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Abstract Objective The aim of this study was to evaluate the serum Syndecan-1 (SDC-1) levels in patients with immunoglobulin-A vasculitis (IgAV) in children and its relation with gastrointestinal involvements. Methods Sixty-eight children with IgAV and 48 healthy children were enrolled in this cross-sectional study. Clinical and related laboratory data were collected from a computerized hospital database. Serum SDC-1 was collected on admission prior to treatment. Results Forty-eight patients fully met the IgAV diagnostic criteria at admission (IgAV group), 20 patients with rash only and diagnosed IgAV during hospitalization (Purpura group). In IgAV group, 30 patients with gastrointestinal involvements (IgAV-GI group) and 18 patients without gastrointestinal involvements (IgAV-NGI group). SDC-1 serum levels were significantly higher in the IgAV group (86.37 ng/mL (IQR 59.16-117.14 ng/mL)) than in the controls (20.37 ng/mL (IQR 15.52-26.45 ng/mL)) and the Purpura group (32.66 ng/mL (IQR 14.87-49.89 ng/mL)). Additionally, SDC-1 (OR = 1.08) was independently associated with IgAV with a cut-off value (sensitivity and specificity) of 66.55 ng/mL (68.8%, 95.0%), and the area under the curve was 0.908. The serum SDC-1 levels of the IgAV-GI group (106.92 ± 50.12 ng/mL) were significantly higher than those in the IgAV-NGI group (67.52 ± 17.59 ng/mL). Logistic regression analysis showed that SDC-1 (OR = 1.03) was independently associated with IgAV-GI with a cut-off value of 89.39 ng/mL. Conclusions SDC-1 serum levels may mirror vascular endothelium injury and mucosal damage in IgAV. Its applicability as a surrogate biomarker in IgAV remains to be determined.
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OBJECTIVE: The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear. METHODS: KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR). RESULTS: KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression. CONCLUSION: KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.
Subject(s)
Humans , Esophageal Neoplasms/genetics , MicroRNAs/genetics , RNA, Long Noncoding/genetics , Esophageal Squamous Cell Carcinoma/genetics , Phosphatidylinositol 3-Kinases , Cell Proliferation/genetics , KCNQ1 Potassium Channel/geneticsABSTRACT
Objective:To investigate the effects of thyroxine (T 4) and propylthiouracil (PTU) on nitric oxide synthase expression in human umbilical vein endothelial cells (HUVEC cells). Methods:HUVEC cells were cultured in vitro, the experiment was divided into 6 groups: control (without T 4 and PTU), 10 -9, 10 -7, 10 -4 mol/L T 4, PTU (5 μg/ml PTU), and 10 -4 mol/L T 4 + PTU, the action time was 24 h. CCK-8 method was used to detect cell activity; nitrate reductase method was used to detect nitric oxide (NO), total nitric oxide synthase (TNOS) and endothelial nitric oxide synthase (eNOS) contents; Western blotting was used to detect eNOS protein expression level. Results:The differences of cell survival rates [(100.00 ± 0.00)%, (96.73 ± 1.17)%, (86.20 ± 7.54)%, (47.37 ± 9.10)%, (53.37 ± 5.47)%, (53.40 ± 8.84)%] among the 6 groups were statistically significant ( F = 29.42, P < 0.05). Compared with the control group, the cell survival rates of 10 -7, 10 -4 mol/L T 4, PTU, and 10 -4 mol/L T 4 + PTU groups were significantly reduced ( P < 0.05). There were statistically significant differences in the contents of NO and TNOS among the 6 groups ( F = 3.93, 3.46, P < 0.05). Compared with the control group, the TNOS content in PTU group was significantly reduced ( P < 0.05); compared with the 10 -4 mol/L T 4 group, the NO contents in PTU and 10 -4 mol/L T 4 + PTU groups were significantly reduced ( P < 0.05). There were no significant differences in eNOS content and protein expression level among the 6 groups ( F = 0.24, 0.17, P > 0.05). Conclusions:High concentration of T 4 can cause damage to the activity of HUVEC cells cultured in vitro, and PTU can alleviate it by regulating NO and TNOS. The specific mechanism of action still needs to be further studied in molecular biological experiments.
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More than 90％ of the iodine intake by the human body is excreted in the urine. Therefore, the urinary iodine excretion is a good indicator for measuring recent iodine intake of the human body. During pregnancy, pregnant women are in a special physiological stage, the intake and discharge of iodine are significantly different from other stages and crowds. At present, the evaluation criteria for urinary iodine levels in pregnant women in China adopt the World Health Organization/United Nations International Children's Emergency Fund/International Committee for the Control of Iodine Deficiency (WHO/UNICEF/ICCIDD) recommendation: the median urinary iodine range is 150 - 249 μg/L. However, this standard is scheduled in 2007, 12 years ago, and due to differences in race, geography, diet, etc., whether the international standards are applicable to China's actual situation deserves further study. This article reviews the current research status of the optimal range of urinary iodine in pregnant women in China, and provides reference for future iodine nutrition monitoring of pregnant women.
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Objective@#To observe the relationship between hyperthyroidism and vascular endothelial injury.@*Methods@#From 2016 to 2017, data of 60 patients with simple hyperthyroidism, autoimmune thyroid disease, cardiovascular and cerebrovascular diseases were collected from the Second Affiliated Hospital of Harbin Medical University. And 60 healthy subjects were enrolled in the same period as a healthycontrol group. The enzyme-linked immunosorbent assay (ELISA) was used to detect the content of vascular endothelial injury markers (vWF), thrombomodulin (TM), endothelin-1 (ET-1), P-selectin in serum of all subjects, as well as the serum thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), anti-thyroglobulin antibody (TgAb), and anti-thyroid peroxidase antibody (TPOAb) in patients with cardiovascular and cerebrovascular diseases levels. The correlation analysis of vascular endothelial injury in the simple hyperthyroidism group, autoimmune thyroid disease group, cardiovascular and cerebrovascular diseases group and healthy control group was conducted.@*Results@#There were statistically significant differences between the healthy control group, the simple hyperthyroidism group, the autoimmune thyroid disease group and the cardiovascular and cerebrovascular diseases group in the serum levels of vWF, TM, ET-1 and P-selectin, respectively(F = 6.56, 9.19, 7.88, 12.45, P < 0.05), and the simple hyperthyroidism group, autoimmune thyroid disease group, cardiovascular and cerebrovascular diseases group were significantly higher than the healthy control group (P < 0.05). Correlation analysis showed that the vascular endothelial injury in the patients with simple hyperthyroidism, autoimmune thyroid disease, and cardiovascular and cerebrovascular diseases groups was statistically significantly different compared with the healthy control group, respectively(χ2 = 5.08, 5.08, 8.16, P < 0.05); the risk of vascular endothelial injury in each diseased group was 2.37, 2.37, and 3.07 times higher than that of the healthy control group, respectively. The abnormal rates of TSH, FT3, FT4, TgAb and TPOAb in patients with cardiovascular and cerebrovascular diseases were 18.33% (11/60), 15.00% (9/60), 15.00% (9/60), 10.00% (6/60) and 11.7% (7/60), respectively.@*Conclusion@#Simple hyperthyroidism and autoimmune thyroid disease are risk factors of vascular endothelial injury.
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Objective To observe the relationship between hyperthyroidism and vascular endothelial injury.Methods From 2016 to 2017,data of 60 patients with simple hyperthyroidism,autoimmune thyroid disease,cardiovascular and cerebrovascular diseases were collected from the Second Affiliated Hospital of Harbin Medical University.And 60 healthy subjects were enrolled in the same period as a healthycontrol group.The enzyme-linked immunosorbent assay (ELISA) was used to detect the content of vascular endothelial injury markers (vWF),thrombomodulin (TM),endothelin-1 (ET-1),P-selectin in serum of all subjects,as well as the serum thyroid stimulating hormone (TSH),free triiodothyronine (FT3),free thyroxine (FT4),anti-thyroglobulin antibody (TgAb),and anti-thyroid peroxidase antibody (TPOAb) in patients with cardiovascular and cerebrovascular diseases levels.The correlation analysis of vascular endothelial injury in the simple hyperthyroidism group,autoimmune thyroid disease group,cardiovascular and cerebrovascular diseases group and healthy control group was conducted.Results There were statistically significant differences between the he althy control group,the simple hyperthyroidism group,the autoimmune thyroid disease group and the cardiovascular and cerebrovascular diseases group in the serum levels of vWF,TM,ET-1 and P-selectin,respectively (F =6.56,9.19,7.88,12.45,P ＜ 0.05),and the simple hyperthyroidism group,autoimmune thyroid disease group,cardiovascular and cerebrovascular diseases group were significantly higher than the healthy control group (P ＜ 0.05).Correlation analysis showed that the vascular endothelial injury in the patients with simple hyperthyroidism,autoimmune thyroid disease,and cardiovascular and cerebrovascular diseases groups was statistically significantly different compared with the healthy control group,respectively (x2 =5.08,5.08,8.16,P ＜ 0.05);the risk of vascular endothelial injury in each diseased group was 2.37,2.37,and 3.07 times higher than that of the healthy control group,respectively.The abnormal rates of TSH,FT3,FT4,TgAb and TPOAb in patients with cardiovascular and cerebrovascular diseases were 18.33％ (11/60),15.00％ (9/60),15.00％ (9/60),10.00％ (6/60) and 11.7％ (7/60),respectively.Conclusion Simple hyperthyroidism and autoimmune thyroid disease are risk factors of vascular endothelial injury.
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Objective To explore the changes and clinical significance of interleukin-1β (IL-1 β) and aquaporin 4 (AQP4) in children with hand-foot-mouth disease (HFMD) combined with encephalitis.Methods From January 2014 to June 2016,30 cases of HFMD patients without encephalitis in Wuxi Children's Hospital were selected as the general group,at an average age of (2.1 ± 1.1) years,including 13 male and 17 female.Thirty cases of HFMD combined with encephalitis were selected as the observation group,at an average age of (2.4 ± 1.2)years,including 12 male and 18 female.Twenty-six non-HFMD patients who underwent minor operations for inguinal hernia or hydrocele of testis were selected as the serum control group,including 25 male and 1 female.Twenty-six patients with non-infectious neurological disorders in the neurology department in the same period were selected as the cerebrospinal fluid control group,including 10 male and 16 female.The levels of AQP4 and IL-1β in children were detected by adopting enzyme-linked immuno sorbent assay(ELISA).Results The levels of IL-1β in cerebrospinal fluid in the acute phase and recovery phase of the observation group were (95.04 ± 20.06) ng/L and (77.63 ±14.51) ng/L respectively,while the levels of AQP4 in cerebrospinal fluid were (16.87 ± 10.02) ng/L and (9.13 ±6.64) ng/L respectively.The levels of IL-1β in serum in the acute phase of the observation group and the general group were (82.40 ± 18.56) ng/L and (50.20 ± 24.22) ng/L respectively.The levels of IL-1β,AQP4 in cerebrospinal fluid were significantly higher in the acute phase of the observation group compared with the controls,and the differences were statistically significant(all P ＜ 0.05).The levels of IL-1β and AQP4 in the recovery phase were lower than those in the acute stage,and the differences were statistically significant(all P ＜ 0.05).The levels of IL-1β in serum was significantly higher in the acute phase of the observation group compared with the general group,and the difference was statistically significant (P ＜ 0.05).The level of IL-1β in serum were significantly higher in the general group compared with the controls,and the difference was statistically significant (P ＜ 0.05).Conclusions AQP4 and IL-1β may participate in the pathological course of HFMD combined with encephalitis by promoting brain edema,which can be used as one of the laboratory indicators for early diagnosis of the severity of the disease.
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<p><b>OBJECTIVE</b>To investigate the incidence of congenital adrenal hyperplasia (CAH) and treatment outcomes in neonates in Ningxia, China.</p><p><b>METHODS</b>The clinical data of CAH screening for 160 046 neonates who were born in midwifery institutions in Ningxia from July 2014 to March 2016 were analyzed.</p><p><b>RESULTS</b>Among the 160 046 neonates who underwent CAH screening, 70 (0.044%) obtained a positive result and 11 were diagnosed with CAH; the incidence rate of CAH was 1/14 550 (0.069‰). Among the 11 neonates diagnosed with CAH, 9 had the salt wasting type (2 died) and 2 had simple virilization. The 9 neonates were given glucocorticoids immediately once diagnosed and all of them achieved good growth and development.</p><p><b>CONCLUSIONS</b>The incidence of neonatal CAH in Ningxia is 1/14 550. It is very necessary to carry out CAH screening in Ningxia, and active treatment can improve the prognosis of neonates with CAH.</p>
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Female , Humans , Infant, Newborn , Male , Adrenal Hyperplasia, Congenital , Diagnosis , Epidemiology , Therapeutics , China , Epidemiology , Follow-Up Studies , PrognosisABSTRACT
Pituitary adenomas (PAs) are well known as a common intracranial benign tumor, and a portion of PAs are refractory to current therapeutic methods. ErbB receptors family signaling pathway regulates the expression of PAs activation associated gene. Inhibition of epidermal growth factor receptor (EGFR) can inhibit proliferation of PAs. Leucine-rich repeats and immunoglobulin-like domains protein 1 ( LRIG1), a negative mediated gene of ErbB receptors family, plays a role in many tumors. However, there are seldom researches about the functional role of LRIG1 in PAs. The aim of this study is to explore the potential effect of LRIG1 and its regulating mechanism in PAs. First, we investigated the role of LRIG1 in cell migration, invasion of PAs with transfected LRIG1 or control. Then, we explored its impact on cell proliferation and apoptosis of PAs in vivo. To study the regulating mechanism of LRIG1, we examined the expression of molecular factor of PI3K/AKT and Ras/Raf/ERK pathway using Western blotting in vitro and RT-PCR in vitro and in vivo. It was found that LRIG1 over-expression inhibited cell migration, invasion and proliferation, and promoted apoptosis of PAs in vivo and in vitro. Furthermore, LRIG1 suppressed the expression of signaling of PI3K/AKT and Ras/Raf/ERK pathways in PAs. LRIG1, as a negative mediated gene of tumor, can inhibit biological function of PAs via inhibiting PI3K/AKT and Ras/Raf/ERK pathways, and it might be a new target for gene therapy of PAs.
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Animals , Female , Humans , Mice , Apoptosis , Genetics , Brain Neoplasms , Genetics , Pathology , Cell Line, Tumor , Cell Movement , Genetics , Cell Proliferation , Genetics , Gene Expression Regulation, Neoplastic , MAP Kinase Signaling System , Genetics , Membrane Glycoproteins , Genetics , Oncogene Protein v-akt , Phosphatidylinositol 3-Kinases , Genetics , Pituitary Neoplasms , Genetics , Pathology , Xenograft Model Antitumor Assays , raf Kinases , GeneticsABSTRACT
Sonic hedgehog(Shh) is a member of the hedgehog family in vertebrate. The Shh signaling pathway is mainly composed of a secreted glycoprotein, named Shh, two transmembrane proteins (Ptch and Smo) and the downstream transcription factor family Glis. It plays a vital role in the embryo development, especially in the neuronal system. Recent study have demonstrated that the Shh pathway is closely associated with the tumorigenesis of various tumors. Glioma, the most common malignant brain tumor of humans, is characterized by the rapid proliferation, infiltrative growth and high rate of relapse, and it is one of the brain tumors with poorest prognosis. Abnormal activation of multiple signaling pathways has been known to enhance the proliferation ability of glioma cells. Moreover, glioma is composed of various tumor cells and the glioma stem cells were endowed with the ability of self-renewal and unlimited proliferation, which plays a key role in the tumorigenesis, progress and relapse. Evidence has been found that Shh signaling pathway is closely assoicated with tumorigenesis of glioma. Herein we review the current knowledge on the components of Shh signaling pathway and its role in the tumorigenesis of glioma and glioma stem cells.
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<p><b>OBJECTIVE</b>To investigate epidermal growth factor receptor (EGFR) gene mutations in exons 19 and 21 of patients with non-small cell lung cancer (NSCLC) and to analyze the relationship of EGFR mutations with clinicopathological features and prognosis.</p><p><b>METHODS</b>The EGFR gene exons 19 and 21 of paraffin-embedded tumor tissue were amplified by PCR, followed by direct sequencing in 282 surgically-removed specimens of NSCLC. The relationship of EGFR gene mutations in NSCLC with clinicopathological features and prognosis were analyzed.</p><p><b>RESULTS</b>EGFR mutations were detected in 120 of 282 (42.6%) patients with NSCLC. There were 61 cases of the mutations in exon 19 and 66 cases of the mutations in exon 21, including 7 cases of the mutations both in exons 19 and 21. Mutations were more frequently observed in women (55.2%, 53/96) than in men (36.0%, 67/186), in 51 to 60-years-old (51.3%, 39/76) than ≤50-years-old (30.4%, 21/69) and >60-years-old (43.8%, 60/137), in non-smokers (54.3%, 69/127) than smokers (32.9%, 51/155), there was negative correlation of EGFR mutations with smoking status (P=0.000, rs=-0.216). EGFR mutations were more frequently observed in adenocarcinomas (47.8%, 64/134), bronchiolo-alveolar carcinomas (73.0%, 27/37), adenosquamous carcinomas (7/9) than squamous cell carcinomas (23.6%, 17/72) and other types (16.7%, 5/30). The EGFR mutation rate in the well differentiated, the middle differentiated, the poorly differentiated and the undifferentiated was 55.7% (68/122), 50.8% (30/59), 22.7% (17/75), 19.2% (5/26) respectively, the incidences of EGFR mutations decreased with the degrading of differentiation, there was positive correlation of EGFR mutations with differentiation of lung cancer (P=0.000, rs=0.296). The patients with EGFR mutations had better prognosis than those with wild-type EGFR (P=0.027). There was no association of EGFR mutations with clinical TNM stage.</p><p><b>CONCLUSIONS</b>EGFR mutations occur frequently in females, non-smokers and adenocarcinomas, bronchioloalveolar carcinomas, and adenosquamous carcinomas. The patients with EGFR mutations have better prognosis. The results may offer a practical approach to select the patients who may benefit from anti-EGFR target therapy.</p>