Effects of mind-regulating acupuncture on pain, negative emotion and sleep quality in patients with postherpetic neuralgia： a randomized controlled pilot trial. / è°ƒç¥žé’ˆæ³•å¯¹å¸¦çŠ¶ç–±ç–¹åŽé—ç¥žç»ç—›æ‚£è€ ç–¼ç—›ç¨‹åº¦ã€è´Ÿæ€§æƒ ç»ªå’Œç¡çœ è´¨é‡çš„å½±å“.

OBJECTIVES: To observe the effect of mind-regulating acupuncture on pain intensity, sleep quality, negative emotion in patients with postherpetic neuralgia (PHN), and evaluate the clinical effect of mind-regulating acupuncture combined with surrounding needling and heavy moxibustion at Ashi points (Extra) in treatment of PHN. METHODS: The patients with PHN were randomly divided into a control group (35 cases, 2 cases dropped out) and a comprehensive therapy group (35 cases). The patients in the control group were treated with surrounding needling and heavy moxibustion at Ashi points. In the comprehensive therapy group, the mind-regulating acupuncture therapy was delivered besides the treatment as the control group. The treatment was given once daily, one course of treatment was composed of 6 days and 2 courses were required in the 2 groups. Before and after treatment, the pain conditions were assessed using pain rating index (PRI), visual analogue scale (VAS) and present pain intensity (PPI), the negative emotions were assessed using Hamilton anxiety scale (HAMA) and Hamilton depression scale (HAMD), and the sleep quality with Pittsburgh sleep quality index (PSQI). One week before and one week after treatment, the average sleep time was recorded. The therapeutic effect of 2 groups was evaluated. The effective cases of 2 groups were followed up in 2 months after treatment completion and the recurrence of neuralgia was recorded. RESULTS: There were no statistical differences in the above indicators between the 2 groups before treatment. After 2 courses of treatment, the scores of PRI, VAS, PPI, HAMA, HAMD and PSQI were reduced when compared with those before treatment in the patients of the 2 groups (P<0.05), and the average sleep time was increased (P<0.05). The scores of PRI, VAS, PPI, HAMA, HAMD and PSQI in the comprehensive therapy group, as well as the average sleep time were all improved when compared with those of the control group (P<0.05). The total effective rate in the comprehensive therapy group (34/35, 97.14%) was higher than that of the control group (27/33, 81.82%, P<0.05) and the recurrence rate was lower (ï¼»2/34, 5.88%ï¼½vsï¼»8/27, 29.63%ï¼½, P<0.05). CONCLUSIONS: The combination of mind-regulating acupuncture with surrounding needling and heavy moxibustion at Ashi acupoint can effectively relieve PHN. Compared with the traditional surrounding acupuncture in pain area combined with moxibustion at Ashi points, this comprehensive therapy is more effective for ameliorating pain intensity, improving sleep quality and reducing negative emotions. It is also effective for declining the recurrence.

Ginkgolide B reduces neuronal cell apoptosis in the traumatic rat brain: possible involvement of toll-like receptor 4 and nuclear factor kappa B pathway.

Ginkgolide B (GB) has been demonstrated to have a variety of pharmacological actions. Accumulating evidence indicates that GB may exert a protective effect on brain injury. The study was designed to investigate the influence of GB on toll-like receptor 4 (TLR-4) and nuclear factor κB (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI). Wistar rats were subjected to 5, 10 and 20 mg/kg GB daily for 5 days, intraperitoneally, following TBI. Rats were sacrificed at hour 2, 6 and 12, as well as day 1, 2, 3 and 5 after TBI. The administration of 10 and 20 mg/kg GB could significantly (least-significant difference test: p < 0.05) suppress gene expressions of TLR-4 and NF-κB, lessen concentrations of tumour necrosis factor α, interleukin-1ß and interleukin-6, as well as reduce the number of apoptotic neuronal cells in traumatic rat brain tissues, but the administration of 5 mg/kg GB did not (p > 0.05). However, a clear concentration-response relationship was not found. Thus, GB may inhibit TLR-4 and NF-κB-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI, which may support the use of GB for the treatment of TBI.

Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury.

OBJECTIVE: To investigate the influence of oxymatrine (OMT) on Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI). MATERIALS AND METHODS: Wistar rats were given an intraperitoneal injection of 60 or 120 mg/kg OMT after TBI once a day till day 5. Rats were killed by decapitation at hours 2, 6 and 12, and days 1, 2, 3 and 5 after TBI. Gene expressions of TLR-4 and NF-κB, concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1ß) and interleukin-6 (IL-6) as well as the number of apoptotic neuronal cells in traumatic rat brain tissues were determined. RESULTS: The administration of 120 mg/kg OMT could significantly suppress gene expressions of TLR-4 and NF-κB, lessen concentrations of TNF-α, IL-1ß and IL-6, and reduce the number of apoptotic neuronal cells in traumatic rat brain tissues by the Mann-Whitney U test (P < 0.05), but the administration of 60 mg/kg OMT could not (P > 0.05). CONCLUSION: OMT may inhibit TLR4/NF-κB-dependent inflammatory responses, and furthermore lessen neuronal cell apoptosis after TBI.

Copeptin is associated with mortality in patients with traumatic brain injury.

BACKGROUND: High serum copeptin levels are associated with injury severity after traumatic brain injury (TBI). However, not much is known regarding its relation with mortality. Thus, we sought to evaluate its relation with disease mortality. METHODS: Fifty healthy controls and 94 patients with acute severe TBI were included. Plasma samples were obtained on admission and at days 1, 2, 3, 5, and 7. Its concentration was measured by enzyme-linked immunosorbent assay. RESULTS: Twenty-six patients (27.7%) died from TBI in a month. After brain injury, plasma copeptin level in patients increased during the 6-hour period immediately, peaked in 24 hours, plateaued at day 2, decreased gradually thereafter, and was substantially higher than that in healthy controls during the 7-day period. A forward stepwise logistic regression selected plasma copeptin level (odds ratio, 1.008; 95% confidence interval, 1.002-1.014; p = 0.010) as an independent predictor for 1-month mortality of patients. A multivariate linear regression showed that plasma copeptin level was negatively associated with Glasgow Coma Scale (GCS) score (t = -7.161; p < 0.001). A receiver operating characteristic curve identified plasma copeptin cutoff level (451.8 pg/mL) that predicted 1-month mortality with the optimal sensitivity (88.5%) and specificity (75.0%) values (area under curve, 0.874; 95% confidence interval, 0.789-0.933; p < 0.001). The area under curve of plasma copeptin level was similar to that of GCS score (p = 0.299). However, copeptin did not statistically significantly improve the area under curve of GCS score (p = 0.413). CONCLUSIONS: Increased plasma copeptin levels are associated with mortality after TBI.

Usefulness of serum interleukin-33 as a prognostic marker of severe traumatic brain injury.

BACKGROUND: Interleukin-33 is recently identified as a brain injury biomarker. We determined whether serum interlerukin-33 concentrations are associated with inflammation, severity and prognosis after traumatic brain injury (TBI). METHODS: We detected serum interlerukin-33 concentrations of 102 healthy controls and 102 severe TBI patients, as well as serum concentrations of 3 inflammatory biomarkers (interleukin-6, tumor necrosis factor-alpha and C-reactive protein) and 7 cell-specific proteins (myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1) in 102 severe TBI patients. The recorded poor prognosis variables included acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury, posttraumatic cerebral infarction and six-month mortality and poor outcome (Glasgow score of 1-3). RESULTS: Median interlerukin-33 concentration of patients (692 pg/mL) was substantially raised, as compared to controls. Interlerukin-33 concentrations were significantly correlated with Glasgow coma scale (GCS) score and the preceding biomarkers concentrations. Interlerukin-33 concentration > 692 pg/mL emerged as an independent prognostic predictor and its discriminatory capability exceeded those of the above-mentioned inflammatory biomarkers concentrations and was in the range of GCS scores and the aforementioned cell-specific proteins concentrations. CONCLUSION: Ascending serum interlerukin-33 concentrations could reflect inflammation, severity and worse prognosis following TBI.

Serum macrophage migration inhibitory factor concentrations correlate with prognosis of traumatic brain injury.

BACKGROUND: Macrophage migration inhibitory factor (MIF) is a well-known pro-inflammatory cytokine. Serum MIF concentrations are associated with the severity and prognosis of ischemic stroke. METHODS: In this prospective, observational study, white blood cell (WBC) count and serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and MIF among 108 severe traumatic brain injury (TBI) patients and 108 controls were measured. We determined whether serum MIF concentrations are associated with inflammation, severity, in-hospital major adverse events (IMAEs) (i.e., in-hospital mortality, acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction) and long-term clinical outcome (i.e., 6-month functional outcome) after TBI. RESULTS: As compared to the controls, serum CRP, IL-6, TNF-α and MIF concentrations were significantly increased. MIF concentrations correlated with WBC count, CRP, IL-6 and TNF-α concentrations and Glasgow coma scale (GCS) scores. MIF in serum was independently associated with IMAEs and long-term clinical outcome. Area under receiver operating characteristic curve of MIF concentrations was similar to GCS scores'. Moreover, MIF concentrations markedly improved the predictive value of GCS scores for 6-month unfavorable outcome. CONCLUSION: Increased serum MIF concentrations have close relation to inflammation, trauma severity and clinical outcomes, substantializing MIF as a good prognostic biomarker after TBI.

Serum thioredoxin and in-hospital major adverse events after traumatic brain injury.

BACKGROUND: In-hospital major adverse events (IMAEs), mainly including acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, are associated with poor prognosis after traumatic brain injury (TBI). Thioredoxin, a potent anti-oxidant, has been identified as an oxidative stress marker. This study was designed to explore the association of serum thioredoxin concentrations with IMAEs of patients with severe TBI. METHODS: This prospective, observational study recruited a total of 108 healthy controls and 108 patients with severe TBI. We investigated the possible relation of serum thioredoxin concentrations to IMAEs and trauma severity (reflected by Glasgow coma scale scores) following TBI using a multivariate analysis. RESULTS: Serum thioredoxin concentrations were higher in the patients than in the controls. Serum concentrations of thioredoxin significantly correlated with admission Glasgow coma scale scores. Thioredoxin in serum independently predicted any IMAEs. As compared to admission Glasgow coma scale scores, thioredoxin concentrations had similar areas under receiver operating characteristic curve for any IMAEs. CONCLUSION: Increased serum thioredoxin concentrations are highly associated with trauma severity and IMAEs, indicating thioredoxin might be a potential prognostic biomarker after TBI.

The change of plasma galectin-3 concentrations after traumatic brain injury.

BACKGROUND: Galectin-3 plays a significant role in microglia activation. Its increased circulating concentration has been associated with some inflammatory diseases. In-hospital major adverse events (IMAEs), including acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, have high prevalence and are strong predictors of mortality after severe traumatic brain injury (STBI). The present study was designed to investigate the relationships between plasma galectin-3 concentrations and trauma severity, in-hospital mortality and IMAEs following STBI. METHODS: Plasma galectin-3 concentrations of 100 STBI patients and 100 controls were determined. Diagnosis of progressive hemorrhagic injury and posttraumatic cerebral infarction was made on the follow-up computerized tomography scan. Acute traumatic coagulopathy was defined based on coagulation test. RESULTS: Plasma galectin-3 concentrations were significantly higher in patients as compared to controls and also associated highly with Glasgow Coma Scale scores and plasma C-reactive protein concentrations. Galectin-3 emerged as an independent predictor for in-hospital mortality and IMAEs. Areas under receiver operating characteristic curve of plasma galectin-3 concentrations were similar to those of Glasgow Coma Scale scores for prediction of in-hospital morality and IMAEs. CONCLUSIONS: Plasma galectin-3 concentrations have close relation to inflammation, trauma severity and clinical outcome, suggesting that galectin-3 should have the potential to be a good prognostic biomarker after STBI.

The prognostic value of plasma nesfatin-1 concentrations in patients with traumatic brain injury.

BACKGROUND: Nesfatin-1 is related to inflammation. Its increased circulating concentrations are associated with the severity and prognosis of subarachnoid hemorrhage. In-hospital major adverse events (IMAEs), including acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, are correlated with mortality after traumatic brain injury (TBI). The present study was designed to investigate the changes of plasma nesfatin-1 concentrations and further assess its association with inflammation, trauma severity, in-hospital mortality and IMAEs following TBI. METHODS: We measured plasma nesfatin-1 concentrations of 100 severe TBI patients and 100 controls. Progressive hemorrhagic injury and posttraumatic cerebral infarction were diagnosed based on a follow-up computerized tomography scan. Acute traumatic coagulopathy was identified according to a coagulation test. RESULTS: Plasma nesfatin-1 concentrations were significantly higher in patients than in controls and associated highly with Glasgow coma scale (GCS) scores and plasma C-reactive protein concentrations. Nesfatin-1 was indicated as an independent predictor for in-hospital mortality and IMAEs. In accordance with area under receiver operating characteristic curve, its predictive value was similar to GCS scores. CONCLUSION: Increased plasma nesfatin-1 concentrations are associated closely with inflammation, trauma severity and clinical outcomes, indicating that nesfatin-1 might be involved in inflammation and become a good prognostic biomarker following TBI.

The prognostic value of plasma thrombospondin-1 concentrations after aneurysmal subarachnoid hemorrhage.

BACKGROUND: Thrombospondin-1 is a homotrimeric glycoprotein with well known functions in hemostasis and angiogenesis. Its expression was increased after experimental intracerebral hemorrhage. We determined whether increased plasma thrombospondin-1 concentrations are predictive of clinical outcomes of aneurysmal subarachnoid hemorrhage (aSAH). METHODS: Plasma thrombospondin-1 concentrations of 118 aSAH patients and 118 age- and gender-matched healthy controls were determined using enzyme-linked immunosorbent assay. Patients were followed up until death or completion of 6months after aSAH. An unfavorable outcome was defined as Glasgow Outcome Scale score of 1-3. Multivariate analyses of significant variables of univariate analyses were performed to determine independent risk factors for the clinical outcomes. RESULTS: Plasma thrombospondin-1 concentrations were significantly higher in aSAH patients than in healthy controls; plasma thrombospondin-1 concentrations were independently associated with clinical severity reflected by the World Federation of Neurological Surgeons score and Fisher score; thrombospondin-1 was identified as an independent predictor of 6-month mortality and 6-month unfavorable outcome; thrombospondin-1 had similar predictive performance compared with the World Federation of Neurological Surgeons score and Fisher score according to receiver operating characteristic curve analysis. CONCLUSION: Higher plasma thrombospondin-1 concentrations are associated with clinical severity and long-term prognosis of aSAH patients.

Plasma 8-iso-Prostaglandin F2α concentrations and outcomes after acute intracerebral hemorrhage.

BACKGROUND: Higher plasma 8-iso-Prostaglandin F2α concentrations have been associated with poor outcome of severe traumatic brain injury. We further investigated the relationships between plasma 8-iso-Prostaglandin F2α concentrations and clinical outcomes in patients with acute intracerebral hemorrhage. METHODS: Plasma 8-iso-Prostaglandin F2α concentrations of 128 consecutive patients and 128 sex- and gender-matched healthy subjects were measured by enzyme-linked immunosorbent assay. We assessed their relationships with disease severity and clinical outcomes including 1-week mortality, 6-month mortality and unfavorable outcome (modified Rankin Scale score>2). RESULTS: Plasma 8-iso-Prostaglandin F2α concentrations were substantially higher in patients than in healthy controls. Plasma 8-iso-Prostaglandin F2α concentrations were positively associated with National Institutes of Health Stroke Scale (NIHSS) scores and hematoma volume using a multivariate linear regression. It emerged as an independent predictor for clinical outcomes of patients using a forward stepwise logistic regression. ROC curves identified the predictive values of plasma 8-iso-Prostaglandin F2α concentrations, and found its predictive value was similar to NIHSS scores and hematoma volumes. However, it just numerically added the predictive values of NIHSS score and hematoma volume. CONCLUSIONS: Increased plasma 8-iso-Prostaglandin F2α concentrations are associated with disease severity and clinical outcome after acute intracerebral hemorrhage.

Plasma copeptin level predicts acute traumatic coagulopathy and progressive hemorrhagic injury after traumatic brain injury.

Higher plasma copeptin levels correlate with poor clinical outcomes after traumatic brain injury. Nevertheless, their links with acute traumatic coagulopathy and progressive hemorrhagic injury are unknown. Therefore, we aimed to investigate the relationship between plasma copeptin levels, acute traumatic coagulopathy and progressive hemorrhagic injury in patients with severe traumatic brain injury. We prospectively studied 100 consecutive patients presenting within 6h from head trauma. Progressive hemorrhagic injury was present when the follow-up computerized tomography scan reported any increase in size or number of the hemorrhagic lesion, including newly developed ones. Acute traumatic coagulopathy was defined as an activated partial thromboplastic time greater than 40s and/or international normalized ratio greater than 1.2 and/or a platelet count less than 120×10(9)/L. We measured plasma copeptin levels on admission using an enzyme-linked immunosorbent assay in a blinded fashion. In multivariate logistic regression analysis, plasma copeptin level emerged as an independent predictor of progressive hemorrhagic injury and acute traumatic coagulopathy. Using receiver operating characteristic curves, we calculated areas under the curve for progressive hemorrhagic injury and acute traumatic coagulopathy. The predictive performance of copeptin was similar to that of Glasgow Coma Scale score. However, copeptin did not obviously improve the predictive value of Glasgow Coma Scale score. Thus, copeptin may help in the prediction of progressive hemorrhagic injury and acute traumatic coagulopathy after traumatic brain injury.

Prognostic significance of plasma copeptin detection compared with multiple biomarkers in intracerebral hemorrhage.

BACKGROUND: Higher plasma copeptin concentrations have been associated with poor clinical outcomes after intracerebral hemorrhage. This study was designed to compare plasma concentrations of copeptin and other biomarkers like myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, tau and ubiquitin carboxyl-terminal hydrolase L1 for analysis of their prognostic prediction. METHODS: We measured plasma concentrations of these biomarkers in 118 healthy controls and in 118 acute patients with a comparison analysis for their prediction of 6-month mortality and unfavorable outcome (modified Rankin Scale score>2). RESULTS: Plasma concentrations of these biomarkers were statistically significantly higher in all patients than in healthy controls, in non-survivors than in survivors and in patients with unfavorable outcome than with favorable outcome. Areas under receiver operating characteristic curves of plasma concentrations of these biomarkers were similar to those of the National Institute of Health Stroke Scale score for prognostic prediction. Plasma copeptin concentration statistically significantly improved the prognostic predictive value of the National Institute of Health Stroke Scale score, but other biomarkers did not. CONCLUSIONS: Copeptin may help in the prediction of long-term clinical outcomes after intracerebral hemorrhage.

Comparison of the performances of copeptin and multiple biomarkers in long-term prognosis of severe traumatic brain injury.

Enhanced blood levels of copeptin correlate with poor clinical outcomes after acute critical illness. This study aimed to compare the prognostic performances of plasma concentrations of copeptin and other biomarkers like myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1 in severe traumatic brain injury. We recruited 102 healthy controls and 102 acute patients with severe traumatic brain injury. Plasma concentrations of these biomarkers were determined using enzyme-linked immunosorbent assay. Their prognostic predictive performances of 6-month mortality and unfavorable outcome (Glasgow Outcome Scale score of 1-3) were compared. Plasma concentrations of these biomarkers were statistically significantly higher in all patients than in healthy controls, in non-survivors than in survivors and in patients with unfavorable outcome than with favorable outcome. Areas under receiver operating characteristic curves of plasma concentrations of these biomarkers were similar to those of Glasgow Coma Scale score for prognostic prediction. Except plasma copeptin concentration, other biomarkers concentrations in plasma did not statistically significantly improve prognostic predictive value of Glasgow Coma Scale score. Copeptin levels may be a useful tool to predict long-term clinical outcomes after severe traumatic brain injury and have a potential to assist clinicians.

Anti-inflammatory Effects of Oxymatrine Through Inhibition of Nuclear Factor-kappa B and Mitogen-activated Protein Kinase Activation in Lipopolysaccharide-induced BV2 Microglia Cells.

Oxymatrine, a potent monosomic alkaloid extracted from Chinese herb Sophora japonica (Sophora flavescens Ait.). possesses anti-inflammatory activittyes. This study was designed to investigate the effects of oxymatrine on nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK)-dependent inflammatory responses in lipopolysaccharide (LPS)-activated microglia. In this paper, BV2 microglia were pretreated with different concentrations of oxymatrine (1, 10 and 20 µg/mL) for 30 min as followed by stimulation with LPS (1 µg/mL) for different times (30 min, 1 h, 3 h, and 6 h). Concentrations of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1ß) and interleukin-6 (IL-6) in supernatant, mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), cytosolic inhibitor of kappa B-alpha (I-κBα) and phospho- I-κBα and nuclear p65 protein levels, and the phosphorylations of MAPK molecules such as extracellular-signal-regulated kinase (ERK) 1/2, p38 MAPK and c-Jun N-terminal kinase (JNK) were determined. It was shown that oxymatrine inhibited the productions of NO, PGE2, TNF-α, IL-1ß and IL-6, attenuated the mRNA levels of iNOS and COX-2, suppressed the phosphorylation of I-κBα in cytosol, decreased the nuclear levels of p65, and also blocked ERK, p38 and JNK pathway in LPS-stimulated BV2 microglial cells in a dose-dependent manner. According to the results; It is suggested that oxymatrine may attenuate inflammatory responses of microglia and could be potentially useful in modulation of inflammatory status in the brain disorders.

Plasma leptin level predicts hematoma growth and early neurological deterioration after acute intracerebral hemorrhage.

Higher plasma leptin levels have been associated with poor clinical outcomes after intracerebral hemorrhage. Nevertheless, their links with hematoma growth and early neurological deterioration are unknown. Therefore, we aimed to investigate the relationship between plasma leptin levels, hematoma growth, and early neurological deterioration in patients with acute intracerebral hemorrhage. We prospectively studied 102 consecutive patients with acute spontaneous basal ganglia hemorrhage presenting within 6h from symptoms onset. Significant hematoma growth was defined as hematoma enlargement >33% at 24h. Early neurological deterioration was defined as an increase of ≥4 points in National Institute of Health Stroke Scale score at 24h from symptoms onset. We measured plasma leptin levels on admission using an enzyme-linked immunosorbent assay in a blinded fashion. In multivariate logistic regression analysis, plasma leptin level emerged as the independent predictor of hematoma growth (odds ratio, 1.182; 95% confidence interval, 1.061-2.598; P=0.008) and early neurological deterioration (odds ratio, 1.193; 95% confidence interval, 1.075-2.873; P=0.004). Using receiver operating characteristic curves, we calculated areas under the curve for hematoma growth (area under curve, 0.844; 95% confidence interval, 0.759-0.908) and early neurological deterioration (area under curve, 0.857; 95% confidence interval, 0.774-0.918). The predictive performance of leptin was similar to, but did not obviously improve that of hematoma volume. Thus, leptin may help in the prediction of hematoma growth and early neurological deterioration after intracerebral hemorrhage.

Plasma high-mobility group box 1 levels and prediction of outcome in patients with traumatic brain injury.

BACKGROUND: High-mobility group box 1 (HMGB1), a marker of inflammation, has been associated with poor outcome of critical illness. The present study was undertaken to investigate the plasma HMGB1 concentrations in patients with traumatic brain injury (TBI) and to analyze the correlation of HMGB1 with TBI outcome. METHODS: We performed an observational, clinical study. Plasma HMGB1 concentration of 106 healthy subjects and 106 patients with severe TBI was measured by ELISA. The correlation with 1-y mortality and unfavorable outcome (Glasgow Outcome Scale score of 1-3) was analyzed. RESULTS: Thirty-one patients (29.2%) died and 48 patients (45.3%) had an unfavorable outcome at 1 y after TBI. Plasma HMGB1 level was substantially higher in patients than in healthy controls. A multivariate analysis selected plasma HMGB1 level as an independent predictor for 1-y mortality and unfavorable outcome of patients. A receiver operating characteristic curve analysis showed plasma HMGB1 level statistically significantly predicted 1-y mortality and unfavorable outcome. The prognostic value of HMGB1 was similar to that of Glasgow Coma Scale score for 1-y clinical outcomes. CONCLUSIONS: Plasma HMGB1 concentration emerges as a novel biomarker for predicting 1-y clinical outcomes of TBI.

The protective role of oxymatrine on neuronal cell apoptosis in the hemorrhagic rat brain.

ETHNOPHARMACOLOGICAL RELEVANCE: Oxymatrine is extracted from the traditional Chinese herb Sophora flavescens Ait, possesses anti-inflammatory, anti-oxidative and anti-apoptotic properties, and has been used for the treatment of chronic viral hepatitis and many other diseases. AIMS OF THE STUDY: This study aimed to investigate the effects of oxymatrine on inflammatory response mediated by Toll-like receptor4 (TLR4) and nuclear factor kappa-B (NF-κB), oxidative injury induced by 12/15 lipoxygenase (12/15-LOX), phosphorylated p38 mitogen activated protein kinase (phosphor-p38 MAPK) and cytosolic phospholipase A2 (cPLA2), and neuronal cell apoptosis in rat brain with intracerebral hemorrhage (ICH). MATERIALS AND METHODS: Wistar rats were treated intraperitoneally with 60 or 120mg/kg of oxymatrine daily for 5 days following ICH. The rats were sacrificed at hour 2, 6, 12, 24, 48, 72, and 120 after ICH. The gene expressions of TLR-4 and NF-κB, the levels of TNF-alpha, interleukin-1beta, interleukin-6, 12/15-LOX, phospho-p38 MAPK and cPLA2, and the number of apoptotic neuronal cells in rat brain were determined. RESULTS: Oxymatrine at 120mg/kg significantly suppressed gene expressions of TLR-4 and NF-κB, decreased levels of TNF-alpha, interleukin-1beta and interleukin-6, inhibited synthesis of 12/15-LOX, phospho-p38 MAPK and cPLA2 protein, and mitigated apoptotic neuronal changes following ICH in rat. CONCLUSION: Oxymatrine at 120mg/kg following ICH inhibits inflammatory responses, oxidative injury, and neuronal cell apoptosis in rats.

Plasma adiponectin as an independent predictor of early death after acute intracerebral hemorrhage.

BACKGROUND: Hyperadiponectinemia or hypoadiponectinemia is associated with different diseases. There is a paucity of data on circulating plasma adiponectin concentrations in human intracerebral hemorrhage (ICH). We investigated the plasma adiponectin concentrations in patients with intracerebral hemorrhage, and analyzed the correlation of adiponectin with the severity of brain injury and early mortality after ICH. METHODS: Thirty controls and 86 patients with acute ICH were included. Plasma samples were obtained on admission and at days 1, 2, 3, 5, and 7 after ICH. Their concentrations were measured by enzyme-linked immunosorbent assay. RESULTS: After ICH, plasma adiponectin level of the patients increased immediately within 6h, peaked within 24h, plateaued at day 2, and decreased gradually thereafter. It was substantially higher than that in the controls in a period of 7 days. A multivariate analysis showed plasma adiponectin level was an independent predictor for 1-week mortality (odds ratio, 1.199; 95% CI: 1.035-1.389; P=0.015) and that it was associated with Glasgow coma scale (GCS) score (t=-3.596, P=0.001) and plasma C-reactive protein level (t=4.194, P<0.001). A receiver operating characteristic curve identified that a plasma adiponectin level >16.4 µg/ml predicted the 1-week mortality of patients with a sensitivity of 65.6% and a specificity of 90.7% (AUC, 0.789; 95% CI: 0.688-0.870). The predictive value of adiponectin concentration was significantly lower than that of GCS score (P=0.007) and hematoma volume (P=0.022). Adiponectin could not improve the predictive values of GCS score (P=0.317) and hematoma volume (P=0.226). CONCLUSIONS: Adiponectin is an independent indicator of early death and may play an anti-inflammatory role after intracerebral hemorrhage.