The fasting and 2 h levels of glucagon, somatostatin ( SS), and C-peptide during 75 g oral glucose tolerance test in 60 patients with type 2 diabetes and 34 normal subjects were determined. Compared with control group, the fasting levels of glucagon and SS and 2 h levels of SS after glucose loading significantly decreased,while the fasting and 2 h levels of C-peptide increased in diabetes group. The 2 h levels of these hormones were significantly higher than the fasting levels in two groups. Compared with control group, the increased folds of glucagon ( 1.40±0.48 vs 1.20±0. 30, P＜0. 05 ) and SS( 2.79±2. 17 vs 1.14±0. 22, P＜0. 01 ) levels after glucose loading were higher and that of C-peptide level ( 3.58 ±3. 10 vs 8. 33 ± 6. 99, P＜0. 01 ) was lower in diabetes group. The levels of fasting glucagon were positively correlated with that of fasting SS in two groups( both P＜0. 01 ). These results suggest that disturbance exists in hormones from α and δ cells besides the dysfunction of β cells in patients with type 2 diabetes.

ed in vitro and in vivo,which was inhibited by aspirin treatment.

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.

Objective:To explore the relationship between microsatellite instability (MSI) and Ki-67 expression level and the clinicopathological features of colorectal cancer, and investigate their impact for prognosis, so as to provide reference for prognostic judgment of colorectal cancer.Methods:The data of 183 patients who underwent radical colorectal cancer surgery and were diagnosed pathologically in the Department of General Surgery, the First Affiliated Hospital of Xinxiang Medical University from January 2017 to December 2019 were retrospectively analysed, including 101 males (55.2%)and 82 females(44.8%), ranged from 20 to 86 years and the mean age was(60.27±13.13)years. According to the results of mismatch repair protein immunohistochemical staining, the patients were divided into MSI-H group ( n=32) and MSI-L/MSS group ( n=151). According to the results of Ki-67 antigen immunohistochemical staining, the patients were divided into low Ki-67 expression group (<82.5%, n=136) and high Ki-67 expression group (≥82.5%, n=47) , among which 62 cases (78.5%) with low Ki-67 expression and 17 cases (21.5%) with high Ki-67 expression were in patients with Ⅲ+ Ⅳ stage colorectal cancer. The data of clinicopathological features, disease-free survival, and overall survival were collected and analyzed. The cotegorical variables were presented as n(%), and the comparisons between groups were performed using Chi-square test or Fisher′s exact test. The multivariate Logistic regression model was used to estimate the correlation between microsatellite instability and Ki-67 expression level and clinicopathologic characteristics of colorectal cancer. Kaplan-Meier survival curve and COX proportional hazards regression model were used to analyze the correlation between microsatellite instability and Ki-67 expression level and disease-free survival and overall survival. Results:Single factor analysis showed that the differences in gender ( χ2=4.37, P=0.037), tumor site ( χ2=26.40, P<0.001), tumor maximum diameter ( χ2=11.12, P=0.001) and nerve invasion ( χ2=5.53, P=0.019) between MSI-H group and MSI-L/MSS group were statistically significant. Multivariate Logistic regression model analysis showed that only gender ( OR=3.013, 95% CI: 1.183-7.672, P=0.021), tumor location ( OR=0.167, 95% CI: 0.067-0.419, P<0.001) and nerve invasion ( OR=0.202, 95% CI: 0.042-0.968, P=0.045) were independently correlative factors for MSI status. In Ⅲ+ Ⅳ stage colorectal cancers, the difference in tumor site between low Ki-67 expression group and high Ki-67 expression group was statistically significant( χ2=3.91, P=0.048). Multivariate Cox proportional hazards regression model analysis revealed that high Ki-67 expression ( HR=0.301, 95% CI: 0.118-0.768, P=0.012; HR=0.275, 95% CI: 0.083-0.912, P=0.035) and MSI-H ( HR=0.072, 95% CI: 0.010-0.525, P=0.009; HR=0.122, 95% CI: 0.017-0.900, P=0.039) were independently protective factors for disease-free survival and overall survival. Conclusions:MSI-H colorectal cancer is common in males, right-sided colonic cancers and non-neuroinvasive patients. In stage Ⅲ+ Ⅳ colorectal cancer, the expression level of Ki-67 in right-sided colonic cancer was lower than in left-sided colorectal cancer. Patients with MSI-H and high Ki-67 expressive colorectal cancer had longer disease-free survival, longer overall survival and better prognosis.

Objective: To study the effect of high-dose methylprednisolone intravenous pulse therapy on immunoglobulins and CD series in patients with active moderate-to-severe Graves′ orbitopathy. Methods: Twenty-seven patients with active moderate-to-severe Graves′ orbitopathy were enrolled in this study. All the patients received iv methylprednisolone pulse therapy for 12 weeks according to the 2016 European Thyroid Association/European Group on Graves′Orbitopathy(EUGOGO) Guidelines. Serum thyroidal autoantibodies, such as thyroid-stimulating hormone receptor antibody (TRAb), anti-thyroperoxidase antibody (TPOAb), and serum immunoglobulins, such as IgG, IgE, IgA, IgM were evaluated at the baseline, at the end of 4th and 12th week. Percentages of CD3⁺ T cells, CD4⁺ T cells, CD8⁺ T cells and CD19⁺ B cells, CD16⁺ or CD56⁺ NK cells were also evaluated at each time point. Results: TRAb, TPOA and IgE, IgG, IgA were significantly decreased both after 4th week and after 12th week (all P<0.05). Percentages of CD3⁺ T cells, CD4⁺ T cells and CD4⁺ /CD8⁺ ratio were gradually decreased after treatment. However, change of CD8⁺ T cells was not significant (P>0.05). Conclusion High-dose methylprednisolone may exert an immunosuppressive effect not only by modifying humoral and cellular immune functions, but also by decreasing serum immunoglobulins.