover, the efficacy of LDC in treating very severe TBI was higher than that of RDC (63.0 % vs. 36.7 %, P < 0.01). The chance of reoperation due to refractory intracranial pressure (ICP) in the LDC group was significantly lower than that of the RDC group (P < 0.05), while the incidences of delayed intracranial hematoma and subdural effusion were significantly higher than those of the RDC group ( P < 0.05).</p><p><b>CONCLUSIONS</b>LDC is superior to RDC in improving the treatment outcome of severe TBI, especially the very severe ones. LDC can also efficiently reduce the chances of reoperation due to refractory ICP. However, it increases the incidences of delayed intracranial hematoma and contralateral subdural effusion.</p>
Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Infant , Male , Middle Aged , Brain Injuries , General Surgery , Craniotomy , Decompression, Surgical , Intracranial PressureABSTRACT
<p><b>OBJECTIVE</b>To study the effect of cuttage time on growth of Lonicera japonica.</p><p><b>METHOD</b>Randomized block of single variable and determination of the selected samples.</p><p><b>RESULT</b>The growth of seeding influenced significantly by the cottage time. The experimental results in two years showed that the survival rate, the number of root, the root weight and root cap ratio that cuttaged on March 2 were better than those cuttaged at other time point.</p><p><b>CONCLUSION</b>The first ten days of March is the best period for cuttaging L. japonica.</p>
Subject(s)
Breeding , Lonicera , Plant Roots , Seedlings , Time FactorsABSTRACT
<p><b>BACKGROUND</b>Glioma is the most common type of malignant brain tumor and the prognosis of glioma is still poor. Moreover, the prognosis of patients diagnosed with grade III gliomas varies significantly. In this study, we assessed the factors that contribute to the prognosis of patients with grade III gliomas.</p><p><b>METHODS</b>Data from 97 patients with grade III glioma who received surgery from 2000 to 2005 were included in this study. Kaplan-Meier survival analysis and Cox regression analysis were used to analyze the prognostic effects of 16 different factors selected from clinical characteristics, results from neuroimaging and pathological examinations, as well as different treatment schemes.</p><p><b>RESULTS</b>The results indicated that age, preoperative Karnofsky Performance Scale score, extent of tumor invasion, tumor resection degree, residual tumor shown by postoperative magnetic resonance imaging (MRI), and postoperative radiotherapy and chemotherapy all correlated with patient prognosis. Furthermore, Cox multivariate analysis also showed the age (P < 0.01), extent of tumor invasion (P < 0.01), residual tumor shown by postoperative MRI (P < 0.05), and postoperative radiotherapy (P < 0.05) significantly correlated with patients' prognosis.</p><p><b>CONCLUSIONS</b>Age, postoperative radiotherapy and residual tumor indicated by MRI after surgery correlated significantly with the prognosis of patients with grade III glioma. The extent of tumor invasion may be an independent prognostic factor for patients with grade III glioma.</p>
Subject(s)
Female , Humans , Male , Middle Aged , Brain Neoplasms , Pathology , General Surgery , Glioma , Pathology , General Surgery , Kaplan-Meier Estimate , Karnofsky Performance Status , Multivariate Analysis , Neoplasm, Residual , Radiotherapy , Prognosis , Proportional Hazards ModelsABSTRACT
<p><b>OBJECTIVE</b>Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality in young people. Inflammatory cytokines play an important part in the pathophysiology of TBI. Recent studies demonstrate that progesterone significantly reduces cerebral edema and enhances functional recovery from TBI and stroke in several animal models. This study was designed to investigate the inhibitory effect of progesterone on inflammatory response after traumatic brain injury.</p><p><b>METHODS</b>Progesterone was injected intraperitoneally using rats as a model of traumatic brain injury, and Western blot technique was applied to detect the expression of three inflammation-related factors: nuclear factor kappa B p65 (NFkappaB p65), glial fibrillary acidic protein (GFAP), and tumor necrosis factor-alpha (TNF-alpha). The water content of injured brain was also examined. A neurological severity score was recorded to evaluate the effect of progesterone on neurodeficit recovery.</p><p><b>RESULTS</b>NFkappaB p65, GFAP, and TNF-alpha were increased in all injured animals. In rats treated with progesterone, the expression level of NFkappaB p65 and TNF-alpha were reduced significantly in comparison with vehicle-treated rats. However, progesterone did not alter the expression of GFAP in the injured rats. Progesterone also reduced the water content of injured brain and the lesion volume. In addition, progesterone-treated injured rats showed significant improvements in the Neurological Severity Score test, compared with vehicle-treated ones.</p><p><b>CONCLUSIONS</b>Progesterone inhibits the inflammatory response after experimental traumatic brain injury and mitigates the severity of brain damage.</p>
Subject(s)
Animals , Male , Rats , Actins , Genetics , Metabolism , Brain , Metabolism , Pathology , Brain Edema , Brain Injuries , Drug Therapy , Metabolism , Gene Expression Regulation , NF-kappa B , Genetics , Metabolism , Neuroprotective Agents , Pharmacology , Progesterone , Pharmacology , Rats, Sprague-Dawley , Tumor Necrosis Factor-alpha , Genetics , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To analyze the role of resistin in insulin resistance (IR) through investigating the variation of plasma resistin levels and single-nucleotide polymorphisms (SNPs) in resistin gene 5' flanking region in stroke patients.</p><p><b>METHODS</b>In 103 atherothrombotic cerebral infarction (ACI) patients, 85 lacunar infarction (LI) patients, 70 intracerebral hemorrhage (ICH) patients, and 86 healthy controls, plasma resistin and insulin levels were measured by ELISA, SNPs in resistin gene 5' flanking region were detected by PCR and direct DNA sequencing. The subjects' body height and weight, the body mass index, quantitative insulin sensitivity check index (QUICKI), blood pressure, and the concentration of fasting plasma glucose, triglyceride, total cholesterol, creatinine, low-density lipoprotein, and high-density lipoprotein were also determined.</p><p><b>RESULTS</b>QUICKI was significantly lower in the ACI and ICH patients (0.316 +/- 0.037 and 0.309 +/- 0.032, respectively) than that in the controls (0.342 +/- 0.043, P < 0.001), while plasma resistin level was significantly higher in the ACI and ICH patients (6.36 +/- 3.79 and 7.15 +/- 4.27 ng/mL, respectively) than that in the controls (5.28 +/- 2.56 ng/mL, P < 0.05), but such difference was not observed in the LI patients compared with controls. There was a statistically negative correlation between plasma resistin level with QUICKI (r = -0.228, P < 0.001). The distributions of allele and genotype frequencies of resistin gene - 420C > G and - 537A > C SNPs were not significantly different among the different groups, and those SNPs were not correlated with other clinical and biochemical parameters.</p><p><b>CONCLUSIONS</b>Plasma resistin is associated with stroke by participating in the development of IR. The SNPs in resistin gene 5' flanking region has no impact on the plasma resistin level.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Blood Glucose , Metabolism , Cerebral Infarction , Blood , Genetics , Creatinine , Blood , Insulin , Blood , Insulin Resistance , Physiology , Intracranial Arteriosclerosis , Blood , Genetics , Lipoproteins , Blood , Polymorphism, Single Nucleotide , Resistin , Blood , Genetics , Stroke , Blood , Genetics , Triglycerides , BloodABSTRACT
<p><b>OBJECTIVE</b>To analyze retrospectively the clinical symptoms, signs, radiological findings and results of treatment of posttraumatic syringomyelia.</p><p><b>METHODS</b>The data of 7 patients with posttraumatic syringomyelia confirmed by computerized tomography (CT) and magnetic resonance imaging (MRI) in our hospital between 1999 and 2004 were reviewed retrospectively. The patients underwent decompressive laminectomy or syringo-subarachnoid (S-S) shunting with microsurgery. Long-term follow-up was available (range: 13-65 months).</p><p><b>RESULTS</b>The major clinical manifestations of posttraumatic syringomyelia usually included the onset of increasing signs and the development of new symptoms after an apparently stable period. The clinical symptoms included pain, sensory disturbance, weakness, and problems in autonomic nerves. Syrinx existed merely at the cervical level in 4 cases and extended downward to the thoracic levels in the other 3 cases. One case underwent decompressive laminectomy, 6 cases were treated by S-S shunting. During the early postoperative period, all the patients showed an improvement of symptoms of syrinx without major complication or death. The decreased size or collapse of the syrinx was demonstrated by postoperative MRI.</p><p><b>CONCLUSIONS</b>Posttraumatic syringomyelia is a disabling sequela of spinal cord injury, developing months to years after spinal injury. MRI is the standard diagnostic technique for syringomyelia. The patients with posttraumatic syringomyelia combined with progressive neurological deterioration should be treated with operations. S-S shunting procedure is effective in some patients with posttraumatic syringomyelia. Decompressive procedure may be an alternative primary surgical treatment for patients with kyphosis and cord compression.</p>
Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Decompression, Surgical , Methods , Laminectomy , Magnetic Resonance Imaging , Retrospective Studies , Spinal Cord Injuries , Syringomyelia , General Surgery , Tomography, X-Ray ComputedABSTRACT
<p><b>OBJECTIVE</b>To investigate the diagnostic method and analyze the result of microneurosurgical treatment for tumors of the fourth cerebral ventricle.</p><p><b>METHODS</b>Tumor of the fourth ventricle was clinically diagnosed in 86 patients basing on the preliminary assessment of symptom and CT or MRI findings. Of these 86 patients treated with micro-neurosurgery, the tumors in 62 were totally removed, subtotally in 19, and partially in 5. Forty-two patients received postoperative radiotherapy.</p><p><b>RESULTS</b>Three patients died postoperatively within ten days, and symptoms in 83 were improved after treatment. The average survival period was over 3 years. The pathology included 32 medulloblastomas, 23 ependymoma, 15 astrocytoma, 10 hemangiblastomas, 2 choroid plexus papillomas, and 4 epidermoid cysts.</p><p><b>CONCLUSION</b>Medulloblastoma, astrocytoma and hemangiblastoma are suggested to be removed totally whenever technically possible according to the site, character and volume of the tumor. For ependymoma, if close to the brain stem, is recommended to be subtotally removed. Postoperative radiotherapy may be beneficial for malignant types.</p>
Subject(s)
Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Astrocytoma , Diagnosis , Diagnostic Imaging , General Surgery , Cerebral Ventricle Neoplasms , Diagnosis , Radiotherapy , General Surgery , Combined Modality Therapy , Ependymoma , Diagnosis , Diagnostic Imaging , General Surgery , Follow-Up Studies , Fourth Ventricle , Pathology , Radiation Effects , General Surgery , Hemangioblastoma , Diagnosis , Diagnostic Imaging , General Surgery , Magnetic Resonance Imaging , Medulloblastoma , Diagnosis , Diagnostic Imaging , General Surgery , Microsurgery , Methods , Mortality , Neoplasm Recurrence, Local , Survival Analysis , Survival Rate , Tomography, X-Ray ComputedABSTRACT
<p><b>AIM</b>To clarify whether the activation of mitochondrial ATP sensitive potassium channel and calcium activated potassium channel can influence the permeability transition of normal and ischemic brain mitochondria.</p><p><b>METHODS</b>spectrophotometry was used to determine the effect of the two mitochondrial potassium channel agonists on the swelling of normal and ischemic brain mitochondria respectively.</p><p><b>RESULTS</b>In normal mitochondria, diazoxide and NS1619 could inhibit the decrease of calcium induced mitochondrial absorbance at 520 nm (A520), which were blocked by atractyloside. When compared with the normal mitochondria, mitochondrial A520 decrease in ischemic brain was even more rapid. Diazoxide and NS1619 could still inhibit the calcium induced mitochondrial A520 decrease, which were blocked by atractyloside.</p><p><b>CONCLUSION</b>Activation of mitochondrial ATP sensitive potassium channel and calcium activated potassium channel can protect brain mitochondria in vitro probably via influencing the mitochondrial permeability transition.</p>
Subject(s)
Animals , Male , Rats , Benzimidazoles , Pharmacology , Brain , Metabolism , Brain Ischemia , Metabolism , Cell Membrane Permeability , Diazoxide , Pharmacology , KATP Channels , Metabolism , Mitochondria , Metabolism , Mitochondrial Membrane Transport Proteins , Potassium Channels, Calcium-Activated , Metabolism , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To investigate the therapeutic effect of Bcl-2 fusion protein on apoptosis in brain following traumatic brain injury.</p><p><b>METHODS</b>Bcl-2 gene was cloned by RT-PCR. Bcl-2 and EGFP genes were linked together and inserted into pAdeno-X vector. This recombinant vector was packaged into infectious adenovirus in HEK293 cells. Ninety Wistar rats were assigned randomly into experimental group (n=45) and control group (n=45). All rats were subjected to traumatic brain injury. Then recombinant adenovirus (for experimental group) or saline (for control group) was injected into the traumatic brain. The expression of Bcl-2 fusion protein was investigated by Western blotting, immunohistochemistry and fluorescence microscopy. Apoptosis in the injured brain was studied by TUNEL. Animals' behavior capacity was evaluated by tiltboard test.</p><p><b>RESULTS</b>In the experimental group, many fluorescent cells were found around the traumatic locus, which were also proven to be Bcl-2 positive by immunohistochemistry. On the contrary, few Bcl-2 positive cells and no fluorescent cell were detected in the control group. Bcl-2 expression of experimental group was much higher than that of control group, which was illustrated by Western blotting. The apoptosis index of experimental group was 0.027+/-0.005, and that of control group was 0.141+/-0.025 (P < 0.01). Two weeks after injury, animals of the experimental group behaved better than those of the control group.</p><p><b>CONCLUSIONS</b>A recombinant adenovirus vector expressing Bcl-2 fusion protein has been constructed. Bcl-2 fusion protein can suppress apoptosis and promote cell survival. Moreover, the behavior recovery of the injured animal is promoted. Bcl-2 fusion protein provides a way to track the target cells in vivo.</p>
Subject(s)
Animals , Rats , Adenoviridae , Genetics , Apoptosis , Base Sequence , Brain Injuries , Therapeutics , Cloning, Molecular , Genes, bcl-2 , Genetic Therapy , Proto-Oncogene Proteins c-bcl-2 , Rats, WistarABSTRACT
<p><b>OBJECTIVE</b>To investigate the clinical characteristics and significance of thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury (TBI).</p><p><b>METHODS</b>Ninety-six inpatients with severe brain injury were randomized into three groups: SBC (selective brain cooling) group (n=24), MSH (mild systemic hypothermia) group (n=30), and control (normothermia) group (n=42). The platelet counts and prognosis were retrospectively analyzed.</p><p><b>RESULTS</b>Thrombocytopenia was present in 18 (75%), 23 (77%) and 15 (36%) patients in SBC group, MSH group and control group, respectively (P<0.01). Thrombocytopenia, in which the minimum platelet count was seen 3 days after hypothermia, showed no significant difference between SBC and MSH group (P>0.05). Most platelet counts (37 cases, 90%) in hypothermia group were returned to normal level after 1 to 2 days of natural rewarming. The platelet count in SBC group reduced by 16%, 27% and 29% at day 1, 3 and 5 respectively compared with the baseline value. Good recovery (GOS score 4-5) rate of thrombocytopenia 1 year after injury for hypothermia group (17 cases, 37%) was significantly lower than that of control group (P<0.01).</p><p><b>CONCLUSIONS</b>Therapeutic hypothermia increases the incidence of thrombocytopenia in severe TBI, and patients with thrombocytopenia after therapeutic hypothermia are associated with unfavorable neurological prognosis.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Brain Injuries , Therapeutics , Hypothermia, Induced , Prognosis , ThrombocytopeniaABSTRACT
<p><b>OBJECTIVE</b>To establish a simple, reproducible, and practical mechanical injury model of hippocampal neurons of Sprague-Dawley rats in vitro.</p><p><b>METHODS</b>Hippocampal neurons isolated from 1-2-day old rats were cultured in vitro. Mild, moderate and severe mechanical injuries were delivered to the neurons by syringe needle tearing, respectively. The control neurons were treated identically with the exception of trauma. Cell damage was assessed by measuring the Propidium Iodide (PI) uptaking at different time points (0.5, 1, 6, 12 and 24 hours) after injury. The concentration of neuron specific enolase was also measured at some time points.</p><p><b>RESULTS</b>Pathological examination showed that degeneration, degradation and necrosis occurred in the injured cultured neurons. Compared with the control group, the ratio of PI-positive cells in the injured groups increased significantly after 30 minutes of injury (P<0.05). More severe the damage was, more PI-positive neurons were detected. Compared with the control group, the concentration of neuron specific enolase in the injured culture increased significantly after 1 hour of injury (P<0.05).</p><p><b>CONCLUSIONS</b>The established model of hippocampal neuron injury in vitro can be repeated easily and can simulate the damage mechanism of traumatic brain injury, which can be used in the future research of traumatic brain injury.</p>
Subject(s)
Animals , Rats , Analysis of Variance , Brain Injuries , Pathology , Equipment Design , Hippocampus , Wounds and Injuries , In Vitro Techniques , Neurons , Pathology , Phosphopyruvate Hydratase , Random Allocation , Rats, Sprague-Dawley , Reproducibility of ResultsABSTRACT
<p><b>OBJECTIVE</b>Malignant middle cerebral artery (MCA) infarction is characterized by mortality rate of up to 80%. The aim of this study was to determine the value of decompressive craniectomy in patients presenting malignant MCA infarction compared with those receiving medical treatment alone.</p><p><b>METHODS</b>Patients with malignant MCA infarction treated in our hospital between January 1996 and March 2004 were included in this retrospective analysis. The National Institute of Health Stroke Scale (NIHSS) was used to assess neurological status on admission and at one week after surgery. All patients were followed up for assessment of functional outcome by the Barthel index (BI) and modified Rankin Scale (RS) at 3 months after infarction.</p><p><b>RESULTS</b>Ten out of 24 patients underwent decompressive craniectomy. The mean interval between stroke onset and surgery was 62.10 h. The mortality was 10.0% compared with 64.2% in patients who received medical treatment alone (P<0.001). The mean NIHSS score before surgery was 26.0 and 15.4 after surgery (P<0.001). At follow up, patients who underwent surgery had significantly better outcome with mean BI of 53.3, RS of 3.3 as compared to only 16.0 and 4.60 in medically treated patients. Speech function also improved in patients with dominant hemispherical infarction.</p><p><b>CONCLUSION</b>Decompressive craniectomy in patients with malignant MCA infarction improves both survival rates and functional outcomes compared with medical treatment alone. A randomized controlled trial is required to substantiate those findings.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Craniotomy , Methods , Decompression, Surgical , Methods , Infarction, Middle Cerebral Artery , Diagnosis , General Surgery , Recovery of Function , Retrospective Studies , Severity of Illness Index , Treatment OutcomeABSTRACT
<p><b>OBJECTIVE</b>To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI).</p><p><b>METHODS</b>In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain.</p><p><b>RESULTS</b>Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP.</p><p><b>CONCLUSIONS</b>In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.</p>
Subject(s)
Animals , Male , Rabbits , Apoptosis , Brain Edema , Metabolism , Pathology , Brain Injuries , Pathology , Cell Count , Disease Models, Animal , In Situ Nick-End Labeling , Intracranial Hypertension , Pathology , Necrosis , Genetics , Pathology , Reference Values , Telencephalon , Metabolism , Water , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the therapeutic effect of mild hypothermia on severe traumatic brain injury.</p><p><b>METHODS</b>Eighty-six in-patients with severe traumatic brain injury treated ordinarily were consecutively randomized into two groups: a hypothermia group (n=43) and a normothermia group (the control group, n=43). In the hypothermia group, the core temperature (i.e., nasopharyngeal or brain temperature) of the patient was reduced to and maintained at 33-35 degrees C with a systemic cooling blanket. Natural rewarming began after 3-5 days (mean: 4.3 days) of hypothermia treatment. In the control group, the patient received no hypothermia treatment. The vital sign, extradural pressure and serum superoxide dismutase were observed and measured during treatment, and the complications as well as the Glasgow outcome scale were evaluated at 2 years after injury.</p><p><b>RESULTS</b>The mean extradural pressure in the hypothermia group (27.38 mm Hg +/- 4.88 mm Hg at 24 hours, 29.40 mm Hg +/- 4.50 mm Hg at 48 hours and 26.40 mm Hg +/- 4.13 mm Hg at 72 hours after injury) was much lower than that in the control group (32.63 mm Hg +/- 3.00 mm Hg, 34.80 mm Hg +/- 6.00 mm Hg and 31.81 mm Hg +/- 4.50 mm Hg respectively at 24, 48 and 72 hours, P<0.05). The mean serum superoxide dismutase levels in the hypothermia group on days 3 and 7 (583.7 microg/L +/- 99.6 microg/L and 699.4 microg/L +/- 217.3 microg/L, respectively) were much higher than those in the control group at the same time period (446.6 microg/L +/- 79.5 microg/L and 497.1 microg/L +/- 101.2 microg/L, respectively, P<0.01). The recovery rates at 2 years after injury were 65.1% in the hypothermia group and 37.2% in the control group (P<0.05). The mortality rates were 25.6% in the hypothermia group and 51.2% in the control group (P<0.05). The complications, including pulmonary infections, thrombocytopenia (platelet count < 100 x 10(9)/L), hemorrhage in the digestive tract, electrolyte disorders and renal malfunction, were managed without severe sequelae.</p><p><b>CONCLUSIONS</b>Mild hypothermia is a safe and effective therapeutic method, which can lower the extradural pressure, increase the serum superoxide dismutase and improve the neurological outcomes without severe complications in the patients with severe traumatic brain injury.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Analysis of Variance , Chi-Square Distribution , Craniocerebral Trauma , Therapeutics , Decompression, Surgical , Glasgow Coma Scale , Hypothermia, Induced , Intracranial Pressure , TherapeuticsABSTRACT
<p><b>OBJECTIVE</b>To establish the diagnostic model of cerebrospinal protein profile for gliomas by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS) and bioinformatics.</p><p><b>METHODS</b>Seventy-five samples of cerebrospinal fluid from patients with gliomas, benign brain tumors and mild brain traumas were collected. A total of 50 samples from gliomas and non-brain-tumors were divided into training sets (33 cases including 17 gliomas and 16 non-brain-tumors) and testing sets (17 cases including 5 gliomas and 12 non-brain-tumors). The cerebrospinal proteins bound to H4 chip were detected by SELDI-TOF MS, the profiles of cerebrospinal protein were gained and then analyzed with artificial neural network algorithm (ANN); and the diagnostic model of cerebrospinal protein profiles for differentiating gliomas from non-brain-tumors was established. Forty-seven of cerebrospinal samples of gliomas and benign brain tumors were divided into training sets (31 cases including 13 gliomas and 18 benign brain tumors) and testing sets (16 cases including 9 gliomas and 7 benign brain tumors), the diagnostic model of cerebrospinal protein profiles for differentiating gliomas from benign brain tumors was established based on the same method. The support vector machine (SVM) algorithm was also used for evaluation, both results were very similar, but the result derived from ANN was more stable than that from SVM.</p><p><b>RESULT</b>The diagnostic model of cerebrospinal protein profiles for differentiating gliomas from non-brain-tumors was established and was challenged with the test set randomly, the sensitivity and specificity were 100% and 91.7%, respectively. The cerebrospinal protein profiling model for differentiating gliomas from benign brain tumors was also developed and was challenged with the test set randomly, the sensitivity and specificity were 88.9%, and 100%, respectively.</p><p><b>CONCLUSION</b>The technology of SELDI-TOF MS which combined with analysis tools of bioinformatics is a novel effective method for screening and identifying tumor biomarkers of gliomas and it may provide a new approach for the clinical diagnosis of glioma.</p>