Objective To explore the effects of Neurogenesin 1 (Ng1) gene on functional recovery after spinal cord injury (SCI) and its mechanism. Methods Thirty-six rats (aging 4 months, weighing 230 g and being male or female), were randomly divided into two groups: experimental group (n=18) and control group (n=18). After spinal cord contusive injury at T10 level was made in all these rats using modified Allen’s method, Ng1 recombinant plasmid and blank plasmid were transfectedinto the damaged areas of exprimental group and control group respectively by Alzet pumps. At 1 day, 1 week, 2 weeks, 3 weeks, and 4 weeks after SCI, Basso-Beattle-Bresnahan (BBB) Rating Scale was used to observe the recovery of motor function. At 1 week after injury, the expressions of Ng1 mRNA and protein in injured spinal cord were detected by RT-PCR and Western blot techniques. And at 2 and 4 weeks, double immunofluorescence and histopathologic examinations were performed to study the prol iferation of the adult endogenous neural stem cells and pathological change after SCI. Results At 1-4 weeks after SCI, the BBB scores in the exprimental group was significantly higher than that in control group (P lt; 0.05), and at 4 weeks the BBB score of the experimental group (16.80 ± 1.79) was significantly higher than that of the control group (9.60 ± 1.67), (P lt; 0.01). RTPCR and Western blot showed that the mRNA and protein expressions of Ng1 were observed in the exprimental group and no expression was seen in the control group. Histologic observation showed that the morphology of spinal cord and neurons in the exprimental group was better than that in the control group and was close to the normal tissue. The mean number of Nestin+/ BrdU+ newborn endogenous neural stem cells in the exprimental group was significantly more than that in control group (P lt; 0.05). Conclusion Ng1 gene could promote the prol iferation of endogenous neural stem cells and protect the injured neurons, which enhances the repair of the motor function after SCI.
ObjectiveTo observe the protective effect of etomidate (ET) on cultured retinal ganglion cells (RGC) with mechanical injury in vitro. MethodsNew Sprague-Dawley rat RGC was cultured in vitro and identified by double immunofluorescent labeling of Thy1.1 and microtubule associated protein 2. The cultured primary cells were randomly divided into control group, RGC scratch group, ET low dose group (1 μmol/L), ET medium dose group (5 μmol/L) and ET high dose group (10 μmol/L). The RGC mechanical injury model was established by using iris knife to culture cells in RGC scratch group and ET group with different concentration. Seven days after modeling, the RGC survival rate of each group was detected by cell count Kit 8 proliferation assay. The apoptosis rate of RGC was detected by Annexin Ⅴ/propyl iodide double staining. Single factor analysis of variance was used to compare the groups. The pairwise comparison between groups was tested by the least significant difference method. ResultsThe survival rates of RGC in RGC scratch group, ET low dose group, ET medium dose group and ET high dose group were (72.60±2.97)%, (73.73±1.14)%, (79.19±1.79)% and (83.88±0.94)%, respectively. The RGC apoptosis rates of control group, RGC scratch group, ET low dose group, ET medium dose group and ET high dose group were (5.08±0.17)%, (18.67±1.24)%, (17.96±0.74)%, (15.11± 0.56)% and (11.67±1.32)%, respectively. Comparison of RGC survival rate between groups: compared with RGC scratch group, the cell survival rate of ET low-dose group, ET medium-dose group and ET high-dose group was increased, and the difference between RGC scratch group and ET low-dose group was not statistically significant (P=0.728); the differences between RGC scratch group, ET medium dose group and ET high dose group were statistically significant (P＜0.001); the difference between ET medium dose group and ET high dose group was statistically significant (P=0.002). Comparison of apoptosis rate of RGC among groups: the apoptosis rate of RGC scratch group was significantly higher than that of control group, the difference was statistically significant (P＜0.001). Compared with RGC scratch group, the apoptosis rate of ET low-dose group, ET medium-dose group and ET high-dose group was decreased, and there was no statistical significance between RGC scratch group and ET low-dose group (P=0.869). The differences of apoptosis rate between RGC scratch group, ET medium dose group and ET high dose group were statistically significant (P＜0.05). The difference of apoptosis rate between ET medium dose group and ET high dose group was statistically significant (P=0.007). ConclusionET has neuroprotective effect on RGC cultured in vitro with mechanical injury, and the protective effect increases with the increase of ET dose in a certain range.
To investigate the effects of fibrin glue on repair and regeneration of acute complete spinal cord injury. Methods Acute complete transaction spinal cord injury model were made in 10 adult healthy SD rats(female, weighing 250-300 g), randomized grouping: treated group(n=5) and control group(n=5). In the treated group, fibrin glue was implanted covering on the injury site and fill ing the lesion gap. In the control group, no treatment was given. At 4 weeks, the locomotor functions of the rats were detected by basso, beattie and bresnahan (BBB) score, then the means of immunohistochemistry were used to observe neurofilament(NF) and gl ial fibrillary acidic protein(GFAP). And image analysis was used to measure the quantify of the nerve fiber and the fibers area ratio of astrocyte. Results The BBB scores were 2.40 ± 0.51 in control group, 3.00 ± 0.45 in treated group, showing no significant difference (P gt; 0.05). By immunohistochemistry: a l ittle positive NF cells and GFAP frame were found in control group; more positive NF cells and GFAP frame were found in treated group, the cells and frame grew toward the center but did not arrive at the center. Image analysis showed the amount of never fibers in treated group (rostral region: 113.10 ± 20.75, caudal region: 73.60 ± 33.61) was more than that in control group (rostral region: 45.50 ± 17.18, caudal region 23.50 ± 8.20), showing significant difference. The fibers area ratio of astrocyte in treated group(rostral region: 33.75% ± 11.06%, caudal region: 27.75% ± 7.15%) was more than that in control group(rostral region: 23.78% ± 5.76%, caudal region: 19.78% ± 5.17%), showing significant difference (P lt; 0.05). Conclusion Fibrin glue can promote repair and regeneration of acute spinal cord injury.
Neuromyelitis optica (NMO) is a kind of demyelinating disorder that preferentially affects the optic nerves and spinal cord and results in permanent vision loss. NMO pathogenesis is thought to involve binding of anti-aquaporin-4 (AQP4) auto-antibodies to astrocytes, which causes complement-dependent cytotoxicity (CDC) and downstream inflammation leading to oligodendrocyte and neuronal injury. Vasculocentric deposition of activated complement is a prominent feature of NMO pathology. In recent years, a number of groups have found complements play an important role in the pathogenesis of NMO, and basic researches in NMO therapy due to its specificity and uniformity. Its inhibition would protect against proteins in the classical complement pathway so that cure the disease. This review will expound the the role of complement signaling pathway in the pathogenesis of NMO, and provide reference for a more in-depth understanding and clinical treatments of NMO.
Objective
To study the expression and its significance of bcl-2 associated death (bad) gene in human optic nerves from traumatic atrophic eyeballs.
Methods
The optic nerves from 8 normal human donor eyes and 31 traumatic atrophic eyes were studied by immunohistochemistry technique.
Results
Bad protein was positively expressed in the normal optic nerve myelin sheath and residual myelin portions of optic nerve tissues from traumatic atrophic eyes. The expression of bad protein in the residual portions of myelin sheath was stained significantly ber than that in normal optic nerves (P＜0.05)。The pathological durations for ocular atrophy was not co-related with the quantites of expression of bad protein. There was no significant difference between pathogenic causes of ocular atrophies and the quantites of bad expression (P＞0.05).
Conclusion
Bad might possess the function of promoting the optic nerve atrophy processes in traumatic atrophic eyes.
(Chin J Ocul Fundus Dis, 2002, 18: 276-278)
ObjectiveTo investigate the relationship between neuroticism and functional gastrointestinal disorders using Mendelian randomized (MR). MethodsBased on the genome-wide association study data of neuroticism and 2 functional gastrointestinal disorders, i.e., functional dyspepsia (FD), and irritable bowel syndrome (IBS), appropriate single nucleotide polymorphisms (SNP) were extracted as instrumental variables, and inverse variance weighted (IVW) was applied as the main analysis method, and sensitivity analyses were performed by Cochran’s Q test, MR-PRESSO test, MR-Egger intercept, and leave one out analysis. Further two-step MR analyses were performed to examine the mediating effects of coffee intake, alcohol consumption, smoking, depression. ResultsThe univariable MR analysis showed that genetically determined neuroticism was positively causally associated with the risk of developing FD and IBS (FD: OR=1.448, 95%CI 1.057 to 1.983, P=0.021; IBS: OR=1.705, 95%CI 1.210 to 2.403, P=0.002). Cochran's Q-test, MR-Egger intercept, MR-PRESSO did not observe significant heterogeneity or horizontal pleiotropy. Leave-one-out analyses also did not find a large effect of individual SNPs on the overall results. Multivariable MR analyses showed that the association between neurotic personality and elevated risk of FD and IBS prevalence persisted even after adjusting for other confounders. Further two-step MR mediation analyses revealed that depression partially mediated this effect, with mediation proportions of 59.41% (95%CI 5.69% to 113.12%) and 67.53% (95%CI 31.55% to 103.51%), respectively. ConclusionThere is a degree of causal association between neuroticism and FD and IBS, and depression may play an important mediating role in this association.
Objective To investigate the management of the soft tissue defect after the Achilles tendon repair. Methods From April 1996 to April 2006, 24 patients(17 males, 7 females; aged 16-59 years), who suffered from postoperative Achilles tendon exposure caused by local soft-tissue necrosis after the Achilles tendon repair, were treated and evaluated. Of the 24patients, 8 had an original open injury (machinecrush injury in 2 patients, heavy-object press injury in 3, motorcycle wheel crush injury in 3) and 16 patients had a closed injury (sports injury). In their treatment, the transferof the sural neurovascular flap was performed on 8 patients and the transfer ofthe saphenous neurovascular flap was performed on 3 patients. The secondary Achilles tendon repair was performed on 13 patients before the neurovascular flap transfer was performed. The time between the injury and the operation was 9-76 days, and the time between the Achilles tendon expousure and the operation was 3-65 days. Results All the flaps survived and the Achilles tendon exposure was well covered by the flaps of good texture. Eighteen patients followed up for 6 months to 24 months had no flap complication, and the two point discrimination of the flaps was 12-20 mm. The AOFASAnkleHindfoot Scale assessment revealed that 8 patients had an excellent result, 6 had a good result, 3 had a fair result, and just 1 had a poor result, with theexcellent and good results accounting for 77.8%. Sixteen patients (89%) were able toperform a tip-toe stance on their operative sides, and only 3 of them complained a loss of plantarflexion strength. However, 2 patients still could not perform the tip-toe stance. Conclusion The Achilles tendon repair, ifnot well performed, can result in the local soft-tissue necrosis and the subsequent Achilles tendon exposure. If those complications occur, the neurovascular flap transfer should be performed as soon as possible; if necessary, the secondary Achilles tendon repair should be performed, too.
Objective To review the biologic characteristics and biologic effect of cholecystokinine (CCK) on the central nervous system. Methods The literatures of recent years on research advancement of cholecystokinine as neurotransmitters/peptides in signal transduction, neuron protection and pain management in the central nervous system are reviewed. Results CCK possesses the ability to suppress the convulsant effects of convulsants. CCK8 is able to reduce the neural damage caused and delay the neural aging. CCK antagonists play an important role in human pain transduction. Conclusion CCK has been proven to be one of the richest neurotransmitters/neuropeptides as well as an important signal factor in the brain, and its important biologic effect is being confirmed.
ObjectiveTo explore the clinical features and the prognostic factors of neuroendocrine carcinoma of the esophagus.
MethodsWe retrospectively analyzed clinical data of 41 cases of neuroendocrine carcinoma of the esophagus admitted in the First Affiliated Hospital of Nanjing Medical University between March 2008 and March 2014. There were 37 males and 4 females at a mean age of 61.1±7.9 years (ranged from 40 to 79 years). All patients underwent surgical resection and lymph node dissection.
ResultsNo severe complications occurred during the perioperative period, and no death occurred during the period of hospitalization.Thirteen patients received postoperative chemotherapy and radiotherapy. Eleven patients received simple postoperative chemotherapy. One patient received postoperative radiotherapy. The remaining 16 patients did not receive any special treatment. The patients were followed up for 6 to 61 (24.0±13.6)months. Twenty-two patients survived, the other 19 patients died. The 1-year, 2-year, 3-year, 4-year, and 5-year survival rate was 80.49%, 39.02%, 21.95%, 7.32%, and 4.88%, respectively. The median survival of single surgical treatment and postoperative comprehensive treatment was 12.0 months and 25.0 months, respectively. The median survival of T2-T4 and T1 was 20.0 months and 37.5 months, respectively. The difference was statistically different (P<0.05). Cox regression analysis showed that the depth of tumor invasion, postoperative adjuvant chemotherapy and radiotherapy were independent factors of prognosis (P<0.05).
ConclusionsNeuroendocrine carcinoma of the esophagus is rare and with a high degree of malignancy. It is expected to increase the long-term survival rate after surgical and postoperative comprehensive treatment.
Objective To evaluate clinical significance of reversed sural neurovascular fasciocutaneous flap for reconstruction of softtissue defects in ankle and foot. Methods From July 1994 to December 2002, 52 cases of soft-tissuedefects in the ankle and foot were reconstructed by use of reversed sural neurovascular fascio-cutaneous flap, including 47 cases of traumatic defects, 3 cases of chronic ulcer and 2 cases of tumors. The flap area ranged from 4 cm×6 cm to 10 cm×21 cm. Results The flaps survived in 48 cases; the distal part necrosed and secondary free-skin graft were further conducted in 4 cases. All soft-tissue defects were repaired and their accompanied bone and tendon exposurehealed. Forty-six cases were followed-up for 5 months to 48 months, the color and texture of the flaps were excellent and 2point discrimination was 11-17 mm(14 mm on average).The functions of ankle joints were good.Conclusion The reversedsural neurovascular fascio-cutaneous flap is convenient in design and dissection. Its use can retained and replace vascular anostomosed flaps to certain degrees.
