In recent decades, with the development of electrophysiological and neuroimaging techniques, the researchers found that spinal cord injury (SCI) not only caused pathological changes in the spinal cord, but also in the brain. This paper reviewed the influence of SCI on the structure and function of the brain in terms of brain neuron degeneration caused by SCI, the changes of neurotrophic factor in brain, and the side-effects of medicine.

Objective To study the risk factors of aortic arch calcification (AoAC) in maintenance hemodialysis (MHD) patients.Methods Retrospective analysis was performed in patients who accepted MHD ≥ 5 years.The clinical data were collected.The images of plan chest radiograph detected during followup period were reviewed by certain imaging physicians,and the AoAC score was calculated.Logistic regression model analysis was proceeded to study the risk factors of AoAC.The patients were divided into AoAC positive group (29 cases) and AoAC negative group (37 cases) respectively.The clinical parameters were compared between the 2 groups.Results Sixty-six patients (21 male,45 female) were selected.The year AoAC scores from the zeroth to fifth year were (0.013 40 ± 0.074 96),(0.018 90 ± 0.078 55),(0.118 50 ± 0.170 06),(0.157 00 ± 0.207 55),(0.166 00 ± 0.205 37),(0.175 50 ± 0.222 29) scores,progressively.There were significant differences in AoAC score from the third year compared with that of the zeroth year (Z =-3.984,-4.021,-4.017;P ＜ 0.01).Logistic regression model analysis result showed that only the age of dialysis beginning was the risk factor for AoAC (relative risk 1.177,regression coefficient 0.163,P =0.002).The age of dialysis beginning,rate of diabetic nephropathy,serum calcium-phosphate product were significantly higher in AoAC positive group than that in AoAC negative group [(59.5 ± 12.6) years vs.(52.9 ± 13.2) years,27.6％(8/29) vs.2.7％(1/37),(5.81 ± 1.63) mmol2/L2 vs.(4.13 ± 0.86) mmol2/L2].Conclusions The AoAC will aggravate with the increased duration of dialysis in MHD patients.The age of dialysis beginning is the risk factor of AoAC.

Objective To study the protective effect of sodium ferulate (SF) on CPB-induced lung ischemia reperfusion injury (IRI) and discuss its possible mechanism. Methods 40 patients undergoing CPB were randomly divided into contral group(CCG, n=20 ) and SF group(SFG, n=20). In SFG, SF was injected (0.2 g in NS 150 ml) intravenously Bid for one week preoperatively. In CCG, SF was replaced by same volume of NS. The changes of TNF-?、IL-6、IL-8、SOD level in the CCG and SFG would be examined before operation, at 15min、30 min after aortic cross clamp(ACC) and 1 hour after operation. By the time of before ACC、15 min and 30 min after ACC was opened, blood samples were taken from the right and left atrium to examine the amount of neutrophils. Lung tissues were cut for pathological studies in 5 patients in each group randomly. Results At 15 min、30 min after ACC and 1h after operation TNF-?、IL-6、IL-8、SOD levels of 2 groups were significantly higher than that before the operation (P

The human brain-derived neurotrophic factor (hBDNF) gene was cloned by polymerase chain reaction and the recombinant adeno-associated viral vector inserted with hBDNF gene (AAV-hBDNF) was constructed. Cultured rat hippocampal neurons were treated with Abeta(25-35) and serued as the experimental Abeta-induced neuronal damage model (AD model), and the AD model was infected with AAV-hBDNF to explore neuroprotective effects of expression of BDNF. Cell viability was assayed by MTT. The expression of bcl-2 anti-apoptosis protein was detected by immunocytochemical staining. The change of intracellular free Ca ion ([Ca2+]i) was measured by laser scanning confocal microscopy. The results showed that BDNF had protective effects against A-induced neuronal damage. The expression of the bcl-2 anti-apoptosis protein was raised significantly and the balance of [Ca2+]i was maintained in the AAv-hBDNF treatment group as compared with AD model group. These data suggested that recombinant AAV mediated a stable expression of hBDNF in cultured hippocampal neurons and resulted in significant neuron protective effects in AD model. The BDNF may reduce neuron apoptosis through increasing the expression of the bcl-2 anti-apoptosis protein and inhibiting intracellular calcium overload. The viral vector-mediated gene expression of BDNF may pave the way of a novel therapeutic strategy for the treatment of neurodegenerative diseases such as Alzheimer's disease.

Objective To investigate the effect of spinal cord ischemia/reperfusion injury on hindlimb dysfunction in rabbits.Methods Twenty-eight health adult rabbits were distributed into normal control group (n =4) and model group (n =24) according to the random number table.The modelof spinal cord ischemia/reperfusion injury was established by selective occlusion of lumbar arteries.The model group were submitted to ischemia for 30 min (Group Ⅰ),60 min (Group Ⅱ) and 90 min (Group Ⅲ) before the reperfusion with 8 rabbits each.Jacobs score,Reuters score and Rivlin inclined plane test were used to evaluate the hindlimb function in each Group at days 1,3 and 7 after reperfusion.Changes in nerve conduction function in each group were observed using the cortical somatosensory evoked potential (CSEP).Results At days 1,3 and 7,the paraplegia rates in group Ⅰ were 50％,38％ and 38％ respectively,in Group Ⅱ were 75％,88％ and 100％,and in Group Ⅲ were all 100％.Paraplegia rate differed significantly among the three groups at 1 d and 3 d (P ＜ 0.01).Paraplegia rate differed significantly in Groups Ⅱ and Ⅲ when compared to that in Group Ⅰ at 7 d (P ＜ 0.01),but there was no significant difference between Groups Ⅱ and Ⅲ (P ＞ 0.05).With the prolongation of reperfusion,the Reuters score in Group Ⅰ dropped but not differed from that in control group (P ＞ 0.05);the Reuters score in Groups Ⅱ and Ⅲ increased and differed from that the control group (P ＜0.01),but the difference between Groups Ⅱ and Ⅲ was insignificant (P ＞ 0.05).Critical angle and obstacle rate of the inclined plane in control group were (68.4 ± 3.0)° and 0％.One day after reperfusion,critical angles of the inclined plane in Groups Ⅰ,Ⅱ and Ⅲ were (58.8 ± 4.1) °,(38.5 ± 2.8) ° and (29.8 ± 1.8) °,and the obstacle rates were (14.5 ± 0.9) ％,(43.6 ± 2.4) ％ and (56.0 ± 2.9) ％.There were significant differences compared to control group (P ＜ 0.01).Slight decrease in critical angle of the inclined plane but a minor increase in the obstacle rate was detected in Groups Ⅱ and Ⅲ at 3 d and 7 d after reperfusion,and the differences were significant compared to control group (P ＜ 0.01).Three days after reperfusion,critical angle of the inclined plane raised and obstacle rate of the inclined plate fell in group Ⅰ,not significantly different from these in control group (P ＞ 0.05).Latencies of CSEP N1 and P1 waves in Group Ⅱ [(33.1 ± 1.8) ms and (58.6 ± 4.0) ms] were longer than these in control group [(23.7±0.5)msand (48.1±4.1)ms]andgroup Ⅰ [(26.2±0.7)ms and (50.2±4.2)ms] (P＜ 0.01) 7 days after reperfusion,but the differences between control group and Group Ⅰ were insignificant (P ＞ 0.05).While the CSEP wave disappeared in Group Ⅲ.Conclusions Severity of spinal cord inschemia/reperfusion injury is related to the duration of ischemia.Hindlimb dysfunction caused by ischemia/reperfusion injury is characterized mainly by spastic paraplegia.

Objective To investigate the clinical features of complex posterior communicating artery aneurysms and the outcome of microsurgical clipping.Methods The clinical and imaging data of the patients with posterior communicating artery aneurysm treated by craniotomy microsurgical clipping were analyzed retrospectively.The patients were divided into either a complex type group or a simple type group according to whether they had complex factors of surgical clipping or not.They were divided into a good outcome group and a poor outcome group according to their Glasgow Outcome Scale scores.Results A total of 55 patients with posterior communicating artery aneurysm were enrolled,and 17 (30.9％) of them were in the simple type group and 38 (69.1％) were in the complex type group.The proportion of higher Fisher grade in the patients of the simple type group was significantly lower than that of the complex type group (Z =-2.068,P=0.019).However,there were no significant differences in the proportions of age,sex,preoperative rupture,and Hunt-Hess grade between the two groups (all P ＞ 0.05).In the complex type group,the complex clipping (73.68％) and anterior clinoidectomy (42.11％) were the most common complex factors.Twenty-four patients (63.16％) had a number of complex factors.In the complex type cases,32 had good outcome,6 had poor outcome (3 of them died); in the simple type cases,15 had good outcome,2 had poor outcome (1 of them died).There was no significant difference in the good outcome rate between the complex type group and the simple type group (84.21％ vs.88.24％;x2 =0.153,P=0.696).In 55 patients with posterior communicating artery aneurysm,the age of the good outcome group was significantly lower than that of the poor outcome group (58.23 ± 12.41 years vs.68.38 ± 8.68 years,t =-2.212; P =0.031),and there were no significant differences in sex,Fisher grade,Hunt-Hess grade,factors of surgical complexity,and surgical clipping level (all P ＞ 0.05).Multivariate logistic regression analysis showed that only age was the independent risk factor for poor outcome of the complex posterior communicating artery aneurysm (odds ratio 1.142,95％ confidence interval 1.029-1.266; P =0.012).Conclusions Using the advanced microsurgical techniques,such as anterior clinoidectomy,anterior choroidal artery microdissection,and complex clipping for the treatment of complex posterior communicating artery aneurysm are no less favorable than the simple type,and age is an independent risk factor for the poor outcome of posterior communicating artery aneurysm.

Objective To elucidate the biocompatibility differences of 4 dialyzers with different membranes in maintenance hemodialysis (MHD)patients. Methods A total of 60 MHD patients were enrolled in the prospective,randomized,control,cohort study.In baseline,synthetic polysulfone(PS)membrane dialyzer was used in all the patients for at least 3 months.Then the patients were randomly divided into three groups:ployethersulfone(PES)membrane group,cellulose triacetate (CTA)membrane group,and synthetic polymethylmethacrylate(PMMA)membrane group.Study duration was 6 months.No dialyzer was reused.The biocompatibility markers were detected repeatedly at different time points and compared with each other in different dialyzer groups. Results The blood levels of high sensitive C reactive protein,interleukin-1β and interleukin-13 were not significantly different among different groups on every time point.However,the blood complements levels and WBC count were significantly different among four kinds of dialyzer.When the dialyzers changed from PS to PMMA membrane,C3a levels and WBC count changed significantly(P＜0.05).Moreover,the change of C5a level was significantly different between PES group and PMMA group on month 3(P＜0.05). Conclusion There are some differences of biocompatibiliy among different dialyzer membranes.

Objective:To detect the value of utilizing bpMRI in prostate biopsy in the detection of prostate cancer with PSA≤20ng/ml.Methods:The clinical data of 394 patients who underwent prostate biopsy in the First Affiliated Hospital of Nanjing Medical University from November 2017 to October 2019 were retrospectively analyzed. Of all the patients, 177 underwent modified systematic biopsy, named TRUS group, 217 patients accepted pre-biopsy bpMRI examination, undergoing modified systematic biopsy if Prostate Imaging Reporting and Data System (PI-RADS) score < 3 or MRI-TRUS cognitive fusion targeted prostate + systematic biopsy if PI-RADS score ≥ 3, named MRI group. The median age of TRUS group was 66 (61, 74) years old, prostate specific antigen (PSA) was 9.52 (7.26, 12.30) ng / ml, and prostate volume (PV) was 36.84 (28.95, 57.72)ml. The median age of MRI group was 66 (59, 72) years old, PSA was 8.84 (6.65, 12.16) ng/ml, and PV was 39.45 (29.25, 58.69)ml. There was no difference in above parameters between the two groups. The χ 2 test was used to compare the detection rate of prostate cancer and clinically significant prostate cancer (CsPCa) between the two groups. Results:There was no significant difference in the detection rates of prostate cancer between TRUS group and MRI group [51.41% (91/177) vs. 48.39% (105/ 217), P = 0.550], but the detection rates of CsPCa were significantly different [26.55% (47/177) vs. 36.41% (79/217), P = 0.037]. In patients with PSA ≤ 10 ng / ml, there was no significant difference in the detection rates of prostate cancer between the two groups [43.62% (41/94) vs. 43.08% (56/130), P = 0.936], but there was a significant difference in the detection rates of CsPCa [17.02% (16/94) vs. 28.46% (37/130), P = 0.047]. There was no significant difference in the detection rates of prostate cancer [60.24% (50/83) and 56.17% (48/87), P= 0.504] and the detection rates of CsPCa [37.35% (31/83) vs. 48.28% (42/87), P = 0.150] between the two groups. The total detection rates of the last two needles in TRUS group and MRI group were 23.16% (41/177) and 36.63% (86/217), respectively, with significant difference ( P=0.001); the detection rates of CsPCa in the last two needles were 11.86% (26/177) and 29.03% (63/ 217), respectively, with significant difference ( P < 0.001). In MRI group, the detection rates of prostate cancer in patients with PI-RADS score <3, 3, 4, 5 were 21.21% (7/33), 25.84% (23/89), 73.24% (52/71), 95.83% (23/24), respectively; the detection rates of CsPCa were 12.12% (4/33), 17.98% (16/89), 54.93% (39/71), 83.33% (23/24), respectively. Conclusions:In patients with PSA ≤ 20 ng / ml, prostate biopsy based on bpMRI may improve the detection of CsPCa, especially in patients with PSA ≤ 10 ng/ml.

Objective To construct MIA3 psicheck2 wild-type and mutant vectors targeting miR-374b,and provide the previous guarantee for the dual luciferase reporter assay.Methods The amplification primer was firstly designed according to mice MIA3-3'UTR sequence information,mice whole blood genomic DNA was taken as the template for PCR amplification of MIA3-3'UTR sequence,and the PCR product was cloned into psicheck2 dual luciferase reporter vector.Then,mutant primer was designed to mutate the MiR-374b seed sequence target TATTATA into AAATTAT so as to construct mutant vector.At last,the vector enzyme digestion evaluation and sequencing method was used to evaluate the constructed vectors.Results It could be seen from the analysis of agarose electrophoresis that the PCR amplification size of vector was consistent with the theoretical size.DNA sequencing evaluation showed that the MIA3-3'UTR-WT vector had been constructed successfully.The construction of mutant vector has successfully mutated the MiR-374b seed sequence target TATTATA into AAATTAT.Conclusion The successful construction of the vector will lay a foundation for the further evaluation on whether there is an actual binding site between the miR-374b and the chondrogenic differentiation-related target gene MIA3.

The human brain-derived neurotrophic factor (hBDNF) gene was cloned by polymerase chain reaction and the recombinant adeno-associated viral vector inserted with hBDNF gene (AAV-hBDNF) was constructed. Cultured rat hippocampal neurons were treated with Aβ25-35 and serued as the experimental Aβ-induced neuronal damage model (AD model), and the AD model was infected with AAV-hBDNF to explore neuroprotective effects of expression of BDNF. Cell viability was assayed by MTT. The expression of bcl-2 anti-apoptosis protein was detected by immunocytochemical staining. The change of intracellular free Ca ion ([Ca2+]i) was measured by laser scanning confocal microscopy. The results showed that BDNF had protective effects against Aβ-induced neuronal damage. The expression of the bcl-2 anti-apoptosis protein was raised significantly and the balance of [Ca2+]i was maintained in the AAV-hBDNF treatment group as compared with AD model group. These data suggested that recombinant AAV mediated a stable expression of hBDNF in cultured hippocampal neurons and resulted in significant neuron protective effects in AD model. The BDNF may reduce neuron apoptosis through increasing the expression of the bcl-2 anti-apoptosis protein and inhibiting intracellular calcium overload. The viral vector-mediated gene expression of BDNF may pave the way of a novel therapeutic strategy for the treatment of neurodegenerative diseases such as Alzheimer's disease.