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1.

Background  

Embryonal central nervous system (CNS) tumors are currently classified into three types: medulloblastoma, atypical rhabdoid/teratoid tumors, and primitive neuroectodermal tumor (PNET). A distinctive subtype of PNET called “embryonal tumor with abundant neuropil and true rosettes” (ETANTR) was reported in 2000.  相似文献   

2.

Objectives  

We examined whether plasma concentrations of amyloid beta (Aβ) as protein derivatives play a central role in the etiology of autistic features.  相似文献   

3.

Background  

Familial hemophagocytic lymphohistiocytosis (FHL) is a rare multisystem congenital disorder characterized by uncontrolled proliferation and infiltration of activated lymphocytes and histiocytes, secreting high amounts of inflammatory cytokines; this may affect multiple organs including liver, spleen, lymph nodes, bone marrow, and central nervous system (CNS; Janka, Eur J Pediatr 166:95–109, 1).  相似文献   

4.
5.

Objective  

To evaluate the effects of the neurological “wake-up test” (NWT), defined as interruption of continuous propofol sedation and evaluation of the patient’s level of consciousness, on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in patients with severe subarachnoid hemorrhage (SAH) or traumatic brain injury (TBI).  相似文献   

6.

Introduction  

Hypotension is common following carotid artery stenting (CAS), and may be mediated by vagal stimulation and/or suppression of spinal sympathetic outflow. Both mixed α/β agonists (dopamine (DA)), and more selective α- agonists (norepinephrine (NE) and phenylephrine (PE)), have been used, but the most effective treatment of post-CAS hypotension is unknown.  相似文献   

7.

Objective  

To describe the pathophysiologic response in cerebral blood flow (CBF) and autoregulation after severe traumatic brain injury (TBI), Glasgow Coma Score (GCS) ≤8 on admission, in children, defining a baseline for future studies.  相似文献   

8.
Objective Our previous study identified Threonine 161 (Thr-161), located in the second intracellular loop of the δ-opioid receptor (DOR), as the only consensus phosphorylation site for cyclin-dependent kinase 5 (Cdk5). The aim of this study was to assess the function of DOR phosphorylation by Cdk5 in complete Freund’s adjuvant (CFA)-induced inflammatory pain and morphine tolerance. Methods Dorsal root ganglion (DRG) neurons of rats with CFA-induced inflammatory pain were acutely dissociated and the biotinylation method was used to explore the membrane localization of phosphorylated DOR at Thr-161 (pThr-161-DOR), and paw withdrawal latency was measured after intrathecal delivery of drugs orTat-peptide, using a radiant heat stimulator in rats with CFA-induced inflammatory pain. Results Both the total amount and the surface localization of pThr-161-DOR were significantly enhanced in the ipsilateral DRG following CFA injection. Intrathecal delivery of the engineered Tat fusion-interefering peptide corresponding to the second intracellular loop of DOR (Tat-DOR-2L) increased inflammatory hypersensitivity, and inhibited DOR- but not μ-opioid receptor-mediated spinal analgesia in CFA-treated rats. However, intrathecal delivery of Tat-DOR-2L postponed morphine antinociceptive tolerance in rats with CFA-induced inflammatory pain. Conclusion Phosphorylation of DOR at Thr-161 by Cdk5 attenuates hypersensitivity and potentiates morphine tolerance in rats with CFA-induced inflammatory pain, while disruption of the phosphorylation of DOR at Thr-161 attenuates morphine tolerance.  相似文献   

9.
Brain-derived neurotrophic factor (BDNF) deficiency has been implicated in pathogenesis of Huntington's disease (HD). 3-Nitropropionic acid (3-NP), an irreversible mitochondrial complex II inhibitor, has been commonly used as a pharmacological model recapitulating HD phenotypes in rodents and nonhuman primates. Herein we test whether BDNF may exert neuroprotective effects against mitochondrial dysfunction caused by 3-NP in primary culture of fetal rat cortical neurons. Preconditioning of neuronal cells with BDNF (100 ng/ml for 8 h) attenuated 3-NP toxicity (2.5 mM for additional 24 h) based on Hoechst and propidium iodide (PI) staining. BDNF effects can be inhibited by the nitric oxide synthase (NOS) inhibitor l-nitroarginine methylester (l-NAME, 100 μM), the cGMP-dependent protein kinase (PKG) inhibitor KT5823 (2 μM), the thioredoxin reductase inhibitor 1-chloro-2,4-dinitrobenzene (DNCB, 5 μM), and a membrane-permeable Bcl-2 inhibitor (12.5 μM). 8-Br-cGMP is a cGMP analogue capable of activating PKG independent of NO. Exogenous application of 8-Br-cGMP (3–30 μM) and purified thioredoxin (3–5 μM) partially mimicked BDNF effects in conferring 3-NP resistance to cortical cells. These results, together with our previous report showing NO donor S-nitrosoglutathione (GSNO)-mediated neuroprotective effects against 3-NP toxicity, suggest that BDNF may protect neurons from mitochondrial dysfunction at least partly via activation of the signaling cascades involving NOS/NO, PKG, thioredoxin and Bcl-2.  相似文献   

10.

Background  

Macrocephaly-cutis marmorata telangiectatica congenita (M-CMTC) is a newly described condition characterized by macrocephaly (megalencephaly), cutis marmorata telangiectatica congenita, macrosomia and/or asymmetric growth, central nervous system abnormalities and neurological manifestations.  相似文献   

11.

Purpose  

To reduce radiation exposure to paediatric neurosurgical patients from computed tomography (CT), a CT scanning protocol — lower radiation dose and selective scan segment (LDSS) protocol was used for CT brain at the authors’ hospital. To evaluate the amount of reduction in radiation exposure by using this LDSS protocol compared to their usual protocol, the authors prospectively documented their findings.  相似文献   

12.

Introduction  

Rotational vertebral artery occlusion (RVAO), sometimes known as “Bow hunter syndrome,” is an important and diagnostically challenging cause of posterior circulation stroke in children. It is caused by impingement of osseous and/or ligamentous structures on the vertebral artery.  相似文献   

13.

Background

In Parkinson's disease (PD), inflammation may lead to the degeneration of dopaminergic (DAergic) neurons. Previous studies showed that inflammatory mediators mainly contributed to this phenomenon. On the other hand, invasive neuromodulation methods such as deep brain stimulation (DBS) have better therapeutic effects for PD. One possibility is that DBS improves PD by influencing inflammation. Therefore, we further explored the mechanisms underlying inflammatory mediators and DBS in the pathogenesis of PD.

Methods

We measured serum levels of two inflammatory markers, namely RANTES (regulated on activation, normal T cell expressed and secreted) and tumor necrosis factor-alpha (TNF-α), using Luminex assays in 109 preoperative DBS PD patients, 49 postoperative DBS PD patients, and 113 age- and sex-matched controls. The plasma protein data of the different groups were then statistically analyzed.

Results

RANTES (p < 0.001) and TNF-α (p = 0.005) levels differed significantly between the three groups. A strong and significant correlation between RANTES levels and Hoehn-Yahr (H-Y) stage was observed in preoperative PD patients (rs = 0.567, p < 0.001). Significant correlations between RANTES levels and Unified Parkinson's Disease Rating Scale III (UPDRS III) score (rs1 = 0.644, p = 0.033 and rs2 = 0.620, p = 0.042) were observed in matched patients. No correlation was observed for TNF-α levels.

Conclusion

The results of this study indicate that PD patients have a persistent inflammatory profile, possibly via recruitment of activated monocytes, macrophages, and T lymphocytes to the central nervous system (CNS). DBS was shown to have a significant therapeutic effect on PD, which may arise by improving the inflammatory environment of the central nervous system.  相似文献   

14.

Background  

This quasi-experimental study was designed to assess two important learning types – procedural and declarative – in children and adolescents affected by posterior fossa tumours (astrocytoma vs. medulloblastoma), given that memory has an important impact on the child's academic achievement and personal development.  相似文献   

15.

Background  

The 17-item Hamilton Depression Rating Scale (HAM-D17) remains the 'gold standard' for measuring treatment outcomes in clinical trials of depressed patients. The Montgomery Ǻsberg Depression Rating Scale (MADRS), Clinical Global Impressions-Severity (CGI-S) and -Improvement (CGI-I) scales are also widely used.  相似文献   

16.
Cold preservation tissue injury remains an unsolved problem during small intestinal transplantation. Pituitary adenylate cyclase-activating polypeptide (PACAP) plays a central role in the intestinal physiology. The aim of our study was to compare the cold ischemic injury in wild-type and PACAP-38 deficient mice after small bowel cold storage. Cold ischemia was produced with small bowel preservation in a University of Wisconsin solution at 4°C in wild-type (n = 35) mice for 1 h (GI), for 3 h (GII), and for 6 h (GIII); and in PACAP-38 deficient (n = 35) mice for 1 h (GIV), for 3 h (GV), and for 6 h (GVI). Small bowel biopsies were collected after laparotomy (Control) and at the end of the ischemia periods. To determine oxidative stress parameters, malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) were measured. Tissue damage was analyzed by qualitative and quantitative methods on hematoxylin/eosin-stained sections. In PACAP-38 deficient animals, tissue lipid peroxidation was elevated. These changes were significant after 6 h (153.04 ± 7.2) compared to sham-operated (110.44 ± 5.5) and compared to wild-type results (120.0 ± 1.1 μmol/g, p < 0.05). Meanwhile, the capacity and activity of the endogenous antioxidant system decreased significantly after 3 and 6 h preservation (GSH: 808.7 ± 5.2; 720.4 ± 8.7 vs. 910.4 ± μmol/g; SOD: 125.1 ± 1.4; 103.3 ± 1.9 vs. 212.11 ± 5.8 IU/g). Qualitative and quantitative histological results showed destruction of the mucous, submucous layers, and crypts in PACAP-38 deficient mice compared to wild-type tissues. These processes depended on the time of the cold preservation periods. Our present study showed that the presence of PACAP-38 in the small bowel tissue has a key role in the protection against intestinal cold preservation injury.  相似文献   

17.

Background  

Cerebrovascular time constant (τ) estimates how fast cerebral blood arrives in cerebral arterial bed after each heart stroke. We investigate the pattern of changes in τ following subarachnoid hemorrhage (SAH), with specific emphasis on the temporal profile of changes in relation to the development of cerebral vasospasm.  相似文献   

18.

Background  

Management of severe traumatic brain injury (TBI) focuses on mitigating secondary insults. There are a number of biomarkers that are thought to play a part in secondary injury following severe TBI. Two of these, S100β and neuron-specific enolase (NSE), have been extensively studied in the setting of neurological injury. This pilot study was undertaken to investigate the relationship of S100β and NSE to clinical markers of severity and poor outcome: intracranial hypertension (ICH), and cerebral hypoperfusion (CH).  相似文献   

19.

Background  

The purpose of this study is to determine whether intraventricular hemorrhage (IVH) exerts a “decompressive” effect that limits intracerebral hemorrhage (ICH) enlargement.  相似文献   

20.

Background  

The literature on the dynamics between community- and hospital services concerning utilization of psychiatric beds is inconclusive. The Norwegian VELO-project provides an opportunity to study this in a natural experiment. Two service-systems are compared. The “central-bed system” have mainly outpatient- and day-hospital services locally, with psychiatric beds at a central mental hospital. The “local-bed system” have only one outpatient clinic, with beds at three local inpatient units. Also utilization of sheltered homes was studied. Hypotheses were predicted from Goldberg and Huxley’s’ stage theory and the Thornicroft and Tansella’s’ hydraulic model.  相似文献   

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