Clinical application of Chinese Nanjing persistent vegetative state scale / 中华医学杂志(英文版)

BACKGROUND@#It is a challenge to characterize the consciousness level of patients with severe disturbance of consciousness and predict their prognosis effectively for Chinese doctors. We aimed to investigate the psychometric property and the diagnostic practicality of severe disturbance of consciousness by Chinese Nanjing persistent vegetative state scale (CNPVSS) which was first set up in 1996 and modified in 2001 and 2011.@*METHODS@#The concurrent validity, inter-rater consistency and diagnostic accuracy of CNPVSS and Chinese version of coma recovery scale-revised (CRS-R) were investigated by assessment of 380 patients with severe disorders of consciousness.@*RESULTS@#Total scores of the CNPVSS were correlated significantly with that of the CRS-R, indicating acceptable concurrent validity. Sub-scale analysis showed moderate to high inter-rater reliability and test-retest reliability. CNPVSS was superior to CRS-R on the diagnosis sensitivity. The CNPVSS was able to distinguish 65 patients in emergence from minimal consciousness state who were misclassified as in minimal consciousness state (MCS) by the CRS-R, and it could also distinguish two patients in MCS who were misclassified as in vegetative state by the CRS-R.@*CONCLUSION@#The CNPVSS is an appropriate measurement and is sensitive to distinguish the MCS patients from the VS patients.

Clinical analysis of the polymorphism of clopidogrel and aspirin-related genes / 临床神经病学杂志

Objective To analyse the polymorphisms of CYP2C19,GPⅢa,PTGS1,GP1BA genes.Methods The basic information of 159 patients in the department of neurology of our hospital during January 2017 to November 2017 was collected. CYP2C19、GPⅢa、PTGS1、GP1BA genes were detected. Results The average age of the patients was (65.32 +12.71)years old,including 112 men (70.4%)and 47 female (29.6%). As for the CYP2C19*2G681Apolymorphism,there were 58 GG-genotype carriers,82 GA-genotype carriers and 19 AC-genotype carriers. For the CYP2C19*3G636Apolymorphism,there were 141 GG-genotype carriers and 18 GA-genotype carriers,for the CYP2C19*17C806Tpolymorphism,there were 155 CC-genotype carriers and 4 CT-genotype carriers. For the GPⅢa polymorphism,the TT genotype had 157 carriers,and the TC genotype had two carriers. For the PTGS1 polymorphism,there were 159 AA-genotype carriers.For the GP1BA polymorphism,the CC genotype had 136 carriers and the CT genotype had 23 carriers. The distribution of genotypes fitted the Hardy-Weinberg equilibrium for all the polymorphisms,except those of PTGS1.Phenotypes:there were 2 clopidogrel ultra metabolizer (1.3%),47 extensive metabolizer (29.6%),82 intermediate metabolizer (51.6%),and 28 poormetabolizer (17.6%). For aspirin,2 resistance (1.3%)and 157 sensitive (98.7%).Conclusion Clopidogrel poor metabolizer is significantly higher than aspirin resistance.

Possible Mechanism of Therapeutic Effect of 3-Methyl-1-phenyl-2-pyrazolin-5-one and Bone Marrow Stromal Cells Combination Treatment in Rat Ischemic Stroke Model / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The functional improvement following bone marrow stromal cells (BMSCs) transplantation after stroke is directly related to the number of engrafted cells and neurogenesis in the injured brain. Here, we tried to evaluate whether 3-methyl-1-phenyl-2-pyrazolin-5-one (MCI-186), a free radical scavenger, might influence BMSCs migration to ischemic brain, which could promote neurogenesis and thereby enhance treatment effects after stroke.</p><p><b>METHODS</b>Rat transient middle cerebral artery occlusion (MCAO) model was established. Two separate MCAO groups were administered with either MCI-186 or phosphate-buffered saline (PBS) solution to evaluate the expression of stromal cell-derived factor-1 (SDF-1) in ischemic brain, and compared to that in sham group (n = 5/ group/time point[at 1, 3, and 7 days after operation]). The content of chemokine receptor-4 (CXCR4, a main receptor of SDF-1) at 7 days after operation was also observed on cultured BMSCs. Another four MCAO groups were intravenously administered with either PBS, MCI-186, BMSCs (2 × 106), or a combination of MCI-186 and BMSCs (n = 10/group). 5-bromo-2-deoxyuridine (BrdU) and Nestin double-immunofluorescence staining was performed to identify the engrafted BMSCs and neuronal differentiation. Adhesive-removal test and foot-fault evaluation were used to test the neurological outcome.</p><p><b>RESULTS</b>MCI-186 upregulated the expression of SDF-1 in ischemic brain and CXCR4 content in BMSCs was enhanced after hypoxic stimulation. When MCAO rats were treated with either MCI-186, BMSCs, or a combination of MCI-186 and BMSCs, the neurologic function was obviously recovered as compared to PBS control group (P < 0.01 or 0.05, respectively). Combination therapy represented a further restoration, increased the number of BMSCs and Nestin+ cells in ischemic brain as compared with BMSCs monotherapy (P < 0.01). The number of engrafted-BMSCs was correlated with the density of neuronal cells in ischemic brain (r = 0.72 , P < 0.01) and the improvement of foot-fault (r = 0.70, P < 0.01).</p><p><b>CONCLUSION</b>MCI-186 might promote BMSCs migration to the ischemic brain, amplify the neurogenesis, and improve the effects of cell therapy.</p>

Neuroprotective effects of edaravone on early brain injury in rats after subarachnoid hemorrhage / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The underlying mechanism of early neurobiological impairment after subarachnoid hemorrhage (SAH) is not well understood, but the system of reactive oxygen superoxide (ROS) might be involved. Edaravone (MCI-186), a potent free radical scavenger that prevents apoptosis of neurons, was thus used in this study to see its possible therapeutic effect in early brain injury due to SAH in a rat model.</p><p><b>METHODS</b>One hundred and twenty male Sprague-Dawley rats were randomly assigned to four groups: group 1, control rats receiving sham operation only; group 2, rats with SAH treated by saline; group 3, rats with SAH treated with 1 mg/kg MCI-186 injected intraperitoneally; and group 4, rats with SAH treated with 3 mg/kg MCI-186. Treated with either saline or MCI-186 twice daily for two consecutive days after SAH, the rats were sacrificed for measurements of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) and histological analysis of caspase-3 protein by Western blotting and immunohistochemical staining. In addition, mortality and neurological scores were statistically analyzed by the chi-square test and Dunn's procedure respectively for each group. One-way analysis of variance followed by the Tukey's procedure was also used in data analysis.</p><p><b>RESULTS</b>The rats in group 2 that received saline only showed neurological impairment as well as elevated mortality, and were found to have significantly increased levels of MDA and caspase-3, but reduced SOD activities in brain tissues (P < 0.05). When treated with MCI-186 at two different dosages, the rats in groups 3 and 4 had markedly decreased levels of MDA and caspase-3 but increased SOD activities in the brain tissue (P < 0.05), along with improved scores of neurological evaluation (P < 0.05).</p><p><b>CONCLUSIONS</b>This study sheds some lights on the therapy of SAH-induced early brain injury by providing the promising data indicating that MCI-186, a radical scavenger, can efficiently diminish apoptosis of neurons and thus prevent the function loss of the brain in rats with SAH.</p>

Prenatal diagnosis of spinal muscular atrophy in Chinese by genetic analysis of fetal cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Spinal muscular atrophy (SMA) is an autosomal recessive disease characterized by degeneration of anterior horn cells of the spinal cord. The survival motor neuron gene is SMA-determining gene deleted in approximately 95% of SMA patients. This study was undertaken to predict prenatal SMA efficiently and rapidly in families with previously affected child.</p><p><b>METHODS</b>Prenatal diagnosis was made in 8 fetuses with a family history of SMA. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were used for the detection of the survival motor neuron gene.</p><p><b>RESULTS</b>The survival motor neuron gene was not found in 6 fetuses, ruling out the diagnosis of SMA. Two fetuses were detected positive and the pregnancies were terminated.</p><p><b>CONCLUSION</b>Our method is effective and convenient in prenatal diagnosis of SMA.</p>