Analysis of iodine nutrition monitoring results of pregnant women in Suqian City, Jiangsu Province from 2016 to 2020 / 中华地方病学杂志

Objective:To learn about the iodine nutritional status of pregnant women in Suqian City, Jiangsu Province, and to provide evidence for scientific supplementation of iodine of pregnant women.Methods:From May 2016 to July 2020, five sampling districts were divided in each county (district) of Suqian City according to the oriation of east, west, south, north and center each year. One township (street) was selected from each district, and 20 pregnant women who lived in the local area for more than half a year were selected from each township (street). The 30 g of household salt samples of pregnant women and 5 ml of urine samples at random once were collected to test the salt iodine and urinary iodine content.Results:A total of 2 483 household salt samples of pregnant women were tested, and the median salt iodine was 23.9 mg/kg; among them, 2 454 were iodized salt, and the coverage rate of iodized salt was 98.8%; the qualified iodized salt was 2 383, the qualified rate of iodized salt was 97.1%, and the consumption rate of qualified iodized salt was 96.0%. There were statistically significant differences in coverage rate of iodized salt, qualified rate of iodized salt and consumption rate of qualified iodized salt between different years (χ 2 = 10.55, 13.23, 11.37, P < 0.05). A total of 2 483 urine samples of pregnant women were tested, and the median urinary iodine was 167.6 μg/L, which was at the appropriate iodine level. However, the median urinary iodine of pregnant women in 2020 was 146.7 μg/L, lower than the WHO/UNICEF/ICCIDD recommendation standard (150 μg/L). The differences of median urinary iodine of pregnant women in different years, pregnancy periods and regions were statistically significant ( H = 26.08, 8.17, 19.87, P < 0.05). Conclusions:The coverage rate of iodized salt, qualified rate of iodized salt and consumption rate of qualified iodized salt in Suqian City , meet the national standard for eliminating iodine deficiency disorders. Iodine nutrition of pregnant women in Suqian City is at an appropriate iodine level, but some pregnant women may have iodine deficiency.

Function of AXL and molecular mechanisms in regulation of nasopharyngeal carcinoma / 中南大学学报(医学版)

OBJECTIVES@#Nasopharyngeal carcinoma (NPC) is a highly invasive epithelial malignant tumor with unique geographical and ethnic distribution characteristics. NPC is mostly found in south China and Southeast Asia, and its treatment mainly depends on radiotherapy and chemotherapy. However, NPC is usually found in the late stage, and local recurrence and distant metastasis are common, leading to poor prognosis. The receptor tyrosine kinase AXL is up-regulated in various tumors and it is involved in tumor proliferation, migration, invasion, and other processes, which are associated with poor prognosis of tumors. This study aims to detect the expression of AXL in NPC cell lines and tissues, and to investigate its biological function of AXL and the underlying molecular mechanisms in regulation of NPC.@*METHODS@#The expression levels of AXL in normal nasopharyngeal epithelial tissues and NPC tissues were analyzed by GSE68799, GSE12452, and GSE53819 data sets based on Gene Expression Omnibus (GEO) database. The Cancer Genome Atlas (TCGA) database was used to analyze the relationship between AXL and prognosis of head and neck squamous cell carcinoma (HNSC). The indicators of prognosis included overall survival (OS), disease-free interval (DFI), disease-specific survival (DSS), and progression-free interval (PFI). Western blotting assay was used to detect the AXL protein expression levels in normal nasopharyngeal epithelial cell line and NPC cell lines. Immunohistochemical method was used to detect AXL expression levels in normal nasopharyngeal epithelial tissues and NPC tissues. Cell lines with stable AXL knockdown were established by infecting 5-8F and Fadu cells with lentivirus interference vector, and cell lines with stable AXL overexpression were established by infecting C666-1 and HK-1 cells with lentivirus expression vector. Real-time PCR and Western blotting were used to detect the efficiency of knockdown and overexpression in stable cell lines. The effects of AXL knockdown or overexpression on proliferation, migration, and invasion of NPC cells were detected by CCK-8, plate colony formation, and Transwell assays, and the effect of AXL knockdown on tumor growth in nude mice was detected by subcutaneous tumor formation assay. The sequence of AXL upstream 2.0 kb promoter region was obtained by UCSC online database. The PROMO online database was used to predict AXL transcription factors with 0% fault tolerance, and the JASPAR online database was used to predict the binding sites of ETS1 to AXL. Real-time PCR and Western blotting were used to detect the effect of ETS1 on AXL protein and mRNA expression. The AXL upstream 2.0 kb promoter region was divided into 8 fragments, each of which was 250 bp in length. Primers were designed for 8 fragments. The binding of ETS1 to AXL promoter region was detected by chromatin immuno-precipitation (ChIP) assay to determine the direct regulatory relationship between ETS1 and AXL. Rescue assay was used to determine whether ETS1 affected the proliferation, migration, and invasion of NPC cells through AXL.@*RESULTS@#Bioinformatics analysis showed that AXL was highly expressed in NPC tissues (P<0.05), and AXL expression was positively correlated with OS, DFI, DSS, and PFI in HNSC patients. Western blotting and immunohistochemical results showed that AXL was highly expressed in NPC cell lines and tissues compared with the normal nasopharyngeal epithelial cell line and tissues. Real-time PCR and Western blotting results showed that knockdown and overexpression efficiency in the stable cell lines met the requirements of subsequent experiments. The results of CCK-8, plate colony formation, Transwell assays and subcutaneous tumor formation in nude mice showed that down-regulation of AXL significantly inhibited the proliferation, migration, invasion of NPC cells and tumor growth (all P<0.05), and the up-regulation of AXL significantly promoted the proliferation, migration, and invasion of NPC cells (all P<0.05).As predicted by PROMO and JASPAR online databases, ETS1 was a transcription factor of AXL and had multiple binding sites in the AXL promoter region. Real-time PCR and Western blotting results showed that knockdown or overexpression of ETS1 down-regulated or up-regulated AXL protein and mRNA expression levels. ChIP assay result showed that ETS1 bound to AXL promoter region and directly regulate AXL expression. Rescue assay showed that AXL rescued the effects of ETS1 on proliferation, migration and invasion of NPC cells (P<0.05).@*CONCLUSIONS@#AXL is highly expressed in NPC cell lines and tissues, which can promote the malignant progression of NPC, and its expression is regulated by transcription factor ETS1.

Role of NO/cGMP signaling pathway in dexmedetomidine-induced reduction of neuropathic pain in rats / 中华麻醉学杂志

Objective To investigate the role of nitric oxide/cyclic guanosine monophosphate (NO/ cGMP) signaling pathway in dexmedetomidine-induced reduction of neuropathic pain (NP) in the rats.Methods Forty-two healthy male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 7 groups (n =6 each) using a random number table:normal control group (C group);NP group;dexmedetomidine group (D group);dimethyl sulfoxide (DMSO) group;a non-selective nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) group (L-NAME group);inactive enantiomer D-NAME group (D-NAME group);a soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxidazole[4,3-a] quinoxalin-1-one (ODQ) group (ODQ group).NP was induced by chronic constriction injury to the sciatic nerve in anesthetized rats.On day 7 after chronic constriction injury,dexmedetomidine 1.5 μg/kg was injected intrathecally in group D,and in DMSO,L-NAME,D-NAME and ODQ groups,DMSO l0 μl,L-NAME 100 μg,D-NAME 100 μg and ODQ 10 μg were injected intrathecally,respectively,and 25 min later dexmedetomidine 1.5 μg/kg was injected intrathecally.The thermal paw withdrawal latency was measured immediately after intrathecal administration and at 30,60,90,120,150,180 and 210 min after intrathecal administration,and the area under the curve of thermal paw withdrawal latency was calculated to reflect the thermal pain threshold.Results Compared with group C,the thermal pain threshold was significantly decreased in the other six groups (P＜0.05).The thermal pain threshold was significantly higher in D,DMSO,L-NAME,ODQ and D-NAME groups than in group NP (P＜0.05).Compared with group D,the thermal pain threshold was significantly decreased in L-NAME and ODQ groups (P＜0.05),and no significant change was found in the thermal pain threshold in D-NAME and DMSO groups (P＞0.05).Conclusion The mechanism by which dexmedetomidine reduces NP is related to activation of NO/cGMP signaling pathway in the rats.

Effects of lactoferrin on activity of PKG in spinal dorsal horn in a rat model of neuropathic pain / 中华麻醉学杂志

Objective To investigate the effects of lactoferrin on activity of PKG in spinal dorsal horn in a rat model of neuropathic pain(NP).Methods Thirty-two male SD rats weighing 200-250 g were randomly divided into4 groups(n = 8 each): sham operation group(group S),NP group,lactoferrin group and KT5823(an inhibitor of PKG)group.Neuropathic pain was produced by placing loosely constrictive ligatures around the common sciatic nerve in group NP,lactoferrin and KT5823,while the sciatic nerve was only exposed but not ligated in groupS.In group S and NP,normal saline 10 μl + 50% dimethyl sulfoxide(DMSO)10 μl were injected intrathecally.Lactoferrin 100 μg + 50% DMSO 10 μl were given intrathecally in group lactoferrin.Lactoferrin 100 μg + KT5823 10 μl were given intrathecally in group KT5823.The paw withdrawal latency(PWL)to a thermal nociceptive stimulus was measured every 30 min within 180 min after administration.The rats were then sacrificed and the spinal cord was removed.The activity of PKG in the spinal dorsal horn was determined by immunofluorescence.Results Compared with group NP and KT5823,the PWL was significantly prolonged after administration in group lactoferrin and the PKG activity was significantly increased in group lactoferrin(P ＜ 0.05).There was no significant difference in the parameters mentioned above between group NP and group KT5823(P ＞ 0.05).Conclusion Lactoferrin reduces NP by inhibiting the activity of PKG in spinal dorsal horn in rats.