Reference intervals established using indirect method for serum ferritin assayed on Abbott Architect i2000SR analyzer in Chinese adults.

BACKGROUND: Serum ferritin (SF) test has been widely used in clinical practice. However, its reference intervals (RIs) vary depending on the analytical method and ethnic origin. This study was to establish the RIs using indirect method for SF in Chinese adults. METHODS: SF was assayed on Abbott i2000SR analyzer. The SF test results of all health examinees (8913 males aged 18-93 years and 5397 females aged 18-90 years) between December 2010 and April 2019 were obtained from our laboratory information system. After Box-Cox transformation of raw data and exclusion of outliers, parametric and non-parametric approaches were used to calculate 95% RIs. The correlation between SF levels and ages, and the differences in SF levels between subgroups were also analyzed. RESULTS: SF levels in females were significantly different from those in males (Z = 88.96, Z* = 23.17; Z > Z*) and showed a weak positive correlation with age (r = .466, P < .0001). The RIs based on parametric approach in males were 66.12-561.58 µg/L, whereas in all females were 3.59-269.59 µg/L, females aged <50 years 3.26-148.02 µg/L and those aged ≥50 years 17.28-303.27 µg/L. The RIs based on non-parametric approach in males were 65.00-571.37 µg/L whereas in all females were 4.00-254.00 µg/L, females aged <50 years 4.00-152.00 µg/L and those aged ≥50 years 16.00-304.05 µg/L. CONCLUSIONS: Our indirect RIs for SF were markedly different from the manufacturer's recommended RIs and might be more suitable for Chinese adults, which would be helpful in interpreting laboratory data and clinical decision-making.

Surgical management of 142 cases of split cord malformations associated with osseous divide.

OBJECTIVES: To investigate the key surgical points in treating split cord malformations associated with osseous divide and scoliosis (SCM-OD-S). MATERIALS AND METHODS: The surgical options and methods of a total of 142 SCM-OD-S cases were retrospectively analyzed, and the surgical precautions and imaging diagnosis were also discussed. RESULTS: The 142 patients were performed osseous divide resection plus dural sac molding, which achieved good results and no serious complication such as spinal cord and nerve injury occurred; certain symptoms such as urination-defecation disorders, muscle strength subsidence, Pes Cavus, and toe movement disorder in partial patients achieved various degrees of relief, and it also created good conditions for next-step treatment against scoliosis. CONCLUSIONS: The diagnosis of SCM-OD mainly depended on imaging inspection, routine magnetic resonance imaging (MRI) combined with computed tomography (CT) 3D reconstruction, which can comprehensively evaluate the types and features of diastematomyelia as well as other concomitant diseases. SCM alone needed no treatment, but surgery will be the only means of treating SCM-OD. Intraoperatively removing osseous divide step-by-step, as well as carefully freeing the spinal cord and remodeling the dural sac, can lay good foundations for relieving tethered cord, improving neurological symptoms, and further scoliosis orthomorphia, thus particularly exhibiting importance for the growth and development of adolescents.

Overexpression of MACC1 protein and its clinical implications in patients with glioma.

Metastasis associated in colon cancer 1 (MACC1) has been regarded as a novel potential therapeutic target for multiple cancers. However, the impact of MACC1 in glioma remains unclear. The aim of this study was to analyze the correlation of MACC1 expression with the clinicopathological features of glioma. MACC1 mRNA and protein expression levels in human glioma tissues were detected by quantitative real-time polymerase chain reaction and immunohistochemistry assays, respectively. MACC1 mRNA and protein expression were both significantly higher in glioma tissues than in corresponding noncancerous brain tissues (both P < 0.001). In addition, statistical analysis suggested that high MACC1 expression was significantly correlated with advanced pathological grade (P = 0.004) and that patients with high expression of MACC1 protein exhibited a poorer prognosis than those with low MACC1 expression. Furthermore, Cox multivariate analysis showed that MACC1 overexpression was an independent prognostic factor for predicting the overall survival of glioma patients. In conclusion, expression of MACC1 in glioma could be adopted as a candidate biomarker for the diagnosis of clinical stage and for assessing prognosis, indicating for the first time that MACC1 may play an important role in the tumor development and progression in glioma. MACC1 might be considered as a novel therapeutic target against this cancer.

Anti-apoptotic and anti-oxidative roles of quercetin after traumatic brain injury.

Experimental studies have demonstrated significant secondary damage (including cell apoptosis, blood-brain barrier disruption, inflammatory responses, excitotoxic damage, and free radical production) after traumatic brain injury (TBI). Quercetin is a natural flavonoid found in high quantities in fruits and vegetables, and may be a potential antioxidant and free radical scavenger. The purpose of this study was to determine the effects of quercetin on TBI-induced upregulation of oxidative stress, inflammation, and apoptosis in adult Sprague-Dawley rats. Animals were subjected to Feeney's weight-drop injury, thus inducing the parietal contusion brain injury model. Quercetin was administered (30 mg/kg intraperitoneal injection) 0, 24, 48, and 72 h after TBI. Quercetin reduced cognitive deficits, the number of TUNEL- and ED-1-positive cells, the protein expressions of Bax and cleaved-caspase-3 proteins, and the levels of TBARS and proinflammatory cytokines, and increased the activity of antioxidant enzymes (GSH-Px, SOD, and CAT) at 1 week after TBI. Our results suggest that in TBI rats, quercetin improves cognitive function owing to its neuroprotective action via the inhibition of oxidative stress, leading to a reduced inflammatory response, thereby reducing neuronal death.

Emodin inhibits inducible nitric oxide synthase in a rat model of craniocerebral explosive injury.

To investigate the effects of emodin on blast-induced traumatic brain injury (bTBI) in a rat model. Eighty rats were randomly divided into 2 groups (the control group and the emodin-treated group; N = 40 per group) and were used to establish the model of blast-induced traumatic brain injury. Ten minutes after the explosion, an isotonic saline solution (10 mg/kg) or emodin (10 mg/kg) were administered via an intraperitoneal injection to the control group and the emodin-treated group, respectively. At each time point (pre-explosion, 2, 6, 12, 24 h after explosion), 2 rats were used for the pathological assessment and 6 rats were used for the biochemical assessment. The concentration of nitric oxide (NO) and the expression and activity of inducible nitric oxide synthase (iNOS) were measured at each time point by spectrophotometry and western blot analysis. Light and electron microscopy showed that the brain damage in the emodin-treated group was less serious than that observed in the control group. The concentration of NO in the emodin-treated group was lower compared with the control group (p < 0.05). Western blot analysis showed that protein expression in the emodin-treated group was lower than the control group (p < 0.05). Emodin can alleviate brain damage after bTBI by inhibiting iNOS. These findings suggest that emodin has a protective effect against bTBI. One possible mechanism may occur by inhibiting the expression and activity of iNOS and consequently decreasing the concentration of NO.

Analyzing time-series microarray data reveals key genes in spinal cord injury.

Although many scholars have utilized high-throughput microarrays to delineate gene expression patterns after spinal cord injury (SCI), no study has evaluated gene changes in raphe magnus (RM) and somatomotor cortex (SMTC), two areas in brain primarily affected by SCI. In present study, we aimed to analyze the differentially expressed genes (DEGs) of RM and SMTC between SCI model and sham injured control at 4, 24 h, 7, 14, 28 days, and 3 months using microarray dataset GSE2270 downloaded from gene expression omnibus and unpaired significance analysis of microarray method. Protein-protein interaction (PPI) network was constructed for DEGs at crucial time points and significant biological functions were enriched using DAVID. The results indicated that more DEGs were identified at 14 days in RM and at 4 h/3 months in SMTC after SCI. In the PPI network for DEGs at 14 days in RM, interleukin 6, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), FBJ murine osteosarcoma viral oncogene homolog (FOS), tumor necrosis factor, and nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor) were the top 5 hub genes; In the PPI network for DEGs at 3 months in SMTC, the top 5 hub genes were ubiquitin B, Ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1), FOS, Janus kinase 2 and vascular endothelial growth factor A. Hedgehog and Wnt signaling pathways were the top 2 significant pathways in RM. These hub DEGs and pathways may be underlying therapeutic targets for SCI.

Operative versus non-operative treatment for clavicle fracture: a meta-analysis.

PURPOSE: The purpose of this study was to assess the effects of operative and non-operative treatment on clavicle fractures. METHOD: Relevant clinical trials on the operative and non-operative treatment for clavicle fractures were retrieved through searching the databases MEDLINE, Embase, OVID and the Cochrane Central Register of Controlled Trials up to December 2011. The quality of the included studies was assessed by two authors. A meta-analysis was carried out on homogeneous studies. Five studies involving 633 clavicle fractures were included. RESULTS: The differences in nonunion [risk ratio (RR) 0.12, 95 % confidence interval (CI) 0.05-0.29], malunion (RR 0.11, 95 % CI 0.04-0.29) and neurological complications (RR 0.45, 95 % CI 0.25-0.81) were statistically significant between operative and non-operative treatment. There was no statistically significant difference in delayed union (RR 0.78, 95 % CI 0.31-1.95). CONCLUSION: Operative treatment is better than non-operative treatment, but decisions should be made in accordance with specific conditions for clinical application.

Modulating Brain Activity with Invasive Brain-Computer Interface: A Narrative Review.

Brain-computer interface (BCI) can be used as a real-time bidirectional information gateway between the brain and machines. In particular, rapid progress in invasive BCI, propelled by recent developments in electrode materials, miniature and power-efficient electronics, and neural signal decoding technologies has attracted wide attention. In this review, we first introduce the concepts of neuronal signal decoding and encoding that are fundamental for information exchanges in BCI. Then, we review the history and recent advances in invasive BCI, particularly through studies using neural signals for controlling external devices on one hand, and modulating brain activity on the other hand. Specifically, regarding modulating brain activity, we focus on two types of techniques, applying electrical stimulation to cortical and deep brain tissues, respectively. Finally, we discuss the related ethical issues concerning the clinical application of this emerging technology.

Low-Dose Ketamine-Induced Deficits in Arbitrary Visuomotor Mapping in Monkeys.

Ketamine, an NMDA antagonist, is widely used in clinical settings. Recently, low-dose ketamine has gained attention because of its promising role as a rapid antidepressant. However, the effects of low-dose ketamine on brain function, particularly higher cognitive functions of primate brains, are not fully understood. In this study, we used two macaques as subjects and found that acute low-dose ketamine administration significantly impaired the ability for arbitrary visuomotor mapping (AVM), a form of associative learning (AL) essential for flexible behaviors, including executions of learned stimuli-response contingency or learning of new contingencies. We conducted in-depth analyses and identified intrinsic characteristics of these ketamine-induced functional deficits, including lowered accuracy, prolonged time for planning and movement execution, increased tendency to make errors when visual cues are changed from trial to trial, and stronger impact on combining associative learning and another key higher cognitive function, working memory (WM). Our results shed new light on how associative learning relies on the NMDA-mediated synaptic transmission of the brain and contribute to a better understanding of the potential acute side effects of low-dose ketamine on cognition, which can help facilitate its safe usage in medical practice.

Continuous renal replacement therapy and blood transfusions in treating patients with crush syndrome: 8 Case studies from the Wenchuan earthquake.

OBJECTIVE: We analyzed the efficacy of continuous renal replacement therapy (CRRT) combined with blood transfusion for patients with crush syndrome from an earthquake. METHODS: Eight patients with crush syndrome were included. CRRT were performed in six of eight patients with crush syndrome, and transfusion was performed in all eight patients. Routine blood tests, urea nitrogen, creatinine, blood coagulation function, electrolyte levels, and serum myoglobin were determined and analyzed. RESULTS: Two patients regained their health completely, four patients required amputation but recovered well, and two patients died. The total amount of red blood cells transfused in the eight cases was 521U (mean volume=68.25U). CRRT was performed 164 times in six patients (mean 27.33 times per person). The routine blood test results and coagulation and renal function parameters improved obviously (P<0.05) in the six surviving patients. CONCLUSIONS: Sufficient blood transfusion and early dialysis treatment effectively improved the conditions of patients with crush syndrome.

Establishment and Evaluation of a Novel High-Efficiency Model of Graded Traumatic Brain Injury in Mice.

BACKGROUND: Although previous studies have made significant contributions to establishing animal traumatic brain injury (TBI) models for simulation of human TBI, the accuracy, controllability, and modeling efficiency of animal TBI models need to be further improved. This study established a novel high-efficiency graded mouse TBI model induced by shock wave. METHODS: A total of 125 mice were randomly divided into sham, 0.7 mm, 0.6 mm, and 0.5 mm groups according to the depth of the cross groove of the aluminum sheets. The stability and repeatability of apparatus were evaluated, and the integrity of the blood-brain barrier, cerebral edema, neuropathologic immunohistochemistry, apoptosis-related protein, and behavioral tests of neurologic function were used to validate this new model. RESULTS: The results showed that 4 mice were injured simultaneously in 1 experiment. They received the same intensity of shock waves. Moreover, the mortality rates caused by 3 different aluminum sheets were consistent with the mortality rates of mild TBI, moderate TBI, and severe TBI. Compared with the sham group, mice in different injured groups significantly increased brain water content, blood-brain barrier permeability, and neuronal apoptosis. And the mice in all injured groups showed poor motor ability, balancing, spatial learning, and memory abilities. CONCLUSIONS: The novel TBI apparatus has advantages in its small size, simple operation, high repeatability, high efficiency, and graded severity. Our TBI apparatus provides a novel tool to investigate the neuropathologic changes and underlying mechanisms of TBI with various levels of severities.

Up-regulation of EphA2 and down-regulation of EphrinA1 are associated with the aggressive phenotype and poor prognosis of malignant glioma.

Malignant gliomas display over-expression of the receptor tyrosine kinase EphA2. However, expression levels of the EphA2 ligand, EphrinA1, have not been fully elucidated. Seventy-eight patients with primary gliomas were included in this study who underwent surgical resection, radiation, and chemotherapy. The expression of EphA2 and EphrinA1 in tumors was assessed by immunohistochemistry and was statistically analyzed in combination with the follow-up data of patients. EphA2 was highly expressed in most malignant gliomas, but EphrinA1 was expressed at low levels in these tumors. The increased EphA2 expression is associated with higher-grade histology and poor patient prognosis. Contrary to this, the increased EphrinA1 expression is associated with lower-grade histology, but not associated with poor patient prognosis. Moreover, patients with tumors positive for EphA2 and negative for EphrinA1 had significantly shorter overall and progression-free survival than patients with tumors positive for both EphA2 and EphrinA1, negative for both EphA2 and EphrinA1, or negative for EphA2 and positive for EphrinA1. RNAi-mediated suppression of endogenous EphA2 in human glioblastoma multiforme cells resulted in increased EphrinA1 levels, as well as decreased cell viability, anchorage independence and in vitro invasion, and increased apoptosis. Furthermore, suppression of EphA2 resulted in delayed tumor growth in mice xenografts. Together, these data indicate that up-regulation of EphA2 and down-regulation of Ephrina1 may correlate with poor prognosis for patients with high-grade glioma. EphA2 suppression partially reversed the aggressive phenotypes of malignant gliomas, possibly through up-regulating EphrinA1 expression, which may help explain how EphA2 modulates the malignant progression of gliomas.

Improvement in cognitive dysfunction following blast induced traumatic brain injury by thymosin α1 in rats: Involvement of inhibition of tau phosphorylation at the Thr205 epitope.

Cognitive impairment is a significant sequela of traumatic brain injury (TBI) especially blast induced traumatic brain injury (bTBI), which is characterized by rapid impairments of learning and memory ability. Although several neuroprotective agents have been postulated as promising drugs for bTBI in animal studies, very few ideal therapeutic options exist to improve cognitive impairment following bTBI. Thymosin α1(Tα1), a 28-amino-acid protein that possesses immunomodulatory functions, has exhibited beneficial effects in the treatment of infectious diseases, immunodeficiency diseases and cancers. However, it remains unclear whether Tα1 has a therapeutic role in bTBI. Thus, we hypothesized that Tα1 administration could reverse the outcomes of bTBI. The blast induced TBI (bTBI) rat model was established with the compressed gas driven blast injury model system. A consecutive Tα1 therapy (in 1 ml saline, twice a day) at a dose of 200 µg/kg or normal saline (NS) (1 ml, twice a day) for 3 days or 2 weeks was performed. Utilizing our newly designed bTBI model, we investigated the beneficial effects of Tα1 therapy on rats exposed to bTBI including: cognitive functions, general histology, regulatory T (Treg) cells, edema, inflammation reactions and the expression and phosphorylation level of tau via Morris Water Maze test (MWM test), HE staining, flow cytometry, brain water content (BWC) calculation, IL-6 assay and Western blotting, respectively. Tα1 treatment seemed to reduce the 24-hour mortality, albeit with no statistical significance. Moreover, Tα1 treatment markedly improved cognitive dysfunction by decreasing the escape latency in the acquisition phase, and increasing the crossing numbers in the probe phase of MWM test. More interestingly, Tα1 significantly inhibited tau phosphorylation at the Thr205 epitope, but not at the Ser404 and Ser262 epitopes. Tα1 increased the percentage of Treg cells and inhibited plasma IL-6 production on 3d post bTBI. Moreover, Tα1 suppressed brain edema as demonstrated by decrease of BWC. However, there was a lack of obvious change in histopathology in the brain upon Tα1 treatment. This is the first study showing that Tα1 improves neurological deficits after bTBI in rats, which is potentially related to the inhibition of tau phosphorylation at the Thr205 epitope, increased Treg cells and decreased inflammatory reactions and brain edema.

A novel model of blast induced traumatic brain injury caused by compressed gas produced sustained cognitive deficits in rats: involvement of phosphorylation of tau at the Thr205 epitope.

Improvised explosive devices (IEDs) represent the leading causes for casualties among civilians and soldiers in the present war (including counter-terrorism). Traumatic brain injury (TBI) caused by IEDs results in different degrees of impairment of cognition and behavior, but the exact brain pathophysiological mechanism following exposure to blast has not been clearly investigated. Here, we sought to establish a rat model of closed-head blast injury using compressed gas to deliver a single blast only to the brain without systemic injuries. The cognitive functions of these bTBI models were assessed by Morris Water Maze test (MWM test). The HE staining, flow cytometry, ELISA and Western Blotting were used to measure the effects of shock wave on general histology, regulatory T (Treg) cells percentage, inflammatory reactions, the expression and phosphorylation level of tau, respectively. In addition, the brain water content and 24 -h mortality were also assessed. As the distance from the blast source increased, the input pressure did not change, the overpressure decreased, and the mortality decreased. Receiver operating characteristic (ROC) curves for predicting 24 -h mortality using peak overpressure fits with the following areas under ROC curves: 0.833. In 2 weeks after blast injury, cognitive tests revealed significantly decreased performance at 20 cm distance from the blast (about 136.44 kPa) as demonstrated by increased escape latency in the acquisition phase, and decreased crossing numbers in the probe phase of MWM test. Interestingly, a single blast exposure (at 20 cm) lead to significantly increased tau phosphorylation at the Thr205 epitope but not at the Ser404 and Ser262 epitopes at 12 h, 24 h, 3d, and 7d after blast injury. Blast decreased the percentage of CD4+T cells, CD8+T cells, Treg cells and lymphocytes at different time points after blast injury, and blast increased the percentage of neutrophils at 12 h after blast injury and significantly increased IL-6 production at 12 h, 24 h and 3d after blast injury. In addition, blast lead to an increase of brain edema at 24 h and 3d after blast injury. However, no obvious alterations in brain gross pathology were found acutely in the blast-exposed rats. In conclusion, we established a rat model of simple craniocerebral blast injury characterized by impairment of cognitive function, Thr205 phosphorylation of tau, decreased Treg cells and increased inflammatory reactions and brain edema. We expect this model may help clarify the underlying mechanism after blast injury and possibly serve as a useful animal model in the development of novel therapeutic and diagnostic approaches.

Digestive system involvement of novel coronavirus infection: Prevention and control infection from a gastroenterology perspective.

An epidemic of an acute respiratory syndrome caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in Wuhan, China, now known as coronavirus disease 2019 (COVID-19), beginning in December 2019, has attracted an intense amount of attention worldwide. As the natural history and variety of clinical presentations of this disease unfolds, extrapulmonary symptoms of COVID-19 have emerged, especially in the digestive system. While the respiratory mode of transmission is well known and is probably the principal mode of transmission of this disease, a possibility of the fecal-oral route of transmission has also emerged in various case series and clinical scenarios. In this review article, we summarize four different aspects in published studies to date: (a) gastrointestinal manifestations of COVID-19; (b) microbiological and virological investigations; (c) the role of fecal-oral transmission; and (d) prevention and control of SARS-CoV-2 infection in the digestive endoscopy room. A timely understanding of the relationship between the disease and the digestive system and implementing effective preventive measures are of great importance for a favorable outcome of the disease and can help climnicians to mitigate further transmission by taking appropriate measures.

Neurosurgery medical robot Remebot for the treatment of 17 patients with hypertensive intracerebral hemorrhage.

OBJECTIVE: To verify the minimally invasive surgical approach and therapeutic effects of using the medical neurosurgery robot Remebot to treat hypertensive intracerebral hemorrhage (HICH). METHODS: Clinical data for 17 HICH patients were analyzed retrospectively. Hematoma evacuation and tube drainage using Remebot frameless stereotaxic techniques were performed for all patients, and urokinase was injected into the hematomas after the operations. RESULTS: Robot-assisted stereotactic techniques can accurately guide hematoma punctures, and no deaths occurred among these patients. The average positioning error was 1.28 ± 0.49 mm. The average drainage duration was 3.4 days. The 3-month postoperative follow-up revealed improved neurological functions and quality of life for all patients. CONCLUSIONS: The medical neurosurgery robot Remebot is minimally invasive, has high positional accuracy, and facilitates surgical planning according to the shape of the hematoma. Therefore, robot-assisted surgery using Remebot represents a safe and effective treatment method for hematoma evacuation and tube drainage in HICH patients.

Establishment of a novel rat model of blast-related diffuse axonal injury.

Although studies concerning blast-related traumatic brain injury (bTBI) have demonstrated the significance of diffuse axonal injury (DAI), no standard models for this type of injury have been widely accepted. The present study investigated a mechanism of inducing DAI through real blast injury, which was achieved by performing instantaneous high-speed swinging of the rat head, thus establishing a stable animal model of blast DAI. Adult Sprague-Dawley rats weighing 150±10 g were randomly divided into experimental (n=16), control (n=10) and sham control (n=6) groups. The frontal, parietal and occipital cortex of the rats in the experimental group were exposed, whereas those of the control group were unexposed; the sham control group rats were anesthetized and attached to the craniocerebral blast device without experiencing a blast. The rats were subjected to craniocerebral blast injury through a blast equivalent to 400 mg of trinitrotoluene using an electric detonator. Biomechanical parameters, and physical and behavioural changes of the sagittal head swing were measured using a high-speed camera. Magnetic resonance imaging (MRI) scans were conducted at 2, 12, 24 and 48 h after craniocerebral injury, only the experimental group indicated brain stem injury. The rats were sacrificed immediately following the MRI at 48 h for pathological examination of the brain stem using haematoxylin and eosin staining. The results indicated that 14 rats (87.5%) in the experimental group exhibited blast DAI, while no DAI was observed in the control and sham control groups, and the difference between the groups was significant (P<0.05). The present results indicated that this experimental design may serve to provide a stable model of blast DAI in rats.

Brain structure alterations and cognitive impairment following repetitive mild head impact: An in vivo MRI and behavioral study in rat.

Mild traumatic brain injury (mTBI) or concussion is a common health issue. Several people repeatedly experience head impact milder than that causing concussion. The present study aimed to confirm the effects of such repeated impact on the brain structure and cognitive abilities. Rat models were established by closed skull weight-drop injury. The animals were anesthetized, subjected to single (s)-sham, s-mTBI, repetitive (r)-sham, and r-mTBI, and recovery times were recorded. MRI, including T2-weighted and diffusion tensor imaging (DTI), as well as, neurological severity scores (mNSS) were assessed for the dynamics of the brain structure and neurological function. Morris water maze (MWM) was used to evaluate the cognitive function. The histological examination of r-mTBI rats revealed the basis of structural changes in the brain. There was no significant difference in the recovery time, MRI, mNSS, and MWM between the s-sham and the s-mTBI groups. Compared with r-sham, r-mTBI induced significant differences in the following aspects. The recovery time was prolonged and beam balance test (BBT) in mNSS increased from day 5. MWM performances were worse even after the BBT was recovered. The volumes of the cortex (CT), hippocampus (HP), and lateral ventricle had changed from day 5, which reached a maximum at day 14. Abnormal DTI parameters were observed in CT, corpus callosum, and HP. Histological analyses showed that both in CT and HP, neuron counts reduced at the end of the experiment. Altogether, these findings indicate that non-symptomatic head injury may result in brain atrophy and cognitive impairment when occurred repeatedly.

NFAT5 protects astrocytes against oxygen-glucose-serum deprivation/restoration damage via the SIRT1/Nrf2 pathway.

Nuclear factor of activated T cells (NFAT) is a multifunctional cytokine family. NFAT5 was recently reported to be involved in many neuronal functions, but its specific function remains unclear. In this study, our aim is to investigate whether NFAT5 overexpression can protect astrocytes against oxygen-glucose-serum deprivation/restoration (OGSD/R) damage. In vivo, rats were subjected to ischemia-reperfusion injury, resulting in increased water content, infarct volume, and expression of NFAT5 protein in rat spinal cord. After primary culture for spinal cord astrocytes, the in vitro OGSD/R model was established. The results of the CCK8 assay and flow cytometry showed that, in the OGSD/R group, astrocyte cell viability was downregulated, but astrocyte apoptosis increased. Caspase 3 activity increased as well. Levels of NFAT5, as detected by real-time quantitative PCR and western blot, decreased under OGSD/R, as did SIRT1. Commercial kits for activity assays were used to show that OGSD/R inhibited SIRT1 activation but accelerated SOD activation after OGSD/R. Next, pcDNA-NFAT5 or NFAT5 siRNA was transfected into astrocytes. Overexpression of NFAT5 not only promoted the survival of the astrocytes and SIRT1 activation under OGSD/R but also inhibited cell apoptosis and SOD activation. Moreover, overexpression of NFAT5 apparently diminished histone acetylation and promoted the nuclear transport of Nrf2. Our results show that NFAT5 protects spinal astrocytes in a manner that depends on activation of the SIRT1/Nrf2 pathway. These findings present a novel potential molecular mechanism for NFAT5 therapy in the context of spinal cord injury.

[Study on short-term therapeutic effect and its impact factors of stereotactic surgery for treating opiate users with opiate dependence in Sichuan].

OBJECTIVE: To investigate the common characteristics of the patients, relapse reasons of patients before and after surgery, evaluate the relapse rate and its impact factors, and therapeutic effect of patients accepted stereotactic surgery to treat opiate dependence in Sichuan. METHODS: An investigation, using uniform questionnaires by face-to-face and telephone interview, and gaining data from medical records of patients, was conducted in Mar to Jun 2005, in Sichuan Province. 208 patients (total 212 patients participated in surgery) were invited to gather information about their common characteristics, drug-taking history and the surgery. Statistical methods including t-test, chi2 test and logistic regression were used to analyze the data. RESULTS: (1) 181 male patients and 27 female patients participated in this study, and their mean age was (29.5 +/- 5.5) years. Most of the respondents were in Sichuan and some peripheral province, graduated from senior high school and over, and with various occupations. (2) All patients abused opiate before the surgery, and the average duration of drug-taking was (7.6 +/- 3.4) years. All patients were detoxified by unconstraint or compulsory abstinence before surgery, with mean drug abstinence of 13.9, but relapse occurred after each detoxification. (3) Suffering with no drugs and abstinence syndrome were the two main reasons of relapse before surgery. Compared with relapse before surgery, validating the effect of the surgery treating drug dependence and temptation by drug surroundings were the two main reasons of relapse after surgery. (4) The complication rate was 38.0% (79/208), no severe complications occurred in patients, and most of the complications disappeared or were healed before they were discharged from hospital. Relapse rate within 7 months after surgery was 22.1% (46/208). A significant decrease of relapse time, relapse dose, subjective feel on drugs and relapse euphoria appeared in patients who relapsed after surgery when compared with those before surgery. The univariate and multivariate analysis shows potential significant predictors of relapse rate after surgery to include education (OR = 3.259), operative time (OR = 2.451), social support (OR = 23.256) and doing simple work (OR = 3.328). CONCLUSION: This investigation showed that the stereotactic surgery can eliminate psychological desire for drugs and abstinence syndrome among most of the patients. Satisfactorily short-term therapeutic effect and substantial decline in relapse rate as well as no severe complications were appeared in these patients. Relapse was greatly associated with education, operative time, neuropsychological factors, and social conditions of patients. Therefore, patients' family and the society should strengthen their care, comprehension as well as support, and create better living and working surroundings to facilitate the complete drug abstinence to occur in patients. average duration of drug-taking was (7.6 +/- 3.4) years. All patients were detoxified by unconstraint or compulsory abstinence before surgery, with mean drug abstinence of 13.9, but relapse occurred after each detoxification. (3) Suffering with no drugs and abstinence syndrome were the two main reasons of relapse before surgery. Compared with relapse before surgery, validating the effect of the surgery treating drug dependence and temptation by drug surroundings were the two main reasons of relapse after surgery. (4) The complication rate was 38.0% (79/208), no severe complications occurred in patients, and most of the complications disappeared or were healed before they were discharged from hospital. Relapse rate within 7 months after surgery was 22.1% (46/208). A significant decrease of relapse time, relapse dose, subjective feel on drugs and relapse euphoria appeared in patients who relapsed after surgery when compared with those before surgery. The univariate and multivariate analysis shows potential significant predictors of relapse rate after surgery to include education (OR = 3.259), operative time (OR = 2.451), social support (OR = 23.256) and doing simple work (OR = 3.328). CONCLUSION: This investigation showed that the stereotactic surgery can eliminate psychological desire for drugs and abstinence syndrome among most of the patients. Satisfactorily short-term therapeutic effect and substantial decline in relapse rate as well as no severe complications were appeared in these patients. Relapse was greatly associated with education, operative time, neuropsycological factors, and social conditions of patients. Therefore, patients' family and the society should strengthen their care, comprehension as well as support, and create better living and working surroundings to facilitate the complete drug abstinence to occur in patients.