[Objective] To study the protective effect of Xing Nao Jing (XNJ) on cultured cortical neurons in rats. [Methods] Primary cultured cortical neurons were applied to observe the effect of XNJ in counteracting the excitotoxicity ofglutamic acid. [Results] XNJ decreased the release of intracellular lactic dehydrogenase induced by glutamic acid and reduced the histological changes of cultured cortical neurons. [Conclusion] XNJ can counteract the excitotoxicity of glutamic acid and protect cultured cortical neurons in rats.

OBJECTIVE:To study the protective effects of Xingnaojing(XNJ)and Ligustrazine(Lig)on rat's cortical neu_ rons of primary culture.METHODS:The effects of XNJ and Lig in counteracting the excitotoxicity of glutamic acid(10?l/L,3h)in rat's cortical neurons of primary culture were observed.RESULTS:Both XNJ and Lig could decrease the release of LDH from cells into culture medium and reduce the changes in cell morphology.CONCLUSION:XNJ or Lig can protect cultured cortical neurons from excitotoxicity of glutamic acid and more obvious effect can be initiated through combined use of them.

Objective To investigate the clinical features of and GJB2 gene mutations in a Chinese Han patient with keratitis-ichthyosis-deafness syndrome (KID syndrome),in hope to offer evidence for the clinical and genetic diagnosis of KID syndrome.Methods Clinical data were collected from a patient with KID syndrome.DNA was extracted from peripheral blood of the patient and his two family members (mother and brother).PCR was performed to amplify the exon 2 and its flanking splicing sites of GJB2 gene followed by bidirectional direct DNA sequencing. Results The patient presented with the typical triad of vascularizing keratitis,ichthyosis and congenital deafness.A G148A mutation in the exon 2 of GJB2 gene,resulting in the substitution of aspartic acid by asparagine at position 50 of the junction protein connexin 26 (Cx26),was identified in the patient,but not in either of his family members.Conclusion The G148A mutation in GJB2 gene may be responsible for the clinical phenotype of KID syndrome in this Chinese patient.

Objective To establish a mouse model of prostate cancer expressing human PSCA for the development of new anti-tumor drugs or vaccines. Methods The total RNA of DU145 cells,a human prostate cancer cell line,was isolated by using TRIzol reagent according to the (RT-PCR),the first-strand cDNA was synthesized using the SuperScript First-Strand synthesis system. The human PSCA gene was amplified with the primers and cloned into the plasmid pcDNA3.1 to generate pcDNA-PSCA. DNA sequencing was used to confirm the constructs. The mouse prostate tumor cell line RM-1 cells,syngeneic to C57BL/6,were transfected with pcDNA-PSCA plasmids followed by selection using G418. RT-PCR analysis was performed to examine the validity of the constructs. Expression of PSCA on the cell surface was determined by staining with anti-PSCA antibody,and the anti-PSCA antibody was detected using an FITC-conjugated goat anti-rabbit IgG antibody,and analyzed by flow cytometry. 4-6-week-old male C57BL/6 mice purchased from the Laboratory Animals Center were inoculated with different amounts of RM-PSCA cells to search for suitable cell population which can form tumor in mouse,and the mice were monitored twice a week. The growth and the survival time of mice were measured,respectively. The tumor volume was measured by vernier caliper according to the formula:V=0.5a×b~2,where a and b are the long and short diameters of the tumor,respectively. Results The plasmid pcDNA-PSCA was successfully constructed and the PSCA was successfully expressed in RM-PSCA 7~# and RM-PSCA 28~# cells by RT-PCR and confirmed by flow cytometry. 1×10~5 RM-PSCA cells were sufficient to get tumor growth in 100% of inoculated mice. The tumor grew quickly and the volume of the tumor reached 12000 mm~3 within 34 days. All the mice died within 40 days and their mean survival time was 37 days. Conclusion A PSCA-expressing tumor model in mice has been successfully established. It can be used to evaluate the activities of drugs or vaccines.

Objective To use warm needling moxibustion plus Julisanjie Bolus for the treatment of hysteromyoma and explore a new way to treat hysteromyoma. Method A treatment group of 40 hysteromyoma patients received warm needling moxibustion plus Julisanjie Bolus; a conventional treatment group of 40 hysteromyoma patients, Julisanjie Bolus; a control group of 40 hysteromyoma patients, mifepristone. The therapeutic effects were compared between the treatment group and the conventional treatment or control group. Result The cure rate and the total efficacy rate were 12.5% and 97.5%, respectively, in the treatment group, 5.0% and 75.0%, respectively, in the conventional treatment group and 5.0% and 72.5%, respectively, in the control group. Conclusion The therapeutic effect was significantly better in the treatment group than in the conventional treatment and control groups (P<0.05). There were no obvious adverse reactions during the clinical trial of warm needling moxibustion plus Julisanjie Bolus for the treatment of hysteromyoma.

Objective To evaluate the application of multi-parameter three-dimension arterial spin labeling (3D-ASL) in observing the brain perfusion of patients with transient ischemic attack (TIA). Methods A total of 42 TIA patients, admitted to our hospital from July 2014 to March 2017, were included in this study. All subjects underwent conventional MRI, diffusion-weighted imaging (DWI), magnetic resonance angiography (MRA) and 3D-ASL scanning. Abnormal signals, and cerebral arterial stenosis or occlusion were observed under MRI, DWI and MRA; cerebral blood flow (CBF) map was drew after analyzing the 3D-ASL imaging, and abnormal reperfusion of ASL-CBF was qualitatively and quantitatively analyzed. The detection rate of abnormal reperfusion in TIA patients by 3D-ASL (PLD=1.5 s, PLD=2.5 s) and MRA were compared. Results Forty-two TIA patients showed no positive findings on conventional MRI and DWI maps, of which 18 patients showed different degrees of cerebral artery stenosis on MRA maps. Twenty-seven patients (PLD=1.5 s, 64.29％) and 21 (PLD=2.5 s, 50％) on ASL-CBF maps showed different sizes and degrees of abnormal hypoperfusion, and significant difference was found in detection rate of hypoperfusion by 3D-ASL (PLD=1.5 s and PLD=2.5 s, χ2=23.333, P=0.000). The detection rates of hypoperfusion by 3D-ASL (PLD=1.5 s and PLD=2.5 s) were 中华神经医学杂志2017年12月第16卷 第12期 Chin J Neuromed, December 2017, Vol.16, No.12 significantly higher than that by MRA (χ2=17.500, P=0.000; χ2=31.500, P=0.000). Conclusions The 3D-ASL can quantitatively analyze the degrees of perfusion of patients with TIA. 3D-ASL can comprehensively reflect the perfusion status in patients with TIA, and short PLD 3D-ASL is more sensitive than long PLD ASL in finding TIA, while long PLD 3D-ASL can reflect the perfusion status more truly.

Objective To investigate the mechanism that receptor activator of NF-κB ligand (RANKL) promotes arterial calcification.Methods Firstly,RANKL was added into the culture media,in which the monocyte precursor cells alone were cultured.Morphological observation and tartrate resistant acid phosphatase(TRAP)stain were used to assess whether RANKL could induce the monocyte precursor cells to differentiate into osteoclast-like cells.During arterial calcification,both in vivo and in vitro expressions of RANKL and osteoprotegerin (OPG,as RANKL inhibitor)were measured via real-time PCR.The extent of osteoclast-like cell differentiation was also assessed.Results It was found that RANKL could induce osteoclast-like cell differentiation.There were no both in vivo and in vitro expressions of osteoclast-like cells in the early stage of calcification.At that time,the ratio of RANKL to OPG was very low.In the late stage of calcification,a small amount of osteoclast-like cell expression coincided with a relatively high ratio of RANKL to OPG.According to the results,the ratio of RANKL to OPG was very low during most of the arterial calcification period.This made it possible for OPG to completely inhibit RANKL-induced osteoclast-like cell differentiation.The ratio of RANKL to OPG was (0.36 ± 0.08) (F =36) and (1.68 ± 0.08) (F =36) respectively in the early and late subgroup of calcification group in the animal model,but was zero in the control group(both P＜0.05).The ratio of RANKL to OPG was(0.42±0.09) (F=16)and(1.50 ± 0.10)(F=16)respectively in the early and late subgroup of calcification group in the cell model,but was zero in the control group(both P＜0.05).Conclusions Our result likely explains why RANKL has the ability to induce osteoclast-like cell differentiation,but acts as a promoter of calcification.