Objective To explore the clinical value of laparoscopic radical cystectomy based on fascia anatomy for bladder cancer treatment.Methods The clinical data of 51 patients with bladder cancer who underwent 3D laparoscopic radical cystectomy during Jan.2015 and Jun.2022 were retrospectively analyzed.The surgery was performed based on membrane anatomy technology along four longitudinal and two transverse planes to complete the radical cystectomy.The pelvic plexus was preserved for patients with normal preoperative sexual function.Results All surgeries were completed without conversion to open operation.The mean operation time was(502.52±108.99)min,mean intraoperative blood loss was(275.96±155.18)mL,mean postoperative drainage time was(4.14±2.41)d,and the mean postoperative hospital stay was(16.37±4.85)d.The mean number of lymph nodes removed was(17.98±11.48).The mean postoperative follow-up was(30.27±19.39)months.At the last follow-up,no Clavien ≥grade 3 complications were observed.The estimated overall survival(OS),tumor-specific survival(TSS),and recurrence-free survival(RFS)were 82.4％,92.2％,and 88.2％,respectively.The lymph node positive patients had shorter OS and RFS(60.0％,60.0％)than the lymph node negative patients(84.8％,91.3％).Among the 19 male patients who underwent radical cystectomy with pre-exposure and preservation of pelvic plexus,daytime and nocturnal continence rate were 83.3％and 72.2％,respectively,and 17 patients recovered potency within 6 months postoperatively.Conclusion Laparoscopic radical cystectomy based on fascia anatomy is safe and effective in laparoscopic radical cystectomy,with standardized surgical procedure,satisfactory oncological outcomes,little hemorrhage,few complications and fast recovery.

Objective:To investigate the correlation between serum ischemia modified albumin (IMA) and calmodulin (CaM) expression levels and neurological impairment in patients with cerebral small vessel disease.Methods:The clinical data of 140 patients with cerebral small vessel disease (CSVD) who received treatment at The Third People Hospital in Liaocheng between April 2020 and December 2021 were retrospectively analyzed. On admission, serum levels of CaM and IMA were measured using an enzyme-linked immunosorbent assay and an albumin-cobalt binding test. Patients' neurological function was evaluated using the National Institutes of Health Stroke Scale (NIHSS). Patients' transient cerebral ischemia, urinary incontinence, and gait disturbance were evaluated using the National Institute of Neurological Disorders and Stroke Scale. Patients' cognitive function was evaluated using the Montreal Cognitive Assessment scale. The influential factors of serum IMA and CaM expression levels in patients with CSVD were analyzed. The factors that affect the severity of neuological imairment in patients with CSVD and their correlation with serum IMA and CaM expression levels were analyzed.Results:The gender, age, presence or absence of gait disorders, and presence or absence of urinary incontinence of patients were not correlated with serum IMA and CaM levels (all P > 0.05). The serum levels of IMA [(38.5 ± 5.3) × 103U/L, (38.5 ± 4.7) × 103U/L, (39.0 ± 4.4) × 103U/L] and CaM [(190.4 ± 34.5) μg/L, (191.2 ± 26.7) μg/L, (199.7 ± 24.8) μg/L] in patients with cognitive impairment, dizziness and vertigo, and transient cerebral ischemia were significantly higher than those in patients with normal cognitive function, patients without dizziness and vertigo, or patients without transient cerebral ischemia [(27.3 ± 4.4) × 103U/L, (21.0 ± 3.8) × 103U/L, (20.5 ± 5.1) × 103U/L, (180.6 ± 29.6) μg/L, (179.5 ± 28.6) μg/L, (168.6 ± 32.4) μg/L, t = 14.10, 24.36, 22.50, all P < 0.05]. There were significant differences in cognitive impairment (38/16/9), dizziness and vertigo (39/16/8), transient cerebral hemorrhage (35/16/9), NIHSS score [(3.6 ± 0.8) points, (7.5 ± 0.9) points, (16.2 ± 3.2) points], CaM levels [(125.3 ± 20.5) μg/L, (185.5 ± 23.6) μg/L, (237.9 ± 54.3) μg/L], and IMA levels [(21.2 ± 3.5)] × 103 U/L, [(38.5 ± 4.3) × 103 U/L, (74.9 ± 5.4) × 103 U/L] among patients with mild, moderate, and severe neurological impairment ( t = 32.87, 11.28, 12.42, 34.59, 151.73, 147.84, all P < 0.05). The results of multivariate analysis indicated that cognitive impairment ( OR = 1.578, 95% CI: 1.043-2.386), transient cerebral ischemia ( OR = 2.396, 95% CI: 1.156-4.969), dizziness and vertigo ( OR = 1.906, 95% CI: 1.086-3.345), NIHSS score ( OR = 2.171, 95% CI: 1.162-4.056), CaM level ( OR = 2.022, 95% CI: 1.268-3.224), and increased IMA levels ( OR = 2.090, 95% CI: 1.313-3.325) were independent influential factors for worsened neurological impairment (all P < 0.05). The serum levels of IMA and CaM in patients with CSVD were significantly positively correlated with the severity of neurological impairment ( r = 5.45, 8.33, both P < 0.05). Conclusion:The elevated serum levels of IMA and CaM in patients with CSVD serve as independent risk factors for neurological impairment, and these levels are positively correlated with the severity of neurological impairment.

Objective To explore the clinical features,treatment and prognosis of glioblastomas(GBM)in adults.Methods A retrospective cohort study was performed on 176 adult GBM patients admitted to our department from January 2015 to December 2021.Chi-square test was used to investigate the clinical differences between isocitrate dehydrogenase(IDH)mutant and wild-type GBM.Kaplan-Meier and Log-Rank tests were employed to plot survival curve and compute the survival analysis.Multivariate Cox regression model was applied to identify the independent prognostic factors.Results IDH wild-type GBM account for 89.2％and had significantly differences from the IDH-mutant GBM in terms of age of onset,Karnofsky(KPS)score at admission,symptoms of neurological deficit,and methylation status of O6-methylguanine-DNA-methyltransferase(MGMT)promoter(P＜0.05).For the IDH wild-type GBM patients receiving conventional therapy,univariate Cox hazard analysis showed gross total resection,methylation of MGMT promoter,initiation of radiation within the 5th to 6th week after surgery,and adjuvant temozolomide(TMZ)chemotherapy ≥6 cycles were favorable prognostic factors for overall survival(OS);GBMs in the left hemisphere,involvement of single lobe,methylation of MGMT promoter,and initiation of radiation within the 5th to 6th week after surgery were favorable prognostic factors for progression free survival(PFS)(all P＜0.05).Moreover,multivariate Cox hazard regression analysis indicated that methylation of MGMT promoter,and initiation of radiation within the 5th to 6th week after surgery,and adjuvant TMZ chemotherapy ≥6 cycles were independent protective factors for OS,and GBMs in the left hemisphere,involvement of single lobe and methylation of MGMT promoter were independent protective factors for PFS in the GBM patients(all P＜0.05).Conclusion The clinical and prognostic features are totally different between IDH mutant and wild-type GBM,and molecular detections are needed for the further pathological classification.Methylation of MGMT promoter is a primary marker of favorite prognosis for IDH wild-type GBM,and slightly delay in radiotherapy(the 5th to 6th week after surgery)can effectively improve the survival prognosis of IDH wild-type GBM.

Objective:To observe the effect of combining robot-assisted gait training (RAGT) with task-oriented training (TOT) on the walking ability of children with dyskinetic cerebral palsy (DCP).Methods:Sixty DCP children were randomly divided into a conventional intervention group, an RAGT group, and a combined intervention group, each of 20. All of the children received conventional rehabilitation therapy, while the RAGT and combined intervention groups were additionally provided with RAGT, and RAGT combined with TOT, respectively. Before the experiment and after 12 and 24 weeks of treatment, the subjects′ walking ability was evaluated using the 10-metre walk test (10MWT), and the D energy zone (standing position) and the E energy zone (walking, running and jumping) of the Gross Motor Function Measurement-88 (GMFM-88) instrument.Results:After 12 and 24 weeks of treatment, the average 10MWT speed and D and E energy zone scores of all three groups had improved significantly. After 24 weeks the combined group′s averages on all three measures were significantly better than those of the other two groups.Conclusion:RAGT combined with TOT and conventional rehabilitation training significantly improves the walking ability of DCP children.

Objective To investigate the mechanism mediating the regulatory effect of lncRNA MAGI2-AS3 on cisplatin(DDP)resistance in non-small cell lung cancer(NSCLC).Methods MAGI2-AS3 and miR-1269a expression levels were detected by qRT-PCR in DDP-sensitive lung cancer cell lines(A549 and H1299)and their resistant counterparts(A549/DDP and H1299/DDP).In A549 and H1299 cells with MAGI2-AS3 silencing and A549/DDP and H1299/DDP cells overexpressing MAGI2-AS3,the effects of 20 μmol/L DDP on cell viability and apoptosis were examined with CCK-8 assay,colony formation assay,flow cytometry and Western blotting,and the changes in epithelial-mesenchymal transition(EMT)were assessed with wound healing and Transwell assays.The interaction between MAGI2-AS3,miR-1269a and PTEN was predicted using GEPIA,StarBase and miRDB and verified with luciferase reporter gene assay and radioimmunoprecipitation(RIP)assay.A miR-1269a mimic and pcDNA3.1-PTEN plasmid were used to perform the rescue assay.Results MAGI2-AS3 expression was significantly downregulated in lung cancer tissues(P<0.05)in association with a poor prognosis(P<0.05).In the two DDP-resistant lung cancer cell lines,MAGI2-AS3 expression was significantly lowered as compared with the sensitive cells.Silencing MAGI2-AS3 significantly enhanced cell viability and promoted EMT of A549 and H1299 cells irrespective of DDP treatment,and also decreased DDP-induced apoptosis of the cells.In A549/DDP and H1299/DDP cells,MAGI2-AS3 overexpression strongly repressed cell viability and EMT irrespective of DDP treatment and promoted DDP-induced cell apoptosis.Luciferase reporter gene and RIP assays confirmed the binding of MAGI2-AS3 with miR-1269a and the binding of miR-1269a with 3'-UTR domain of PTEN.The rescue assay demonstrated that MAGI2-AS3 acted as a sponge for miR-1269a to promote PTEN expression and downregulate AKT phosphorylation,thus inhibiting EMT and promoting DDP-induced apoptosis of A549/DDP cells.Conclusion MAGI2-AS3 enhances DDP sensitivity of NSCLC by targeted regulation of the miR-1269a/PTEN/AKT signaling axis.

Objective:Previous studies have revealed a correlation between eosinophils and allergic rhinitis,but the causal relationship has not been fully confirmed.This study aims to evaluate the causal link between blood eosinophils and allergic rhinitis using the Mendelian randomization(MR)method. Methods:Summary data from the Genome-Wide Association Study Catalog(GWAS)for eosinophil count(exposure variable)and allergic rhinitis(outcome variable)were collected.GWAS data for the exposure variable were obtained from the IEU Open GWAS Project developed by the Integrative Epidemiology Unit at the University of Bristol,while data for the outcome variable were sourced from the FinnGen Biobank(Finland)database.The causal relationship between eosinophils and allergic rhinitis was analyzed using the two-sample MR method with inverse variance weighted(IVW)analysis.Sensitivity analyses were conducted using the weighted median method,MR-Egger regression,leave-one-out analysis,and funnel plots. Results:An increase in blood eosinophil count showed a potential causal relationship with an increased risk of allergic rhinitis(OR=1.187,95%CI 1.051 to 1.341,P=0.006).This finding was consistent across the weighted median method and MR-Egger regression.Leave-one-out analysis indicated that no single nucleotide polymorphism significantly influenced the causal inference. Conclusion:There is a causal association between increased eosinophil count and a higher risk or worsening of allergic rhinitis.

Objective To investigate the mechanism mediating the regulatory effect of lncRNA MAGI2-AS3 on cisplatin(DDP)resistance in non-small cell lung cancer(NSCLC).Methods MAGI2-AS3 and miR-1269a expression levels were detected by qRT-PCR in DDP-sensitive lung cancer cell lines(A549 and H1299)and their resistant counterparts(A549/DDP and H1299/DDP).In A549 and H1299 cells with MAGI2-AS3 silencing and A549/DDP and H1299/DDP cells overexpressing MAGI2-AS3,the effects of 20 μmol/L DDP on cell viability and apoptosis were examined with CCK-8 assay,colony formation assay,flow cytometry and Western blotting,and the changes in epithelial-mesenchymal transition(EMT)were assessed with wound healing and Transwell assays.The interaction between MAGI2-AS3,miR-1269a and PTEN was predicted using GEPIA,StarBase and miRDB and verified with luciferase reporter gene assay and radioimmunoprecipitation(RIP)assay.A miR-1269a mimic and pcDNA3.1-PTEN plasmid were used to perform the rescue assay.Results MAGI2-AS3 expression was significantly downregulated in lung cancer tissues(P<0.05)in association with a poor prognosis(P<0.05).In the two DDP-resistant lung cancer cell lines,MAGI2-AS3 expression was significantly lowered as compared with the sensitive cells.Silencing MAGI2-AS3 significantly enhanced cell viability and promoted EMT of A549 and H1299 cells irrespective of DDP treatment,and also decreased DDP-induced apoptosis of the cells.In A549/DDP and H1299/DDP cells,MAGI2-AS3 overexpression strongly repressed cell viability and EMT irrespective of DDP treatment and promoted DDP-induced cell apoptosis.Luciferase reporter gene and RIP assays confirmed the binding of MAGI2-AS3 with miR-1269a and the binding of miR-1269a with 3'-UTR domain of PTEN.The rescue assay demonstrated that MAGI2-AS3 acted as a sponge for miR-1269a to promote PTEN expression and downregulate AKT phosphorylation,thus inhibiting EMT and promoting DDP-induced apoptosis of A549/DDP cells.Conclusion MAGI2-AS3 enhances DDP sensitivity of NSCLC by targeted regulation of the miR-1269a/PTEN/AKT signaling axis.

As a common psychiatric disorder, the etiology and pathogenesis of depression are complex and not yet fully elucidated.The diagnosis of depression mainly depends on the patients’ medical history, clinical symptoms and related examinations.Identification of biomarkers will provide important clues for the specific diagnosis and targeted treatment of depression.In addition to the widely recognized neurotransmitter dysregulation, hypothalamus-pituitary-adrenal axis hyperactivity, neuroplasticity, and neuro-inflammation theory, oxidative stress is also involved in the pathogenesis of depression in multiple ways.Many studies showed that the heat shock protein 70(HSP70)levels will increase in early stage to cope with the stress in patients with depression.However, lower HSP70 levels are often correlated with more severe depressive symptoms.HSP70 may be involved in depression through multiple pathways of oxidative stress, glucocorticoid receptors, neuroinflammation and neuroplasticity.Furthermore, increasing HSP70 expression results in significant improvement in depression-like behavior in animals.Thus, HSP70 possesses potential value as an early warning marker for depression as well as a therapeutic target.

Objective:To explore the influence of chronic rhinitis on depressive symptoms of college freshmen and the mediating effect of avoidant personality.Methods:A cluster sampling method was used to survey 8 079 college freshmen from April 2018 to October 2018 using the Beck depression inventory and the avoidant personality diagnosis questionnaire based on DSM-Ⅳ.SPSS 25.0 software was used for descriptive statistics and Spearman correlation analysis, and the macro program PROCESS version 3.3 was used for the mediating effect.Results:(1) The detection rates of chronic rhinitis, avoidant personality and depressive symptoms were 22.90% (1 850/8 079), 19.22% (1 553/8 079) and 6.28% (507/8 079). The scores for avoidant personality disorder and depressive symptoms were 1.00 (0, 3.00) and 1.00 (0, 4.00), respectively. (2) The chronic rhinitis, avoidant personality and depressive symptoms were positively correlated ( rchronic rhinitis-avoidant personality=0.094, rchronic rhinitis-depressive symptoms=0.095, ravoidant personality-depressive symptoms=0.416, all P<0.001). (3) Chronic rhinitis could positively predict depressive symptoms ( β=1.113, P<0.001). (4) Avoidant personality played a mediating role between chronic rhinitis and depressive symptoms ( β=1.094, P<0.001), and accounted for 44.92%(0.500/1.113) of the total effect. Conclusion:Chronic rhinitis directly affect the depressive symptoms of college freshmen, and indirectly affect the depressive symptoms of college freshmen through the mediating role of avoidant personality.

Objective:To study the genetic profile of neonatal hyperbilirubinemia with unknown etiology in Guangdong Province and the clinical significance of jaundice-related genetic screening.Methods:From July to September, 2021, neonates with hyperbilirubinemia of unknown etiology born in different hospitals in Guangdong Province were studied. 24 neonatal jaundice-related exons were sequenced using targeted capture and high-throughput sequencing technology. The pathogenic variants were analyzed.Results:A total of 331 cases, 139 (42.0%) cases showed positive screening results with five diseases, including 65 (19.6%) cases of Gilbert syndrome, 48 (14.5%) cases of glucose-6-phosphate dehydrogenase (G6PD) deficiency,18 (5.4%) cases of sodium taurocholate cotransporting polypeptide deficiency, 4 (1.2%) cases of Citrin deficiency and 4 (1.2%) cases of Dubin-Johnson syndrome. 149 (45.0%) cases carried one or more genetic variants and 43 (13.0%) cases showed no clinically significant variants. The 8 high-frequency mutation loci (carrier rate >1%) are UGT1A1 gene c.211G>A and c.1091C>T, G6PD gene c.1466G>T and c.1478G>A, SLC10A1 gene c.800C>T, SLC25A13 gene c.852_855del TATG, HBB gene c.126_129delCTTT and c.316-197C>T.Conclusions:Genetic factors are important for neonatal hyperbilirubinemia with unknown etiology in Guangdong. The common pathogenic genes are UGT1A1, G6PD, SLC10A1, and SLC25A13 and the population carries high-frequency mutation loci. Therefore, genetic screening in neonates with hyperbilirubinemia of unknown etiology has important clinical significance.