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Objective·To investigate the effectiveness of nerve transfer in repairing defecation function after spinal cord injury by the pseudorabies virus (PRV) retrograde tracing. Methods·The spinal cords were transected between L6 and S1 nerve root in 20 rats. The nerve transferring surgery was then conducted in 10 rats (Group B) and the remaining rats were control (Group A). After six months, all rats were injected with 6 μL PRV, sacrificed after 3 d and perfused with paraformaldehyde. Spinal cords were then harvested and frozen sections were prepared for observation. Results·There was no detectable infection of PRV proximal to the injury level in Group A, while infected neurons proximal to the injury level were widely observed in Group B.Conclusion·Nerve transfer has potent effect on defecation reconstruction after spinal cord injury in rats. PRV retrograde tracing can prove the existence of new neuron pathway.
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Objective·To investigate the effectiveness of nerve transfer in repairing defecation function after spinal cord injury by the pseudorabies virus (PRV) retrograde tracing. Methods·The spinal cords were transected between L6 and S1 nerve root in 20 rats. The nerve transferring surgery was then conducted in 10 rats (Group B) and the remaining rats were control (Group A). After six months, all rats were injected with 6 μL PRV, sacrificed after 3 d and perfused with paraformaldehyde. Spinal cords were then harvested and frozen sections were prepared for observation. Results·There was no detectable infection of PRV proximal to the injury level in Group A, while infected neurons proximal to the injury level were widely observed in Group B.Conclusion·Nerve transfer has potent effect on defecation reconstruction after spinal cord injury in rats. PRV retrograde tracing can prove the existence of new neuron pathway.
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Objective To investigate the effect of early cerebrospinal fluid replacement on nuclear factor-κB (NF-κB) level and clinical outcomes in patients with aneurismal subarachnoid hemorrhage (aSAH) after endovascular embolization.Methods Patients with aSAH received aneurysm embolization were enrolled.They were divided into a cerebrospinal fluid replacement group and a non-cerebrospinal fluid replacement group according to the treatment scheme.All patients were treated with cerebral aneurysm coil embolization within 3 days after admission.The cerebrospinal fluid replacement group performed lumbar puncture cerebrospinal fluid replacement within 24 h after coil embolization,once every other day,20-30 ml of cerebrospinal fluid was replaced each time and 3 mg dexamethasone was injected intrathecally.The NF-κB levels in cerebrospinal fluid were detected at day 1,7 and 14 after the coil embolization.The primary outcome measures were the clinical outcomes determined by the modified Rankin scale (mRS) and the Glasgow outcome scale (GOS) at 3 months after onset.Good outcome was defined as mRS score 0-2 or GOS ＞ 3.The secondary outcome measures included severe complications (hydrocephalus,cerebral vasospasm,cerebral infarction,and rebleeding) and death.Results A total of 81 patients with aSAH received aneurysm embolization were enrolled,including 42 in the cerebrospinal fluid replacement group and 39 in the non-cerebrospinal fluid replacement group.There was no significant differences in the baseline data between the cerebrospinal fluid replacement group and the non-cerebrospinal fluid replacement group (all P ＞0.05).The duration of neck stiffness in the cerebrospinal fluid replacement group was significantly shorter than that in the non-cerebrospinal fluid replacement group (11.3 ± 3.2 d vs.16.5 ± 3.5 d;t =6.985,P ＜ 0.001).The cerebrospinal fluid NF-κB levels were progressively reduced at day 1,7 and 14 after coil embolization in the cerebrospinal fluid rephcement group and non-cerebrospinal fluid rephcement group (all P ＜0.05),but the ccerebrospinal fluid levels of NF-κB in the cerebrospinal fluid replacement group at each time point were significantly lower than those in the non-cerebrospinal fluid replacement group (all P ＜ 0.01).The good outcome rates evaluated according to the mRS score (92.9％ vs.56.4％;x2 =14.446,P ＜ 0.001) and GOS score (97.6％ vs.76.9％;x2 =8.004,P=0.005) in the cerebrospinal fluid replacement group at 3 months were significantly higher than those in the non-cerebrospinal fluid replacement group,and the incidence of cerebral vasospasm was significantly lower than that in the non-cerebrospinal fluid replacement group (14.3％ vs.33.3％;x2 =4.086,P =0.043).Conelusiom Cerebrospinal fluid replacement therapy can reduce the incidence of cerebral vasospasm in patients with aSAH receiving aneurysm embolization and improve clinical outcomes.Its mechanism may be associated with the decrease of NF-κB level in cerebrospinal fluid.
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<p><b>OBJECTIVE</b>To explore the effect of BCR-ABL gene transcripts on Leukemia-free survival (LFS) and prognosis of patients with Philadelphia chromosome positive acute lymphoblastic leukemia (PhALL) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).</p><p><b>METHODS</b>The clinical data of 107 cases of PhB-ALL patients received allo-HSCT from July 2006 to November 2014 in the First Affiliated Hospital of Soochow University were collected and the relationship between the clinical characteristics and LFS after transplantation was analyzed.</p><p><b>RESULTS</b>Out of 107 PhALL patients (64 males and 43 females) with a median age of 30(7 to 54)years old, 35.5% (38/107) cases relapsed after transplantation within a median time of 6.9 (1.5 to 40.7) months. A total of 39 (36.4%) cases died within a median time of 19.8 (3.6 to 83.7) months after HSCT, of which 51.3% (20/39) due to disease relapse and 25.6% (10/39) due to infection. BCR-ABL gene transcripts of 49 cases turn into negative before transplantation, of which the expected 5-year cumulative incidence of relapse (CIR), non-relapse mortality (NRM) and overall survival (OS) were 26.5%, 29.5% and 41.6%, respectively. Another 49 cases still had a positive BCR-ABL gene transcripts before transplantation, of which the life expectancy of 5 year CIR, NRM and OS were 64.4%,8.9% and 48.9%, respectively. Compared with BCR-ABL positive patients, BCR-ABL negative patients showed a lower CIR (P<0.001), a higher NRM (P=0.030) and a similar OS (41.6% versus 48.9%, P=0.497). Multivariate analysis showed that BCR-ABL positive (P=0.016) and a disease statusphase ≥CR2 (P<0.001) before HSCT were independent risk factors for LFS, while the age underwent HSCT was the principal element affecting prognosis (P<0.001).</p><p><b>CONCLUSION</b>Both the relapse and infection are the main causes of death in the patients after transplantation. A disease status ≥CR2 and the BCR-ABL positive before transplantation are 2 independent risk factors of LFS in the patients with PhALL after allo-HSCT.</p>
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<p><b>OBJECTIVE</b>To investigate the roles of prostatic infarction, prostatic inflammation and the type of prostatic hyperplasia in acute urinary retention (AUR) in patients with benign prostatic hyperplasia (BPH).</p><p><b>METHODS</b>We retrospectively analyzed 102 cases of BPH, 49 complicated by AUR and the other 53 without AUR. We compared the incidences of prostatic infarction and prostatic inflammation, the types of prostatic hyperplasia, the patients' age, the level of prostate specific antigen (PSA), the prostate volume, and international prostate symptom score (IPSS) between the AUR and non-AUR groups.</p><p><b>RESULTS</b>The PSA level was significantly increased in the AUR group as compared with the non-AUR group (P < 0.05). There were no statistically significant differences between the two groups in the mean age, prostate volume and IPSS (P > 0.05). The type of prostatic hyperplasia showed no correlation with AUR. The incidence rate of AUR was 5.620 and 2.326 times higher in the BPH patients with prostatic infarction and prostatic inflammation respectively than in those without (P < 0.05).</p><p><b>CONCLUSION</b>Prostatic infarction and prostatic inflammation are important risk factors of AUR in BPH patients.</p>
Subject(s)
Aged , Aged, 80 and over , Humans , Male , Middle Aged , Case-Control Studies , Inflammation , Prostate , Pathology , Prostate-Specific Antigen , Chemistry , Prostatic Hyperplasia , Pathology , Retrospective Studies , Risk Factors , Urinary Retention , PathologyABSTRACT
Objective To investigate the effect of sulforaphane on 1-methyl-4-phenylpyridinium (MPP +)-induced cell viability loss in cultured PC12 cells and to explore the possible mechanism.Methods MPP + induced damage in PC12 cells was prepared as oxidative damage model.Sulforaphane (0.5,1.O,2.5,5.0 and 10.0 μmol/L) was added in each group cell growth medium.Subsequent experiments were divided into 4 groups:(A) normal control group,(B) sulforaphane group,(C) MPP+ injury group,(D)sulforaphane pretreatment + MPP+ injury group.Cell viability was detected by MTT assay,and the sulforaphane pretreatment PC12 cell viability was observed in different concentrations.Flow cytometry was used to detect changes in the rate of apoptosis in different packet PC12 cells,and protein expression levels of nuclear factor erythroid2-related factor 2 (Nrf2),heme oxygenase (HO-1) and human NAD (P) H dehydrogenase,quinone 1 (NQO1) were detected by Western blot when the PC12 cells were incubated with sulforaphane (2.5 μmol/L) and (or) MPP+ (500 μmol/L) for 24 h in vitro.Results Compared to control group (cell survival rate was 98.70％),the survival percents of PC12 cells were significantly decreased in MPP+-treated group (58.16％).A significant difference was showed between group A and C (F =21.83,P ＜ 0.05),and the cell survival rate in group D was significantly improved.Compared to control group,the rate of apoptosis in MPP+ injury group was increased,and the rate of apoptosis after pretreatment of the sulforaphane was significantly reduced.Compared to MPP+ injury group,the levels of Nrf2,HO-1 and NQO1 protein expression were significantly increased in sulforaphane pretreatment group.Conclusion Sulforaphane have a protective effect against MPP+-induced PC12 cell model damage,and the protective effect may be achieved by activating the Nrf2-antioxidant response element pathway.
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Keap1 -Nrf2/ARE pathway plays a wide role of cell protection function in anti-tumor,antistress,anti-apoptosis,anti-inflammatory response.It has become a focus of the neuroprotective effects in nervous system.We will review on the latest research of Keap1-Nrf2/ARE pathways in cerebral ischemia.It will provide a basis for the prevention and treatment of central nervous system.
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<p><b>OBJECTIVE</b>To investigate the effect of PI-3K and p38MAPK signal pathways on the cyclooxygenase-2 (COX-2) expression induced by the epidermal growth factor (EGF) in PC-3 cells.</p><p><b>METHODS</b>PC-3 cell proliferation was detected by methylthiazolyl tetrazolium (MTT) assay after stimulated by EGF (0 microg/L), EGF (10 microg/L), EGF (10 microg/L) + LY294002 (20 micromol/L) and EGF (10 microg/L) + SC203580 (20 micromol/L), and so was the COX-2 expression in the PC-3 cells by RT-PCR and Western blot assay after stimulated the same way for 24 hours. ELISA was used to determine the changes of PGE2 in the culture medium.</p><p><b>RESULTS</b>LY294002 and SC203580 signficantly inhibited PC-3 cell proliferation (P < 0.05), COX-2 expression and PGE2 production after EGF stimulation (P < 0.05).</p><p><b>CONCLUSION</b>EGF can stimulate PC-3 cells into proliferation and induce COX-2 mRNA and the upregulation of its protein expression, while LY294002 and SC203580 can inhibit EGF from the above effects on PC-3 cells.</p>