Aim To investigate the effect of isoflurane on the phosphorylation of p38 mitogen-activated protein kinase (MAPK)in the hippocampus of neonatal rats, and the effect of p38 MAPK pathway on isoflurane-in-duced neuronal apoptosis.Methods Forty-eight neo-natal rats on postnatal day 7 were assigned randomly into four groups:DMSO group (group Air +DMSO), p38 MAPK inhibitor SB203580 group (group Air +SB20 ),isoflurane +DMSO group (group Iso +DM-SO),and isoflurane +SB203580 group (group Iso +SB20 ).Rats were exposed to air or isoflurane (volume fraction of 0.01 1 )for 4h.The p38 inhibitor SB203580 (20 nmol)or DMSO (volume fraction of 0.1 )5μl was intraventricularly administered 30 min before the expo-sure.The brains of some rats in each group were per-fused and embedded by paraffin 6h after the exposure. Neuronal apoptosis in the hippocampal CA1 area was detected by terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling (TUNEL)(n =6). The hippocampal tissues of the other rats in each group were dissected 6h after the exposure,and the protein expressions of phospho-p38 (p-p38 ),p38,cleaved caspase-3,phospho-NF-κB (p-NF-κB ),Bcl-2 and Bax were detected by Westem blot (n =6).Results The number of TUNEL positive cells in the hippocam-pal CA1 region in group Iso +DMSO increased by 4.8 fold compared with that in group Air +DMSO (P <0.01 ),while the number of TUNEL positive cells in group Iso +SB20 decreased by 3 /5 compared with that in group Iso +DMSO (P <0.01 ).The protein expres-sion of cleaved caspase-3 in group Iso +DMSO signifi-cantly increasd (P =0.003)compared to that in group Air +DMSO,which was significantly decreasd in group Iso +SB20 (P =0.007 ).In addition,isoflurane also increased the protein expression of p-p38,p-NF-κB and Bax,decreased the level of Bcl-2,and reduced the ratio of Bcl-2 /Bax compared with control animals (P <0.01 ,P =0.004,P <0.01 ,P <0.01 ,P <0.01 ,respectively).Howerver,SB203580 partly at-tenuated the isoflurane-induced protein change above. Conclusion Isoflurane induces neuroapoptosis in neo-natal rat hippocampus by the activation of p38 MAPK pathway.

Objective To evaluate the effects of sevoflurane on proteome in the cortices of neonatal rats.Methods Thirty neonatal rats at postnatal day 7 (6 rats each litter,5 litters in total) were randomly assigned into 2 groups (n =15 each):control group (C group) and sevoflurane group (S group).The rats were exposed to air and 1.8 ％ sevoflurane for 4 h in C and S groups,respectively.One rat from each litter was chosen in each group at the end of anesthesia and the puncture needle was inserted into the left ventricle via the chest wall.Arterial blood samples were then collected for blood gas analysis and for determination of blood glucose.One rat from each litter was sacrificed in each group at 3 and 72 h after the end of anesthesia,and their cortices were then dissected.Two-dimensional differential in-gel electrophoresis (2-D DIGE) was used to identify patterns of protein expression in cortices cross-labeled with different CyDyes.The differentially expressed proteins were analyzed by using matrixassisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS).Results Acid-base imbalance,anoxia or lycopenia were not found at 3 h after the end of anesthesia in both groups.The analysis showed there were 6 differentially expressed proteins at 3 h after the end of anesthesia in S group compared with C group.Among the 6 proteins,the expression of 4 proteins (class 2 c beta-tubulin,neuron-specific class Ⅲ beta-tubulin,CRMP-1 and CRMP-4) which belonged to cytoskeleton/neuronal growth proteins was down-regulated,the expression of 1 protein (ATP synthase beta subunit) which belonged to hydrolyses and transferases was down-regulated,and the expression of 1 protein (guanine nucleotide binding protein beta1) which belonged to signal transduction proteins was up-regulated (P ＜ 0.05).No significant changes in protein expression were identified at 72 h after 1.8％ sevoflurane anesthesia (P ＞ 0.05).Conclusion 1.8％ sevoflurane-induced 4 h anesthesia can induce short-time changes in the expression of proteins which are related to neuronal migration,differentiation,energy metabolism and signal transduction in cortices of neonatal rats,which may contribute to its neurodegenerative effects in brains of rats during the development period.

Objective To investigate the effects of sevoflurane ( Sevo ) on dendritic development and the expression of collapsin response mediator proteins ( CRMP ) in the hippocampus of developing rats. Methods Twenty-four neonatal Sprague Dawley (SD) rats at postnatal day 7 (P7) were randomly divided into control group or sevoflurane group ( 12 rat pups for each group) .Rats in the control group were exposed to air for 4 h,whereas rats in the sevoflurane group were exposed to 2.8%sevoflurane for 4 h.The hippocam-pus of some rats were collected,and the expressions of CRMP1,CRMP2 and CRMP4 proteins and phospho-rylation of CRMP2 protein at Ser522,Thr514 and Thr555 were detected by Western blot 6h after exposure ( n=6) .The rest rats were housed till P30,the expression of CRMP1,CRMP2 and CRMP4 proteins in the hip-pocampus were detected by Western blot ( n=6) and the morphology changes of dendrites in the dentate gy-rus ( DG) of hippocampal neurons were detected by Golgi-Cox Staining ( n=6) .Results The expression of CRMP1,CRMP2 and CRMP4 proteins of rats at P7 in the sevoflurane group was decreased by 35.0%( P=0.004) ,27.5%( P=0.015) and 12.0%( P=0.003) ,respectively,and the phosphorylation of CRMP2 pro-tein at Ser522 and Thr514 in the sevoflurane group were increased by 68.3%( P<0.01) ,74.5%( P<0.01) , respectively,6 h after exposure compared with control rats.However,the phosphorylation of CRMP2 protein at Thr555 was not significantly changed after sevoflurane exposure.At P30,both total dendrite length ( P=0.001) and the dendrites length at level 2 and 3 ( P=0.033, P<0.01,respectively) were shorter and the dendritic branching at 120,140 and 160 μm rings in Sholl analysis were less ( P=0.009, P=0.028, P=0.048,respectively) for rats in the sevoflurane group,compared with control rats.There were no significant changes at the expressions of CRMP1,CRMP2 and CRMP4 proteins.Conclusion Sevoflurane inhibits the development of dendrites in the hippocampal DG area of developing rats,which may be related to inhibition of CRMP1,CRMP2 and CRMP4 proteins expression and hyperphosphorylation of CRMP2 Ser522 and Thr514.

Objective To investigate the effects of the c-Jun N-terminal kinase (JNK)pathway on isoflurane induced neuronal apoptosis and the proteins expression of phospho-JNK,Bcl-2 and Bax in the hippocampi of neonatal rats.Methods Forty-eight neonatal rats at postnatal day 7 (P7) were randomly assigned into 4 groups:DMSO control group (group D),SP600125 control group (group SP30),isoflurane + DMSO group (group Iso +D),isoflurane + SP600125 group (group Iso + SP30).Rats were exposed to air (control group) or 1.1％ isoflurane (isoflurane group) for 4 h.The JNK inhibitor SP600125 at 30 μg or 12％ DMSO 5 μl was intraventricularly administered 20 min before the exposure.The brains of some rats in each group were perfused and embedded by paraffin 6 h after the exposure.Neuronal apoptosis in the hippocampi CA1 area was detected by TUNEL (n =6).The fresh hippocampi of other rats in each group were dissected 6 h after the exposure and the proteins expression of phospho-JNK,Bcl-2 and Bax were detected by Western blot (n =6).One way ANOVA were used for data analysis among groups.Results The number of TUNEL positive cells in the hippocampal CA1 regions in group Iso +D (135.72 ±21.26 per mm2) increased by 5 folds compared with group D (24.07 ± 1.35 per mm2) (P＜0.01) ;while the number of apoptotic cells in group Iso + SP30 (42.49 ± 5.56 per mm2) decreased by 84％ (P ＜ 0.05)compared with group Iso + D.The expression of phospho-JNK p46 kd in group Iso + D increased by 44.1％ (P ＜0.01),while both phospho-JNK at p46kd and at p54kd in group Iso + SP30 decreased significantly (P＜0.05,P ＜0.01) compared with group Iso + D.The protein expression of Bax increased 1.5 folds (P＜0.05) and Bcl-2 decreased by 42.2％ (P＜0.05) in group Iso + D compared to group D;while SP600125 significantly decreased expression of Bax (P ＜0.05) and increased expression of Bcl-2 (P＜0.01).Conclusion JNK activation contributes to isoflurane-induced neuroapoptosis in the developing brain.Maintaining Bcl-2 expression and inhibiting Bax expression may be involved in the neuroprotective effects of SP600125.

Objective To induce fluconazole resistance in T.asahii by culture in medium containing increasing concentrations of fluconazole,and to evaluate the stability of the induced resistance.Methods Two T.asahii strains with a highest sensitivity to fluoconazole,including a clinical isolate CBS2479 (minumum inhibitory concentration (MIC) =0.25 μg/ml) and an environmental isolate CBS8904 (MIC =1.5 μg/ml),were selected from 11 T.asahii strains stored in the laboratory of the Department of Dermatology,General Hospital of Beijing Military Region.Both strains were respectively and serially subcultured in potato dextrose agar (PDA) medium containing growing concentrations of fluconazole (from 0.5 MIC to 256 μg/ml).E-test was performed to evaluate the susceptibility of T.asahii to fluconazole after each passage.To evaluate the stability of fluconazole resistance,the T.asahii isolates with induced resistance (MIC ＞ 256 μg/ml) were serially subcultured in drug-free PDA medium,and drug susceptibility assay was performed after each subculture.Results After serial culture in PDA medium containing fluconazole,high level of fluconazole resistance (MIC ＞ 256 μg/ml) developed in both of the fluconazole-susceptible T.asahii strains CBS2479 and CBS8904.The MIC value of fluconazole remained unchanged in the fluconazole-resistant strain CBS2479R,but gradually decreased to 64 μg/ml in the other resistant strain CBS8904R after 18-day culture in fluconazole-free PDA medium.Conclusions Fluconazole resistance can be induced in T.asahii strains from different origins by serial culture in medium containing growing concentrations of fluconazole,and the stability of the induced fluconazole resistance varies between strains of different origins.

Objective To investigate psychosocial factors for post-stroke depression (PSD). Methods 405 in-pa-tients with stroke were first screened for depression using Comprehensive International Diagnostic Interview-3.0. 22 pa-tients with depression were recruited as the depression group. From 383 patients without depression, 44 patients were se-lected and served as the non depression controlled group according to the sex and age paired with 1:2. Both groups were measured by using questionnaires including Life Event Scale, Simplified Coping Style Questionnaire, Social Support Rat-ing Scale, Activities of Daily Living Scale and Quality of Life Enjoyment and Satisfaction Questionnaire, Short Form. Re-sults The score of passive coping was significantly higher in depression group than in non depression group [(1.2 ± 0.5) vs. (0.8±0.7), P<0.05]. The score of subjective support was significantly lower in depression group than in non depression group [(17.5±4.0) vs. (20.7±4.6), P<0.05]. Logistic regression analysis showed, minority nationality (OR=2.564, 95%CI:1.039~6.327) and passive coping style (OR=2.223, 95%CI:1.052~5.192) were risk factors for PSD, while subjective sup-port was protective factor for PSD (OR=0.884, 95%CI:0.793~0.986). Conclusions Passive coping style and low subjec-tive support may be the important psychosocial factors of PSD.

PURPOSE: We investigated the effects of different stimulation frequencies on the inhibition of bladder overactivity by sacral neuromodulation (SNM) in pigs. METHODS: Implant-driven stimulators were used to stimulate the S3 spinal nerve in 13 pigs. Cystometry was performed by infusing normal saline (NS) or acetic acid (AA). SNM (pulse width, 210 µsec) at frequencies ranging from 5 to 50 Hz was conducted at the intensity threshold at which observable perianal and/or tail movement was induced. Multiple cystometrograms were performed to determine the effects of different frequencies on the micturition reflex. RESULTS: AA-induced bladder overactivity significantly reduced the bladder capacity (BC) to 34.4%±4.7% of the NS control level (354.4±35.9 mL) (P<0.05). During AA infusion, SNM at 5 Hz did not significantly change the BC (48.1%±6.9% of the NS control level) (P>0.05), but SNM at 15, 30, and 50 Hz significantly increased the BC to 54.5%±7.1%, 55.2%±6.5%, and 57.2%±6.1% of the NS control level (P<0.05), respectively. No significant differences were found among the results obtained using frequencies of 15, 30, and 50 Hz (P>0.05). CONCLUSIONS: This study demonstrated that 15 Hz was an appropriate frequency for SNM and that frequencies higher than 15 Hz did not lead to better surgical outcomes.
Acetic Acid ; Reflex ; Spinal Nerves ; Swine* ; Tail ; Urinary Bladder* ; Urinary Bladder, Overactive ; Urination

Purpose: To investigate the video-urodynamic and pelvic floor electrophysiological characteristics in patients with traumatic spinal cord injury (SCI). Methods: This retrospective reviewed the clinical records, urodynamic and pelvic floor electrophysiological data of 647 patients with traumatic SCI and out of spinal shock. Patients were classified based on American Spinal Injury Association (ASIA) Impairment Scale and urodynamic findings. Results: Of the 647 patients, detrusor overactivity (DO) with or without detrusor sphincter dyssynergia (DSD) was found in 79.5%, 61%, 35.2%, 35%, and 19.2% of patients with cervical, thoracic (T1–9), thoracic (T10–12), lumbar, and conical cauda injury, respectively. Other patients manifested detrusor areflexia (DA). Patients with DO and/or DSD had a longer duration of SCI at each injury level than patients with DA. In suprasacral injury patients with DA, 63.0% (58 of 92) had a normal bulbocavernosus reflex (BCR) response. Compared with patients without bladder sensation (BS), bladder capacity during urine leakage was far higher in those with BS. The manifestation of BCR and somatosensory-evoked potential (SEP) was associated with the level of injury. Conclusions This study showed a significant correlation between the level of SCI and video-urodynamic findings, but clinical examination cannot by predict bladder function; urodynamic testing is also necessary. In addition, the role of BCR and SEP for guiding bladder management is limited. Moreover, BS is important for urinary control in patients with traumatic SCI.

Purpose: To determine the risk factors predicting upper urinary tract (UUT) damage using a grading system for upper urinary tract dilation (UUTD) and a descriptive system for all urinary tract dysfunction (AUTD) in patients with myelodysplasia. Methods: Six hundred thirty-seven patients with myelodysplasia were evaluated at our center from January 2008 to November 2019. Clinical data, ultrasonography, magnetic resonance urography, and video-urodynamics (VUDS) parameters were collected. Univariate and multivariate analyses were used to determine the risk factors predicting UUT damage. Results: Three hundred eighty-three males and 254 females were included. The average course of lower urinary tract symptoms (LUTS) was 14.08±7.07 years (range, 3–31 years). The urodynamic diagnoses of all patients were as follows: detrusor overactivity, 26.8%; detrusor underactivity, 6.44%; and acontractile detrusor, 66.72%. UUT damage was determined in 66.56% of the patients. Of the patients, 28.73 % had vesicoureteral reflux (VUR) during filling (bilateral, n=50; unilateral, n=133) on fluoroscopy during VUDS testing. Two hundred thirty-four patients had UUTD (bilateral, n=203; unilateral, n=31). The occurrence of hydronephrosis based on ultrasonography was closely related to ipsilateral VUR (P<0.05). Absent of bladder sensation, long-term course of LUTS, decreased maximum cystometric capacity (MCC) and bladder compliance (BC), and increased postvoid residual urine (PVR) were shown to be independent risk factors in logistic regression analysis. Conclusions This retrospective study using UUTD and AUTD systems indicated that patients with myelodysplasia have a high incidence of UUT damage. Absence of bladder sensation, long-term course of LUTS, decreased MCC and BC, and increased PVR were independent risk factors predicting UUT damage.

Objective:To explore the influence of peer support education on psychosocial adaptation and psychological distress of breast cancer patients.Methods:Using non-simultaneous experimental research methods, a total of 51 breast cancer patients admitted to the department of breast surgery, the First Affiliated Hospital of Nanchang University from June to August 2019 were selected as the control group, and 53 breast cancer patients admitted from September to December 2019 were selected as the intervention group. The control group received routine education, while the intervention group received peer education on the basis of routine education. After 4 months of intervention, the differences of psychosocial adaptation and psychological pain were compared between the two groups.Results:After 4 months of intervention, 49 cases in the control group and 51 cases in the intervention group completed the study. In the psychosocial adaptation scale, the scores of anxiety/depression, self-esteem, self-acceptance, self-control and self-efficacy belonging in the intervention group were (29.43±2.83), (32.08±3.07), (28.10±2.62), (28.08±3.27), (31.53±3.73) points, which were higher than (27.67±3.96), (30.14±2.54), (25.94±2.91), (25.16±2.95), (30.02±2.70) points in the control group after the intervention, and difference statistically significant ( t values were -4.680 to -2.312, P<0.05). The score of psychological pain in the intervention group (2.37±1.15) points was significantly lower than that in the control group (3.57±0.98) points, and difference was statistically significant ( t value was 4.867, P<0.05). The number of patients with mild and moderate psychological pain in the intervention group was 51 cases accounting for 100% (51/51), which was higher than 48 cases accounting for 98% (48/49) in the control group, and difference was statistically significant ( χ2 value was 12.272, P<0.05). Conclusions:Peer education can effectively improve the psychosocial adaptability of breast cancer patients and reduce their pain level.