Neurological Research (NEUROL RES)
Neurological Research is an international peer-reviewed journal publishing original and fundamental studies as well as clinical research in areas of neurology, neurosurgery and neurosciences, together with such subspecialty areas as: neuro-oncology, neuropsychiatry, neurotraumatology, neuroradiology, neuropathology and molecular biology. Each issue comprises articles of clinical significance and scientific excellence with original research, case reports, and broad-based review articles, with rapid publication turnaround.
Journal Impact: 1.00*
Journal impact history
|2016 Journal impact||Available summer 2017|
|2015 Journal impact||1.00|
|2011 Journal impact||2.95|
|2010 Journal impact||1.88|
|2009 Journal impact||1.60|
|2008 Journal impact||2.41|
|2007 Journal impact||2.26|
|2006 Journal impact||2.13|
|2005 Journal impact||2.09|
|2004 Journal impact||1.49|
|2003 Journal impact||1.31|
|2002 Journal impact||1.00|
|2001 Journal impact||1.13|
|2000 Journal impact||0.77|
Journal impact over time
|Website||Neurological Research website|
|Other titles||Neurological research|
|Document type||Journal / Magazine / Newspaper|
Publications in this journal
- [Show abstract] [Hide abstract] ABSTRACT: During physical activity in McArdle patients, little or no lactate is released in the skeletal muscle. However, excessive ammonia production has frequently been reported in these patients. Production of ammonia is catalysed by AMP deaminase (AMPD) and adenylate kinase (AK). The activities of AMPD and AK along with housekeeping enzyme phosphoglucoisomerase (PGI) were measured in 11 genetically confirmed McArdle patients and compared with 27 healthy controls. The AMPD and AK activities were not significantly different in patients and controls. The activity of PGI was significantly higher in patients than in controls suggesting compensation of the impaired glycogenolysis in McArdle. The ratios of activities of AMPD and AK over PGI were significantly lower in patients than in controls. High ammonia production in McArdle patients is not based on enzyme induction of AMPD and AK but possibly due to kinetic activation of the enzyme AMPD by increased concentration of the substrate AMP.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: To investigate whether promotion of neuronal differentiation of human umbilical cord mesenchymal stem cells (HUMSCs) by progesterone (PROG) involves changes in brain-derived neurotrophic factor (BDNF) levels. Methods: We used rat brain tissue extracts to mimic the brain microenvironment. Quantitative sandwich enzyme-linked immunosorbent assay was performed to measure levels of BDNF in cultured medium with or without PROG. Results: Progesterone increased levels of BDNF in HUMSCs. Conclusion: Progesterone enhancement of brain-derived neurotrophic factor levels may be involved in PROG activated-pathways to promote neuronal differentiation of HUMSCs.
- [Show abstract] [Hide abstract] ABSTRACT: Background: Few epidemiological studies of the prevalence of neuromuscular disorders have been undertaken. The aim of the study was to estimate the prevalence of the most common types of neuromuscular disorders in Qena governorate/Egypt. Methods: A random sample was taken from 11 districts, involving 9303 inhabitants with 57.3% urban residents and 42.7% rural residence. Patients were diagnosed using a screening questionnaire for the diagnosis of neuromuscular disorders. All positive cases were referred to Qena University hospital where they underwent full clinical, electrophysiological, and laboratory investigations. Results: Out of 9303 participants 448 cases were identified positive during survey. Four hundred and twenty-six cases proved to have neuromuscular disorders giving a crude prevalence rate (CPR) of 4.57%; 408 cases had definite neuropathy and 18 cases had muscular disorders equivalent to CPR of 4.39% and 193/10⁵ respectively. There was a higher prevalence in the rural than urban population. The CPR of focal compression neuropathies was 1.8%, with the majority of cases having carpal tunnel syndrome (CPR = 1.67%). CPR of diabetic neuropathy was 1.67%. The CPR of compressive radiculopathy was 0.34%. Traumatic nerve injury had a CPR 0.06%. The lifetime prevalence of Bell’s palsy was 0.16%. Hereditary motor and sensory neuropathy had a CPR 0.08%. The CPR of idiopathic neuropathy was 0.09% and Infective Leprotic neuropathy was 0.04%. Five patients were diagnosed as having muscular dystrophy and another 5 patients had myotonia with CPR of 54/10⁵ for each. Two cases of myasthenia gravis and another two cases with systemic myopathy were recorded giving a CPR of 21/10⁵. Conclusion: The overall CPR of neuromuscular disorders in the general population in Qena governorate/Egypt was higher than reported in other countries.
- [Show abstract] [Hide abstract] ABSTRACT: Reactive species play important physiological functions. Overproduction of reactive species, notably reactive oxygen (ROS) and nitrogen (RNS) species along with the failure of balance by the body antioxidant enzyme system’s results destruction of cellular structures, lipids, proteins, and genetic materials such as DNA and RNA. Moreover, the effects of reactive species on mitochondria and their metabolic processes eventually cause a rise in ROS/RNS levels, leading to oxidize mitochondrial proteins, lipids, and DNA. Oxidative stress has been considered to be linked to the etiology of many diseases, including neurodegenerative diseases (NDDs) such as Alzheimer diseases, Amyotrophic lateral sclerosis, Friedreich’s ataxia, Huntington’s disease, Multiple sclerosis and Parkinson’s diseases. In addition, oxidative stress causing protein mis-fold may turn to other NDDs include Creutzfeldt-Jakob disease, Bovine Spongiform Encephalopathy, Kuru, Gerstmann-Straussler-Scheinker syndrome and Fatal Familial Insomnia. An overview of the oxidative stress and mitochondrial dysfunction linked NDDs has been summarized in this review.
- [Show abstract] [Hide abstract] ABSTRACT: Objectives: Posterior communicating artery aneurysms (PcoAA) account for 30–35% of intracranial aneurysms. The anatomical factors involved in the formation of PCoAA are poorly known. The study aimed to investigate the anatomical variations in the posterior communicating artery (PcoAs) and the presence of PCoAA. Methods: All 154 patients hospitalized from January 2008 to December 2013 at the department of neurology of our hospital were included in this study; 76 were confirmed with PCoAA upon cerebral angiography and 78 were confirmed without cranial artery aneurysm (controls). According to the blood supply pattern, variations of the PCoAA were classified as Type P0, P-I, or P-II. The angles of C7 and C6 of the internal carotid artery on each side were analyzed. Results: Compared with controls, patients with PCoAA had a higher frequency of abnormal posterior communicating artery (Types P-I and P-II) (p < 0.001). The angles of C7 and C6 on the contralateral side in the PCoAA group were significantly greater than on the affected side, and significantly lesser than in controls (p < 0.001). There was no difference in the angle between the culprit artery and the contralateral one. Discussion: Abnormal PCoAs (Types P-I and P-II) might be more vulnerable to PCoAA development, and Type P-II was the most vulnerable. There was a correlation between the angles of C7 and C6 part of the internal carotid artery and the presence of symptomatic PCoAA, with smaller angles being associated with increased frequency of symptomatic PCoAA.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: The role of inflammation in cognitive alterations in a post-operative setting is still not fully understood. Surgical interventions can cause systemic inflammations which eventually can induce neuroinflammation. However, the main causes of functional changes after surgery are still elusive. In this study, we investigated the role of CD38, a TNFα-inducible NADH⁺ cyclase and hydrolase. We assume that CD38 overexpression impairs mitochondrial ATP synthesis. Within the hippocampus, the resulting cellular death could lead to cognitive impairment. Methods: Seventy-nine Wistar-HAN rats were subjected for three hours either to partial hepatectomy under sevoflurane anaesthesia (‘surgery’), sevoflurane anaesthesia alone (‘anaesthesia’) or control. Rats were randomly selected to determine levels of CD38, TNFα, IL-6, and ATP, for GFAP immunohistochemistry and for Morris Water Maze testing. Results: Plasma TNFα and IL-6 levels were significantly higher in the surgery group in the immediate post-operative phase. GFAP expression and hippocampal CD38 concentration were significantly elevated 24 h after the intervention in the surgery group as compared to anaesthesia alone and controls. ATP levels did not differ significantly between the three groups. No treatment differences in spatial cognition parameters were found. Conclusions: Surgery in the form of partial hepatectomy activated the peripheral immune system and induced hippocampal glial activation and a CD38 increase. These changes, however, were not associated with rats’ cognitive impairment ≥24 h after surgery.
- [Show abstract] [Hide abstract] ABSTRACT: Background: Numerous dura substitutes are commercially available, but no absorbable synthetic dura repair product has been used for both onlay and suture applications. Objective: The safety and effectiveness of a new absorbable synthetic substitute composed of Poly-L-lactide microfibers as onlay dural graft were evaluated. Methods: Physical properties and performance of the microfibrous synthetic dural substitute implanted as an onlay or suturable grafts were compared with these commercial products, including CODMAN ETHISORB™ Dura Patch and DuraGen™ Dural Graft Matrix, in a canine duraplasty model. The cerebrospinal fluid (CSF) leakage, macroscopic and microscopic observation at 30 and 90 days after implantation were investigated. Results: The absorbable synthetic dural substitute exhibited good wettability and conformability. When implanted as an onlay graft, it can prevent CSF leakage and integrate with the surrounding tissue to repair dural defects, indicating its good efficacy and biocompatibility as an onlay graft. Conclusion: Based on the excellent physical properties and performances mentioned above, the new absorbable synthetic substitute can be applied as a dural graft for both onlay and suturable applications.
- [Show abstract] [Hide abstract] ABSTRACT: Our previous studies showed that bone marrow mononuclear cells (BMMNCs) from 5-fluorouracil (5-FU) pre-treated rats (named BMRMNCs) had a better therapeutic efficacy in ischemia/reperfusion rats as compared to BMMNCs from untreated rats. This study was undertaken to further explore the potential mechanisms underlying the neuroprotective effects of BMRMNCs in the same model. Rats were intravenously pre-treated with 5-FU, and BMRMNCs were collected 7 days later and subjected to flow cytometry for detection of CD34, CD45 and CD90. Middle cerebral artery occlusion (MCAO) was induced in rats, and BMMNCs and BMRMNCs were independently transplanted via the tail vein at 24 h after MCAO. NISSL staining was performed 14 days after cell transplantation and the viable cells in the hippocampus were counted. Stromal cell-derived factor 1 (SDF-1) mRNA expression was detected in the penumbra at 7 and 14 days after treatment. The contents of pro-inflammatory cytokines and growth factors as well as microvessel density (MVD) were determined at 14 days. Results showed more BMRMNCs were positive for CD34, CD45 and CD90. After transplantation, more viable cells were observed in the hippocampus of BMRMNCs treated rats. In addition, BMRMNCs transplantation significantly increased MVD, reduced pro-inflammatory cytokines and raised growth factors in the penumbra. However, the SDF-1 mRNA expression was comparable between BMRMNCs group and BMMNCs group. Our results indicate that BMRMNCs are likely to more effectively improve the local microenvironment to increase viable cells and elevate angiogenesis, exerting neuroprotective effects on cerebral ischemia in rats.
- [Show abstract] [Hide abstract] ABSTRACT: Huntington’s disease (HD) is a neurodegenerative disease caused by the expansion of unstable CAG repeats in the HTT gene. There are scarce data about HD in China. Fifty-eight HD patients were consecutively recruited and assessed using the Unified HD Rating Scale (UHDRS) motor section and UHDRS behaviour assessment (UHDRS-b). Genetic analyses were also conducted. Thirty-three women and Twenty -five men were diagnosed with a mean age of 46.1 ± 11.2 years and a mean number of CAG triplet repeats 44.6 ± 4.4. CAG triplet repeat number was negatively correlated with age at onset, and positively correlated with UHDRS-b total score, and its subdomains including depressed mood, low self-esteem, anxiety and irritability. On the other hand, negative correlations were identified between age at onset and UHDRS-b total score, and its subdomains include low self-esteem, anxiety, suicidal thought, irritability and apathy. Disease durations were correlated with UHDRS motor scores and anxiety domain of UHDRS-b. This is the largest series of Chinese HD patients with demographic, clinical and genetic data confirms the demographic features of Chinese HD patients are comparable to those in other ethnic backgrounds. CAG triplet repeat number may also predict the severity of behaviour problems in HD patients besides its predication for age of onset.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: Vincristine, a microtubule-destabilizing drug, was found to exhibit anti-angiogenic effects and anti-tumoral activity. However, the precise mechanism by which vincristine inhibits angiogenesis in glioblastomas is not well understood. Our aim was to investigate whether vincristine affects vascular endothelial growth factor (VEGF) expression in glioblastoma cells and determine whether it is mediated by the downregulation of hypoxia-inducible factor-1α (HIF-1α). Methods: We investigated the expression of HIF-1α in glioblastoma tissues resected from patients and in human glioblastoma cell lines using immunohistochemistry, Western blot analysis, and immunocytochemistry. In addition to an MTT assay assessing the effect of vincristine on cell proliferation and viability, the effects of vincristine on VEGF mRNA expression and HIF-1α protein were examined using real-time RT-PCR and Western blot analysis under 1% O2 (hypoxia). Results: HIF-1α was expressed in the majority of glioblastoma tissues and was detected mainly in the nucleus. Strong immunoreactivity for HIF- 1 α was found often in the hypercellular zones. Under hypoxic conditions, HIF-1α protein levels in the glioblastoma cell lines increased, primarily localizing into the nucleus similar to glioblastoma tissues. Exposure of glioblastoma cells to vincristine resulted in enrichment of the G2-M fraction of the cell cycle, which suggests that vincristine-mediated growth inhibition of glioblastoma is correlated with mitotic inhibition. Using doses lower than those found to reduce the viability and proliferation of cells by 50% (IC50), vincristine decreased both the expression of VEGF mRNA and the level of HIF-1α protein in hypoxic glioblastoma cells. In addition, following exposure to vincristine, the expression of VEGF mRNA was correlated with HIF-1α protein levels. Conclusions: Our results suggest that the mechanism by which vincristine elicits an anti-angiogenic effect in glioblastomas under hypoxic conditions might be mediated, in part, by HIF-1α inhibition.
- [Show abstract] [Hide abstract] ABSTRACT: Introduction: Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of stroke worldwide and, in particular, has been implicated as a leading cause of recurrent ischemic stroke. We developed a new rat model to study intracranial atherosclerosis. Methods: Twelve-week-old male Sprague-Dawley rats were divided into a control (on a maintain diet) and a high-cholesterol group (on a daily 1% cholesterol diet) for up to 6 weeks. During the first two weeks, NG-nitro-L-arginine methylester (L-NAME, 3 mg/mL) was added to the drinking water in the high-cholesterol group to induce intimal changes making the rats susceptible to atherosclerosis. Blood lipids, including low-density lipoprotein (LDL), cholesterol (CHO), triglycerides (TG), and high-density lipoprotein (HDL), were measured after 3 and 6 weeks. Histological sections of the brains, including internal carotid artery (ICA), middle cerebral artery (MCA), and basilar artery (BA), were prepared to study intracranial artery morphometry and intimal thickening. The levels of CD68, an inflammatory marker, within the vessel walls as determined by immunohistochemistry were also measured. Results: The high-cholesterol diet increased the levels of classic blood markers of atherosclerosis, LDL, CHO, and TG as well as decreased HDL, which became progressively more intensive with time. Rats showed increased intimal thickening in the ICA, MCA, and BA. This protocol also increased the levels of CD68 immunoreactivity within the vessel walls. Conclusions: A rat model of intracranial atherosclerosis was effectively developed by high-cholesterol diet and L-NAME administration. This clinically relevant model would be beneficial for studying ICAS.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: To investigate the effect of thrombin preconditioning (TPC) on the intracerebral hemorrhage (ICH)-induced proliferation, migration, and function of subventriclular zone (SVZ) cells and to find new strategies that enhance endogenous neurogenesis after ICH. Methods: Male Sprague-Dawley rats were randomly divided into 3 groups (ICH, TPC, and control group). Rats of each group were randomly divided into 5 subgroups (3-d, 7-d, 14-d, 21-d, and 28-d subgroup). ICH was caused by intrastrial stereotactic administration of collagenase type IV. Brdu was used to label newborn SVZ cells. Organotypic brain slices were cultured to dynamically observe the migration of SVZ cells at living brain tissue. Migration of Dil-labeled SVZ cells in living brain slices was traced by time-lapse microscopy. To assess whether SVZ cells migrating to injured striatum had the ability to form synapses with other cells, brain slices from each group were double immunolabeled with Brdu and synapsin I. Results: The number of Brdu-positive cells markedly increased in the ipsilateral SVZ and striatum 3 days after TPC, peaked at 14 days (P < 0.01), continued to 21 days, and then gradually decreased at 28 days with significant difference compared to the ICH group at each time point (P < 0.01). Migration of Dil-labeled SVZ cells in brain slices in each group was observed and imaged during a 12-h period. Dil-labeled SVZ cells in the TPC group were observed to migrate laterally toward striatum with time with a faster velocity compared to the ICH group (P < 0.01). Our study also demonstrated that TPC induced strong colocalization of Brdu and synapsin I in the ipsilateral striatum between 3 and 28 days after injury.TPC made colocalization of Brdu and synapsin I appear earlier and continue for a longer time compared to the ICH group. Conclusions: Our results demonstrated that TPC could promote proliferation, migration, and function of SVZ cells after ICH, which may provide a new idea for enhancing endogenous neurogenesis and developing new therapeutic strategies against ICH-induced brain injury.
- [Show abstract] [Hide abstract] ABSTRACT: Background/objective: Despite many data suggesting a role of genetic factors in the risk for essential tremor (ET), the responsible genes have not been identified. We analyzed in ET Spanish families three single nucleotide polymorphisms (SNPs): DRD3 rs6280, SLC1A2 rs3794087, and MAPT rs1052553) previously related to an increased risk for developing the disease. Methods: We recruited 45 subjects with ET and 13 subjects without tremor belonging to 11 families who were evaluated because of familial tremor. Diagnosis of probable or definite ET was done according to TRIG criteria. Genotyping of the 3 SNPs was done using TaqMan-based qPCR assays. Data were compared with those of healthy controls of our laboratory. Family-based association testing for disease traits was performed as well. Results: rs6280 and rs3794087 genotype and allelic frequencies did not differ significantly between subjects with ET and healthy controls. However, rs1052553AA genotype and the allele rs1052553A allele were significantly more frequent among ET patients. rs1052553A allele was non-significantly overrepresented in ET patients compared with controls when considering only the more severely affected member of each ET family. Family-based association test for disease traits showed lack of association between ET and the three SNPs studied. Conclusions: Our results showed a lack of association between rs6280 and rs3794087 with the risk for ET, though a marginal increased risk for ET was observed among the rs1052553A allele carriers, which was not confirmed with a family-based association study.
- [Show abstract] [Hide abstract] ABSTRACT: Objectives: Amyloid-beta (Aβ) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer's disease (AD), but soluble oligomeric Aβ is considered to be more potent and has been hypothesized to directly impair learning and memory. Also, evidences from some clinical studies indicated that Aβ oligomer formation is the major cause for early AD onset. However, the biochemical mechanism involved in the oligomer-induced toxicity is not very well addressed. So, thise present study was undertaken to study the effects of single intracerebroventricular (icv) injection of protofibrillar Aβ 1-42 on the behavioral and biochemical profile in rats. Methods: Rats were divided into two groups (n = 8 per group): (1) sham control group and (2) Aβ 1-42 injected group. A single dose of protofibrillar Aβ 1-42 (5 ul) through icv injection was bilaterally administered into the dorsal hippocampus, while sham control animals were administered with 5 µl of vehicle. Results: The results demonstrated that the protofibrillar Aβ significantly inhibited long-term memory retention and increased anxiety levels as shown by the behavioral studies. The amyloid deposits were present inside the brain even six weeks after injection as confirmed by thioflavin-T staining and the neurodegeneration induced by these deposits was confirmed by Nissl's staining in hippocampal and cortical regions. The amyloid aggregates induced reactive oxygen species (ROS) production, acetylcholinesterase activity, nitrite levels, lipid peroxidation, and inhibited antioxidant enzyme activity in hippocampus, cortex, and striatum regions of rat brain after six weeks. Discussion: The present study indicated that protofibrillar Aβ 1-42 injection altered long term memory, induced anxiety-like behavior and also developed Alzheimer's disease like pathology in rats.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: The main aim of this study was to identify the prognostic factors that contribute to complete recovery at 6 weeks and 6 months in patients with Bell's palsy. Material and methods: This is a prospective, longitudinal, and descriptive study that included 123 patients diagnosed with facial nerve palsy (FNP) at a hospital in Guimarães, Portugal. However, only 73 patients with Bell's palsy (BP) were included in the assessment of recovery at 6 weeks and 6 months. We analyzed the demographic and clinical characteristics of the patients, including sex, age, paralyzed side, occupation, previous and associated symptoms, seasonal occurrence, familial facial palsy, patient perception, intervention options, and baseline grade according to the House-Brackmann facial grading system (HB-FGS). Results: Of the 123 cases with FNP, 79 (64.2%) patients had BP. Age, sex, and baseline HB-FGS grades were significant predictors of complete recovery at 6 weeks. Patients with HB-FGS grade III or lower (6 weeks baseline) had significant recovery of function at 6 months. Conclusions: Baseline severity of BP, elderly patients, and male sex were early predictors of poor prognosis. Patients with mild and moderate dysfunction according to the HB-FGS achieved significant normal facial function at 6 months. Further prospective studies with longer observation periods and larger samples are needed to verify the results.
- [Show abstract] [Hide abstract] ABSTRACT: Background: The low-density lipoprotein cholesterol/high-density lipoprotein cholesterol (LDL-C/HDL-C) ratio has been recognized as a strong risk predictor of cardiovascular diseases. However, the association between the LDL-C/HDL-C ratio and the prognosis of acute intracranial hemorrhage (ICH) is unclear. Thus, we prospectively investigated whether a low LDL-C/HDL-C ratio could predict all-cause mortality and whether LDL-C/HDL-C ratio is superior to traditional lipid profiles in predicting mortality among Chinese patients with acute ICH. Methods: A prospective cohort study of 356 patients with acute ICH was conducted, and the mean follow-up time point was 80.4 days. Participants were divided into four categories based on LDL-C/HDL-C ratio quartiles. Three-month outcomes were evaluated by in-person or telephone interviews with patients or their family members. The end point was three-month mortality from all causes. Results: Forty-seven deaths from all causes were documented. The multivariate analysis found that LDL-C/HDL-C ratio [hazard ratio (HR) = 0.49, p = 0.008] and LDL-C (HR = 0.27, p = 0.044) were significantly associated with all-cause mortality. The Kaplan-Meier curves show that patients in the lowest quartiles had the highest cumulative incidence rates (log-rank p = 0.027). After adjusting for covariates, a low LDL-C/HDL-C ratio was associated with a 3.55-fold increase in the risk of all-cause mortality (HR, 3.55 [95% confidence interval, 1.04-12.14]; P-trend = 0.011) when the highest and lowest quartiles were compared. The C-statistic of the LDL-C/HDL-C ratio was significantly larger than other traditional lipid profiles (all p < 0.05). Conclusions: A low LDL-C/HDL-C ratio was independently associated with an increased risk of all-cause mortality at three months in patients with ICH. Moreover, the LDL-C/HDL-C ratio appeared to be a best lipid predictor of all-cause mortality than traditional lipid profiles.
- [Show abstract] [Hide abstract] ABSTRACT: Objectives: Valproic acid (VPA) is a broad-spectrum antiepileptic drug used for a variety of neurologic disorders. The relatively short half-life seen with intermittent intravenous bolus doing may lead to serum concentration variability. Continuous infusion VPA therapy is an approach to mitigate these effects. The objective of this study is to characterize the pharmacokinetics of continuous infusion of VPA in acutely ill patients and to determine dosing regimens that most frequently obtain goal steady-state serum concentrations. Methods: This is a retrospective pharmacokinetics study in adult patients receiving continuous infusion VPA per institutional protocol for seizure or status migrainosus. Pharmacokinetic parameters were reviewed for 234 patients (25 critically ill) and compared between the two groups (non-critically ill vs. critically ill). Intermittent and continuous infusion dosing strategies were modeled utilizing Monte Carlo simulations for both cohorts. Frequencies of serum concentration attainment were reported. Results: The percent target attainment for the non-critically ill group and critically ill group were 69.4 and 58.3% (p = 0.282) post-loading dose and 69.7 and 37.5% (p = 0.004) steady state, respectively. The volume of distribution was significantly different between the two groups (0.35 vs. 0.68 L/kg, p = < 0.0001). Highest frequency of target attainment (50-100 mcg/ml) occurred in the continuous infusion 2 mg/kg/h simulation for both critically ill (45.19%) and acutely ill (48.16%) groups. Discussion: Critically ill patients have an increased volume of distribution. Increasing the volume of distribution requires higher loading doses of VPA to obtain desired therapeutic concentrations. Continuous infusion VPA provides more consistent serum steady-state concentrations while mitigating pharmacokinetic variability.
- [Show abstract] [Hide abstract] ABSTRACT: The present study was designed to investigate the beneficial effects of cornel iridoid glycoside (CIG), a main component extract from Cornus officinalis, on neurotrophin expression in mouse experimental autoimmune encephalomyelitis (EAE), a classical model of multiple sclerosis (MS). After EAE initiation, CIG was intragastrically administered daily for 32 days and reduced disease severity. Histopathological staining and western blotting both showed that CIG could prevent brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) loss in the spinal cord of EAE mice. In conclusion, our findings indicated that CIG treatment suppressed disease severity of EAE partially through blocking downregulation of neurotrophic factor expression such as BDNF and NGF, suggesting that CIG may have beneficial effects for the treatment of demyelinating diseases such as MS.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: This study aimed to investigate the influence of low-intensity pure tone auditory stimulation on patients with rapid eye movement (REM), sleep behavior disorder (RBD), and attempt to identify a new method of RBD intervention. Methods: Patients diagnosed with idiopathic RBD (iRBD) or symptomatic RBD (sRBD) were given auditory stimulation of low-intensity pure tones during their REM sleep. Sleep parameters including sleep process, sleep architecture as well as eye movements (EMs) frequency, and amplitude were recorded by polysomnography monitoring at pre-, intra-, and post-stimulation. Results: Thirteen iRBD and 18 sRBD patients completed this study. Auditory stimulation significantly reduced the EMs frequency and amplitude in iRBD and sRBD patients (p < 0.05). In the iRBD group, the intra-stimulated FSL increased significantly than the pre-stimulated FSL (p < 0.05). After stimulation, patients had similar sleep latency (FSL), rapid eye movement sleep latency (RSL) and periodic limb movements in sleep (PLMS) compared with control. In the sRBD group, the intra-stimulated total sleep time, sleep efficiency was significantly increased, whereas the RSL and PLMS were significantly reduced compared with the pre-stimulated ones (all p < 0.05). The sRBD patients had similar time in bed, FSL and RBD episodes compared with control (all p < 0.05) in spite of significant difference before stimulation (all p < 0.05). However, the sleep architecture was not influenced by the stimulation despite the decrease in N3% in iRBD group (p < 0.05). Conclusion: Low-intensity pure tone auditory stimulation may be a potentially effective intervention for RBD, especially for sRBD.
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