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      Dynamic changes of α-melanocyte-stimulating hormone levels in the serum of patients with craniocerebral trauma

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          Abstract

          The aim of the study was to investigate dynamic changes in α-melanocyte-stimulating hormone (α-MSH) levels in the serum of patients with craniocerebral trauma. Forty-eight patients with acute craniocerebral injury were selected between January 2015 and October 2016. The patients were divided into three groups: severe (18 cases), moderate (16 cases) and mild (14 cases), according to the Glasgow Coma Scale (GCS) score at the time of admission. At the same time, 10 adults with a similar age distribution to the patients were also selected as a control group. Venous blood was extracted from patients at 1, 3, 5 and 7 days after injury. Serum α-MSH and tumor necrosis factor (TNF)-α levels were measured using an enzyme-linked immunosorbent assay (ELISA). The correlation between α-MSH and TNF-α was analyzed using Pearson's correlation analysis. Serum α-MSH levels in patients with craniocerebral injury were lower than those in the healthy control group (P<0.05). Decreased serum α-MSH levels were usually accompanied with higher degrees of craniocerebral injury. Serum α-MSH levels initially decreased and then later increased, with the lowest α-MSH levels in the mild at 5 days, moderate at 5 days, and severe groups at 3 days after injury (P<0.05). Serum TNF-α levels in all the patient groups were higher than those in the control group at different time points after injury, with higher TNF-α serum levels accompanying higher degrees of brain injury. In all three groups, serum TNF-α levels initially increased and then decreased post-injury, with peak serum TNF-α levels found at 3-day post-injury in all the patient groups (P<0.05). A negative correlation between serum α-MSH content and serum TNF-α levels in patients with craniocerebral trauma at different time points, was noted (P<0.05). Serum α-MSH content in the survival group was higher than that in the death group (P<0.05). Serum α-MSH levels in patients with non-systemic inflammatory response syndrome (SIRS) were higher than in patients with SIRS (P<0.05). Serum α-MSH levels during the early stages after craniocerebral trauma can be used as a factor for the prediction of secondary SIRS, with constant low levels of serum α-MSH suggest poor prognosis.

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          The epidemiology and impact of traumatic brain injury: a brief overview.

          Traumatic brain injury (TBI) is an important public health problem in the United States and worldwide. The estimated 5.3 million Americans living with TBI-related disability face numerous challenges in their efforts to return to a full and productive life. This article presents an overview of the epidemiology and impact of TBI.
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            Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial.

            Corticosteroids have been used to treat head injuries for more than 30 years. In 1997, findings of a systematic review suggested that these drugs reduce risk of death by 1-2%. The CRASH trial--a multicentre international collaboration--aimed to confirm or refute such an effect by recruiting 20000 patients. In May, 2004, the data monitoring committee disclosed the unmasked results to the steering committee, which stopped recruitment. 10008 adults with head injury and a Glasgow coma score (GCS) of 14 or less within 8 h of injury were randomly allocated 48 h infusion of corticosteroids (methylprednisolone) or placebo. Primary outcomes were death within 2 weeks of injury and death or disability at 6 months. Prespecified subgroup analyses were based on injury severity (GCS) at randomisation and on time from injury to randomisation. Analysis was by intention to treat. Effects on outcomes within 2 weeks of randomisation are presented in this report. This study is registered as an International Standard Randomised Controlled Trial, number ISRCTN74459797. Compared with placebo, the risk of death from all causes within 2 weeks was higher in the group allocated corticosteroids (1052 [21.1%] vs 893 [17.9%] deaths; relative risk 1.18 [95% CI 1.09-1.27]; p=0.0001). The relative increase in deaths due to corticosteroids did not differ by injury severity (p=0.22) or time since injury (p=0.05). Our results show there is no reduction in mortality with methylprednisolone in the 2 weeks after head injury. The cause of the rise in risk of death within 2 weeks is unclear.
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              Inflammatory reaction after traumatic brain injury: therapeutic potential of targeting cell-cell communication by chemokines.

              Traumatic brain injury (TBI) affects millions of people worldwide every year. The primary impact initiates the secretion of pro- and anti-inflammatory factors, subsequent recruitment of peripheral immune cells, and activation of brain-resident microglia and astrocytes. Chemokines are major mediators of peripheral blood cell recruitment to damaged tissue, including the TBI brain. Here we review the involvement of specific chemokine pathways in TBI pathology and attempts to modulate these pathways for therapeutic purposes. We focus on chemokine (C-C motif) ligand 2/chemokine (C-C motif) receptor 2 (CCL2/CCR2) and chemokine (C-X-C motif) ligand 12/chemokine (C-X-C motif) receptor 4 (CXCL12/CXCR4). Recent microarray and multiplex expression profiling have also implicated CXCL10 and CCL5 in TBI pathology. Chemokine (C-X3-C motif) ligand 1/chemokine (C-X3-C motif) receptor 1 (CX3CL1/CX3CR1) signaling in the context of TBI is also discussed. Current literature suggests that modulating chemokine signaling, especially CCL2/CCR2, may be beneficial in TBI treatment.
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                Author and article information

                Journal
                Exp Ther Med
                Exp Ther Med
                ETM
                Experimental and Therapeutic Medicine
                D.A. Spandidos
                1792-0981
                1792-1015
                September 2017
                12 July 2017
                12 July 2017
                : 14
                : 3
                : 2511-2516
                Affiliations
                Department of Neurosurgery, Shandong Jiaotong Hospital, Jinan, Shandong 250031, P.R. China
                Author notes
                Correspondence to: Dr Baozhong Dong, Department of Neurosurgery, Shandong Jiaotong Hospital, 12 Wuyingshan Middle Road, Jinan, Shandong 250031, P.R. China, E-mail: dxg05n@ 123456163.com
                Article
                ETM-0-0-4793
                10.3892/etm.2017.4793
                5609151
                28962188
                7e868513-7db5-4636-a87f-42106771e48d
                Copyright: © Du et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 17 March 2017
                : 04 July 2017
                Categories
                Articles

                Medicine
                α-melanocyte-stimulating hormone craniocerebral trauma,inflammatory factors,systemic inflammatory response syndrome,tumor necrosis factor-α

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