BACKGROUND:The pathogenesis of diabetic peripheral neuropathy has not yet been clarified,and TAM(Tyro3,Axl,and MerTK)receptor tyrosine kinases can control apoptotic cells and suppress inflammatory responses in the central nervous system. OBJECTIVE:To investigate the difference of Mer receptor tyrosine kinase(MerTK)levels in plasma and sciatic nerve tissue of Sprague-Dawley rats with type 2 diabetes and diabetic peripheral neuropathy,and to study the correlation between MerTK and diabetic peripheral neuropathy. METHODS:Forty male Sprague-Dawley were randomly divided into control group with 15 rats,type 2 diabetes group with 10 rats,and diabetic peripheral neuropathy group with 15 rats.The control group was fed with ordinary diet,while the experimental groups were fed with high-fat and high-sugar diet.After 6 weeks,intraperitoneal injection of streptozotocin at the minimum dose of 35 mg/kg was administered in the two experimental groups.After 14 days,tail vein blood was collected to detect blood glucose.If blood glucose≥16.7 mmol/L,the model of type 2 diabetes was successfully established.Rats in the diabetic peripheral neuropathy group continued to be fed with a high-sugar and high-fat diet for 8 weeks.The sciatic nerve conduction velocity of rats was detected through live isolation under anesthesia.Blood samples were collected from the abdominal aorta,and the sciatic nerve tissue was collected.Histological changes of nerve fibers in each group were observed under a light microscope to confirm the success of diabetic peripheral neuropathy modeling.ELISA was used to detect peripheral blood glucose,blood lipids and serum MerTK levels in rats;hematoxylin-eosin staining was used to observe the histological changes in the sciatic nerve;immunofluorescence,immunohistochemistry and western blot were used to detect the expression of MerTK in the sciatic nerve tissue. RESULTS AND CONCLUSION:The Sprague-Dawley rat models of type 2 diabetes and type 2 diabetes peripheral neuropathy were successfully constructed,and the modeling rate of diabetic peripheral neuropathy was 80%.Compared with the control group,the blood glucose levels of rats in the type 2 diabetes and diabetic peripheral neuropathy groups were significantly higher(P<0.000 1),while the blood glucose level in the diabetic peripheral neuropathy group was higher than that in the type 2 diabetes group;and the sciatic nerve conduction velocity was significantly decreased(P<0.05),which was lower in the diabetic peripheral neuropathy group than the type 2 diabetes group.Histological examination:Compared with the control group,the sciatic nerve nuclei were reduced in the type 2 diabetes group,with some vacuolar degeneration and phagocytosis;in the diabetic peripheral neuropathy group,the cell body was swollen,the nuclear spacing was increased,vacuolar degeneration was observed,and the myelin sheath was partitioned and unsmooth,and lattice-like axons appeared.Serum MerTK levels were significantly higher in the diabetic peripheral neuropathy group than the control group.Expression of MerTK in the sciatic nerve tissue was significantly upregulated in the diabetic peripheral neuropathy group compared with the control group(P<0.05).To conclude,elevated levels of MerTK in plasma and sciatic nerve tissue of rats with diabetic peripheral neuropathy are presumably related to its anti-inflammatory and immunomodulatory effects.

Methods: This study enrolled 40 patients with AIS, 20 patients with congenital scoliosis (CS), and 20 patients with spinal degenerative disease (SDD). All patients underwent open posterior surgery in our hospital, and a paravertebral muscle (multifidus muscle) biopsy was performed intraoperatively. This study included many indexes that describe muscle, especially dystrophin staining. The above pathological results were compared among the AIS, CS, and SDD groups. The correlation between the Cobb angle and Nash–Moe classification and the above pathological results was analyzed in patients with AIS. Results: Significant reductions in the dystrophin staining of dystrophin-1 (p<0.001), dystrophin-2 (p<0.001), and dystrophin-3 (p<0.001) were observed in the AIS group than in the CS and SDD groups. The higher the Nash–Moe classification in the AIS group, the more significant the loss of dystrophin-2 (p=0.042) in the convex paraspinal muscles. Additionally, a significantly positive correlation was observed between the reductions of dystrophin-2 on the concave side of the AIS group and Cobb angle (p=0.011). Conclusions Dystrophin protein deficiency in the paraspinal muscles plays a crucial role in AIS formation and progression. The severity of scoliosis in patients with AIS is correlated with the extent of dystrophin loss in the paravertebral muscles. Therefore, dystrophin dysfunction may be relevant to AIS occurrence and development.

Methods: This study enrolled 40 patients with AIS, 20 patients with congenital scoliosis (CS), and 20 patients with spinal degenerative disease (SDD). All patients underwent open posterior surgery in our hospital, and a paravertebral muscle (multifidus muscle) biopsy was performed intraoperatively. This study included many indexes that describe muscle, especially dystrophin staining. The above pathological results were compared among the AIS, CS, and SDD groups. The correlation between the Cobb angle and Nash–Moe classification and the above pathological results was analyzed in patients with AIS. Results: Significant reductions in the dystrophin staining of dystrophin-1 (p<0.001), dystrophin-2 (p<0.001), and dystrophin-3 (p<0.001) were observed in the AIS group than in the CS and SDD groups. The higher the Nash–Moe classification in the AIS group, the more significant the loss of dystrophin-2 (p=0.042) in the convex paraspinal muscles. Additionally, a significantly positive correlation was observed between the reductions of dystrophin-2 on the concave side of the AIS group and Cobb angle (p=0.011). Conclusions Dystrophin protein deficiency in the paraspinal muscles plays a crucial role in AIS formation and progression. The severity of scoliosis in patients with AIS is correlated with the extent of dystrophin loss in the paravertebral muscles. Therefore, dystrophin dysfunction may be relevant to AIS occurrence and development.

Methods: This study enrolled 40 patients with AIS, 20 patients with congenital scoliosis (CS), and 20 patients with spinal degenerative disease (SDD). All patients underwent open posterior surgery in our hospital, and a paravertebral muscle (multifidus muscle) biopsy was performed intraoperatively. This study included many indexes that describe muscle, especially dystrophin staining. The above pathological results were compared among the AIS, CS, and SDD groups. The correlation between the Cobb angle and Nash–Moe classification and the above pathological results was analyzed in patients with AIS. Results: Significant reductions in the dystrophin staining of dystrophin-1 (p<0.001), dystrophin-2 (p<0.001), and dystrophin-3 (p<0.001) were observed in the AIS group than in the CS and SDD groups. The higher the Nash–Moe classification in the AIS group, the more significant the loss of dystrophin-2 (p=0.042) in the convex paraspinal muscles. Additionally, a significantly positive correlation was observed between the reductions of dystrophin-2 on the concave side of the AIS group and Cobb angle (p=0.011). Conclusions Dystrophin protein deficiency in the paraspinal muscles plays a crucial role in AIS formation and progression. The severity of scoliosis in patients with AIS is correlated with the extent of dystrophin loss in the paravertebral muscles. Therefore, dystrophin dysfunction may be relevant to AIS occurrence and development.

Anxiety disorders are characterized by high prevalence and recurrence rate.Selective serotonin reuptake inhibitors(SSRIs)and cognitive behavioral therapy(CBT)are recommended as first-line treatments for anxiety disorders,while some patients do not response to either of these treatments.Therefore,exploring the neurobiological mechanisms associated with treatment response and valuable prognostic marker is of great value in guiding clinical decision making.Previous studies have reported an altered electroencephalogram(EEG)pattern in patients with anxiety disorders after treatment,and revealed a correlation between baseline EEG and treatment response,suggesting that EEG is of great value in predicting the treatment response in anxiety disorders.The purpose of this article is to delineate findings from a systematic review of the literature investigating the EEG signal in prognostic prediction and exploration of neurobiological mechanisms,so as to provide electrophysiological evidence for individualized treatment of anxiety disorders.Results of this review show that patients responding more strongly to negative emotional stimuli before treatment are more likely to benefit from SSRIs and CBT.After the CBT,no statistical difference is found in the amplitude of error-related negativity(ERN)and P1 component between pre-and post-procedure measurements,suggesting that CBT may not reduce anxiety symptoms by improving attention bias and behavioral monitoring.EEG indicators related to emotion perception under negative emotional stimuli at baseline,such as late positive potential(LPP),may be promising markers for predicting response to treatment in anxiety disorders.

Objective To investigate the interference effect of nitrite on the determination of 24 h urine total protein by pyrogallol red method and evaluate the feasibility of using vitamin C to correct this interference.Methods According to the CLSI EP7-A3 document,fresh urine specimens with 24 h urine total protein concentrations of 150 mg/L,500 mg/L and 1 000 mg/L were selected as control samples,and interfering samples containing different concentrations of sodium nitrite were prepared.The interference of nitrite was con-firmed through paired difference experiments,and the relationship between nitrite concentration and interference level was clarified u-sing dose-effect experiments.The effects of different concentrations of vitamin C on correcting the interference caused by 200 μg/mL so-dium nitrite were evaluated.Additionally,61 nitrite-positive and 40 nitrite-negative clinical specimens were collected to compare the relative differences before and after vitamin C correction to assess its clinical application value.Results In the paired difference exper-iments,200 μg/mL sodium nitrite had relative interferences of-157.8％and-36.2％on the determination of urine total protein of 150 mg/L and 500 mg/L respectively,which were significantly greater than 1/2TEa(22％).Although there was a-20.5％negative interference for the high concentration of 1 000 mg/L urine total protein,the interference was within the acceptable range.The dose-effect experiment results showed that as the nitrite concentration in urine increased,the negative interference on urine total protein de-tection also gradually increased.In the presence of 200 μg/mL sodium nitrite as the final concentration,the addition of 0.2 mg/mL vi-tamin C corrected the urine total protein at 150 mg/L and 500 mg/L to 148 mg/L(-1.1％)and 402 mg/L(-19.5％),respectively,both within the acceptable range.The relative differences produced by vitamin C correction in the nitrite-positive clinical specimen group were significantly higher than those in the nitrite-negative group(P＜0.01).Conclusions Nitrite produced negative interference on the determination of urine total protein by the pyrogallol red method,especially when the urine total protein is 150 mg/L,which needs attention of clinical laboratories.The addition of 0.2 mg/mL vitamin C could effectively correct the interference of nitrite in low-concentration of urine total protein specimens,showing potential clinical application value.

Objective:To explore the predictive value of the prognostic nutritional index (PNI) in concurrently infected patients with acute-on-chronic liver failure (ACLF).Methods:220 cases with ACLF diagnosed and treated at the First Affiliated Hospital of Xi'an Jiaotong University from January 2011 to December 2016 were selected. Patients were divided into an infection and non-infection group according to whether they had co-infections during the course of the disease. Clinical data differences were compared between the two groups of patients. Binary logistic regression analysis was used to screen out influencing factors related to co-infection. The receiver operating characteristic curve was used to evaluate the predictive value of PNI for ACLF co-infection. The measurement data between groups were compared using the independent sample t-test and the Mann-Whitney U rank sum test. The enumeration data were analyzed using the Fisher exact probability test or the Pearson χ2 test. The Pearson method was performed for correlation analysis. The independent risk factors for liver failure associated with co-infection were analyzed by multivariate logistic analysis. Results:There were statistically significant differences in ascites, hepatorenal syndrome, PNI score, and albumin between the infection and the non-infection group ( P ?

To explore the value of CNVPLUS ?-array in the diagnosis of the DMD gene. A retrospective study was performed on 96 children who were clinically diagnosed with Duchenne or Becker muscular dystrophies(DMD/BMD) at the Department of Pediatric Endocrinology and Genetics of Xinhua Hospital affiliated to Shanghai Jiaotong University School of Medicine from January 2014 to March 2023. DNA was extracted from these children′s peripheral blood and divided into two parts. Variations of the DMD gene were detected by using CNVPLUS ?-array and sequential testing of MLPA—NGS—Sanger. In the sequential method, single exon deletions detected by MLPA were first verified by polymerase chain reaction (PCR) and then were tested by Sanger′s sequencing if PCR results were normal. The results showed that, among 96 samples, 91 cases with the pathogenic variation of the DMD gene were detected by the CNVPLUS ?-array, including 76 cases with large deletion/duplication (copy number variation, CNV) and 15 cases with small variation (single nucleotide variant or small insertion/deletion, SNV/Indel). All samples were tested and diagnosed within 5 days. In contrast, 76 cases with pathogenic CNV and 20 cases with pathogenic SNV/Indel were detected in the DMD gene by sequential method. However, all of the experiments and diagnoses were completed within 48 days. Moreover, 5 cases with SNV/Indel in the DMD gene were correctly clustered after the operation mode was optimized. In summary, as a new micro-array integrating CNV and SNV probes, CNVPLUS ?-array can detect CNV and SNV/Indel in the DMD gene simultaneously while the application of CNVPLUS ?-array could save a lot of time and manpower. CNVPLUS ?-array had an excellent diagnostic performance for CNV of the DMD gene. As for SNV/Indel, the diagnostic performance was slightly poor and the operation mode should be optimized. If necessary, other testing technologies should be supplemented to reduce the risk of missed diagnosis.

Objective:To assess the application value of CNVPLUS ?-array for the genetic analysis of spinal muscular atrophy (SMA). Methods:From June 2021 to December 2022, CNVPLUS ?-array technique was employed to test the SMN1 and SMN2 genes among peripheral blood samples from 17 suspected SMA patients, 18 core families with suspected SMA, and 25 healthy individuals. The results were compared with those of multiple ligation-dependent probe amplification (MLPA) assay. Samples with inconsistent results were subjected to nested PCR or comprehensive analysis of SMA. This study was approved by the Shanghai Institute for Pediatric Research, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine (Ethics No. XHEC-D-2024-038). Results:CNVPLUS ?-array has identified 35 SMA patients, 36 carriers, and 25 healthy individuals. In comparison, MLPA has identified 34 SMA patients, 36 carriers, and 26 healthy individuals. The two methods demonstrated a high consistency ( Kappa = 0.968, P<0.001). Additionally, CNVPLUS ?-array has identified one patient with compound heterozygous variants of SMN1 and one carrier with a [2+ 0] genotype. Conclusion:CNVPLUS ?-array not only can accurately determine the copy numbers of SMN1 and SMN2 genes, but also identify point mutations in SMN1 and [2+ 0] carriers, which has offered a new method for the genetic testing of SMA.

To explore the value of CNVPLUS ?-array in the diagnosis of the DMD gene. A retrospective study was performed on 96 children who were clinically diagnosed with Duchenne or Becker muscular dystrophies(DMD/BMD) at the Department of Pediatric Endocrinology and Genetics of Xinhua Hospital affiliated to Shanghai Jiaotong University School of Medicine from January 2014 to March 2023. DNA was extracted from these children′s peripheral blood and divided into two parts. Variations of the DMD gene were detected by using CNVPLUS ?-array and sequential testing of MLPA—NGS—Sanger. In the sequential method, single exon deletions detected by MLPA were first verified by polymerase chain reaction (PCR) and then were tested by Sanger′s sequencing if PCR results were normal. The results showed that, among 96 samples, 91 cases with the pathogenic variation of the DMD gene were detected by the CNVPLUS ?-array, including 76 cases with large deletion/duplication (copy number variation, CNV) and 15 cases with small variation (single nucleotide variant or small insertion/deletion, SNV/Indel). All samples were tested and diagnosed within 5 days. In contrast, 76 cases with pathogenic CNV and 20 cases with pathogenic SNV/Indel were detected in the DMD gene by sequential method. However, all of the experiments and diagnoses were completed within 48 days. Moreover, 5 cases with SNV/Indel in the DMD gene were correctly clustered after the operation mode was optimized. In summary, as a new micro-array integrating CNV and SNV probes, CNVPLUS ?-array can detect CNV and SNV/Indel in the DMD gene simultaneously while the application of CNVPLUS ?-array could save a lot of time and manpower. CNVPLUS ?-array had an excellent diagnostic performance for CNV of the DMD gene. As for SNV/Indel, the diagnostic performance was slightly poor and the operation mode should be optimized. If necessary, other testing technologies should be supplemented to reduce the risk of missed diagnosis.