Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Chemical cleaning and disinfection are crucial steps for eliminating infection in root canal treatment.However,irrigant selection or irrigation procedures are far from clear.The vapor lock effect in the apical region has yet to be solved,impeding irrigation efficacy and resulting in residual infections and compromised treatment outcomes.Additionally,ambiguous clinical indications for root canal medication and non-standardized dressing protocols must be clarified.Inappropriate intracanal medication may present side effects and jeopardize the therapeutic outcomes.Indeed,clinicians have been aware of these concerns for years.Based on the current evidence of studies,this article reviews the properties of various irrigants and intracanal medicaments and elucidates their effectiveness and interactions.The evolution of different kinetic irrigation methods,their effects,limitations,the paradigm shift,current indications,and effective operational procedures regarding intracanal medication are also discussed.This expert consensus aims to establish the clinical operation guidelines for root canal irrigation and a position statement on intracanal medication,thus facilitating a better understanding of infection control,standardizing clinical practice,and ultimately improving the success of endodontic therapy.

Objective:To explore the risk factors of diabetic nephropathy in type 2 diabetes patients, establish a risk prediction model for diabetic nephropathy and provide scientific reference for the prevention and screening of diabetic nephropathy.Methods:Clinical data of 1 223 patients admitted at Department of Endocrinology, General Hospital of Ningxia Medical University from January 2018 to December 2022 were retrospectively collected. In the training set, LASSO regression analysis and 10-fold cross-validation were used to screen the optimal feature variables by RStudio 4.2.1 software, and then multivariate logistic regression analysis was used to determine the final predictors selected from LASSO regression to construct the risk prediction model and draw the nomogram diagram. The receiver operating characteristic curve, C-index, calibration curve, and Hosmer-Lemeshow test were used to assess the discrimination and accuracy of the model; and the decision curve analysis was used to assess the clinical validity of the model.Results:The multivariate logistic regression analysis showed that the duration of diabetes, glycosylated hemoglobin [odds ratio ( OR) = 1.14, 95% confidence interval ( CI): 1.05-1.24], serum creatinine ( OR = 1.02, 95% CI: 1.01-1.04), 25-(OH)-D ( OR = 0.97, 95% CI: 0.95-1.00) were the best predictors of diabetic nephropathy in patients with type 2 diabetes ( P < 0.05). The predictive model was constructed by plotting the nomogram graph based on the predictor variables. In the training cohort, the diabetic nephropathy risk model displayed medium predictive power with a C-index of 0.762 (95% CI: 0.734-0.790). Meanwhile, the risk model was also well validated in the validation set, where the C-index was 0.742 (95% CI: 0.689-0.790). Hosmer-Lemeshow test showed excellent degree of fit ( P = 0.108), and the results of the decision curve analysis showed that the prediction model could be clinically beneficial. Conclusion:The establishment of the risk prediction nomogram model provides clinicians with a more convenient and scientific method for early screening and prevention of diabetic nephropathies.

Objective:To investigate the prevalence of influenza, pneumococcal, hepatitis B virus (HBV), human papillomavirus (HPV), and varicella zoster virus (VZV) vaccination in patients with systemic lupus erythematosus (SLE), and to analyze the factors related to vaccination.Methods:Data were obtained from 1 203 patients with SLE, via a multi-center web-based survey using an online questionnaire. Data about their social conditions, clinical presentations, willingness for being vaccinated, vaccination within 5 years were collected. Demographic data were shown by descriptive analysis. Chi-square and logistic regression analysis were used to assess the power of related indexes as predictors of vaccination.Results:The vaccination rates of influenza, pneumococcal, HBV, HPV, and VZV were 5.49% (66/1 203), 0.66% (8/1 203), 2.08% (25/1 203), 3.82% (46/1 203), and 0.17% (2/1 203), respectively. Data analysis showed that higher education ( χ2=30.94, P<0.001) and higher income ( χ2=10.70, P=0.001) had greater effects on influenza vaccination. There was a relationship between HPV vaccination and higher education ( χ2=20.96, P<0.001), higher income ( χ2=20.56, P<0.001), younger age ( χ2=8.54, P=0.001), and single ( χ2=5.63, P=0.018). Male ( χ2=10.27, P=0.001) and higher education ( χ2=4.52, P=0.034) were associated with HBV vaccination. The multivariate logistic regression analysis revealed that higher education [ OR (95% CI)=2.14 (1.10, 4.18), P=0.026], having children under 18 years-old [ OR(95% CI)=1.802(1.02, 3.18), P=0.042], and hydroxychloroquine usage [ OR(95% CI)=2.55(1.06, 6.15), P=0.037], had a positive correlation with influenza vaccination. Male [ OR(95% CI)=4.24(1.37, 13.08), P=0.012], had an impact on HBV vaccination. The factors related to HPV vaccination included age <45 [ OR (95% CI)=0.93(0.89, 0.97), P=0.001], higher education [ OR(95% CI)=2.28(1.11, 4.65), P=0.024], higher income [ OR(95% CI)=2.68(1.32, 3.41), P=0.006] and the usage of immunosuppressive agents [ OR(95% CI)=1.92(1.03, 3.59), P=0.041]. Conclusion:The prevalence of vaccination in patients with SLE is low. Patients with higher education and income are more likely to being vaccinated.

Objective:To investigate the efficacy and adverse reactions of moderately hypofractionated intensity modulated radiation therapy (IMRT) combined with androgen deprivation therapy (ADT) for locally advanced prostate cancer (LAPC).Methods:This study retrospectively analyzed the medical records of 40 LAPC patients who were admitted in The Second Hospital of Dalian Medical University during 2014-2020. The planning gross target volume (PGTV) dose for prostate gland and seminal vesicle gland was 64.8-70.0 Gy/25-28 f, 2.4-2.8 Gy/f and the dose of PGTVnd in 20 cases with positive pelvic lymph nodes was 60.0-64.4 Gy/25-28 f, 2.3-2.4 Gy/f. The dose of planning target volume (PTV) for the drainage area of pelvic lymph nodes was 45.0-50.4 Gy/25-28 f. The enrolled patients were treated with long-term ADT, including neoadjuvant, simultaneous, and adjuvant therapies. The efficacy and adverse reactions were evaluated. The prognostic factors affecting the biochemical failure-free survival (BFFS) were analyzed.Results:The median follow-up time was 31 months. The 2- and 3-year overall survival (OS) rates were 100% and 96.9%, respectively. The 1-, 2-, and 3-year BFFS rates were 90%, 76.8% and 72%, respectively. The 1-, 2-, and 3-year distant metastasis-free survival (DMFS) rates were 92.2%, 82.8% and 75.1%, respectively. Gleason (GS) score ( χ2=10.00, P < 0.05) and adjacent tissue invasion ( χ2=8.85, P<0.05) were prognostic factors related to BFFS for LAPC. Adjacent tissue invasion and GS 9-10 were independent poor prognostic factors. The incidence of acute urinary adverse reaction and rectal injury (grade≥2) was 7.5% and 20%, respectively. The incidence of late urinary adverse reaction and rectal injury (grade≥2) was 12.5% and 17.5%, respectively. Adverse reactions at grade 3-4 did not occur. Conclusions:The moderately hypofractionated IMRT combined with ADT is feasible for LAPC treatment, achieving satisfactory survival effects. 70 Gy/25-28 f, 2.5-2.8 Gy/f is a safe and effective moderate hypofraction scheme. Adjacent tissue invasion and GS score are prognostic factors related to BFFS for LAPC.

Abstract Flexibleis an important classification of flat foot. Flatfoot occurs due to a variety of reasons and causes the medial longitudinal arch to collapse or disappear. However, many children still do not develop a normal foot arch as the grow, and a failure to intervene in a timely manner will greatly harm a child s normal mobility development. Timely detection and intervention are the key to improve the prognosis. There is a lack of uniform quantitative criteria for the diagnosis of flexible flatfoot. Currently, the commonly used diagnostic methods include physical examination, foot printing, plantar pressure test and imaging examination. This article reviews the risk factors, diagnosis, prevention and treatment of Flexible Flatfoot.

Objective:To investigate the role and mechanism of N 6-methyladenosine (m 6A) methyltransferase-like 3 (METTL3) in vascular calcification (VC) of chronic kidney disease (CKD) through apoptosis-associated protein. Methods:(1) Real-time fluorescence quantitative PCR was used to test METTL3 mRNA in serum of maintenance hemodialysis (MHD) patients. (2) Western blotting was used to detect the expression of METTL3 protein in high-phosphorus stimulated vascular smooth muscle cells (VSMCs), and immunofluorescence double lable was used to observe the distribution of METTL3 and Runt-related transcription factor 2 (Runx2). The METTL3 overexpressed and knockdown plasmids were constructed and transfected into VSMCs. Alizarin red staining was used to detect calcification degree. Western blotting was used to detect the expressions of osteogenic markers [Runx2, bone morphogenetic protein-2(BMP-2), collagen Ⅰ] and apoptosis- related proteins Bax and Bcl-2. (3) SD rats were randomly divided into control group, CKD-VC group and S-adenosylhomocysteine (SAH) intervention group. The calcification of thoracic aorta was evaluated by von Kossa staining, and the protein expressions of Runx2, Bax and Bcl-2 were detected by immunohistochemistry and Western blotting.Results:(1) METTL3 mRNA expression in MHD patients with VC was significantly lower than that in non-VC patients ( P<0.05), and was negatively correlated with coronary artery calcium score ( r=-0.65, P<0.001). (2) The expression of METTL3 in VSMCs stimulated by high phosphorus was decreased and showed a time dependence. Immunofluorescence double label showed that METTL3 and Runx2 were co-expressed in the nucleus. METTL3 was overexpressed in high-phosphorus induced VSMCs, and the expressions of Runx2, collagen I and BMP-2 were significantly decreased, accompanied by the decrease of calcified nodules and Bax/Bcl-2 ratio (all P<0.05). Conversely, METTL3 knockdown aggravated VSMCs calcification by inducing apoptosis. (3) Furthermore, METTL3 inhibitor SAH was administered in vivo, and it was found that inhibition of METTL3 expression significantly increased the calcification of rat thoracic aorta, and the Bax/Bcl-2 ratio and Runx2 expression were up-regulated. Conclusions:Serum METTL3 level is reduced in MHD patients with VC. In vivo and in vitro studies demonstrate that METTL3 inhibits VC in CKD by mediating the apoptosis-related protein Bax/Bcl-2.

Objective　To investigate the etiology,clinical manifestations and neuroimaging features of the lesions of the middle cerebellar foot caused by different diseases.Methods　The general clinical data of 9 patients with bilateral middle cerebellar peduncle lesions admitted to our hospital from May 2016 to October 2021 were retrospectively analyzed,and the clinical manifestations and imaging characteristics of different diseases were analyzed.Results　Abnormal lesions were seen in 9 patients with middle cerebellar feet,including case 1:Speech slurred,left limb weakness for 3 months,dizziness,walking instability for 10 days previous pontine infarction,diagnosed as Walle’s degeneration.Case 2:Dizziness and unstable walking for 1 year after pontine hemorrhage,diagnosed as pontine hemorrhage and Waller’s degeneration of the bridge arm.Case 3:Presented with dizziness and walking instability for 2 years and was diagnosed with mu-ltiple system atrophy.Case 4:Memory loss for 2 months,aggravation for 10 days,previous rheumatoid arthritis,diagnosed as lupus encephalopathy.Case 5:Seizures of limbs,loss of consciousness for 3 days,chronic renal insufficiency in the past,diagnosed as renal encephalopathy.Case 6:Left lower limb weakness for 4 months,dizziness,seppch impairment for 2 days,diagnosed as neuromyelitis optic specturum disease.Case 7:Dizziness,walking instability for 15 days,HIV positive,diagnosed as HIV encephalopathy.Case 8:Clumsy handholding for 4 years,involuntary shaking for 2 days,diagnosis of Wilsonl’s disease.Case 9:Dizziness,unstable walking for 3 months,previous history of Hodgkin’s lymphoma,diagnosed as Hodgkin’s lymphoma with central nervous system damage.Conclusion　The etiology of the lesions of middle cerebellar foot is complex,attentions are needed in order to reduce clinical misdiagnosis and missed diagnosis.