Corrigendum to "SDF2L1 Inhibits Cell Proliferation, Migration, and Invasion in Nasopharyngeal Carcinoma".

[This corrects the article DOI: 10.1155/2020/1970936.].

Win55,212-2 improves neural injury induced by HIV-1 glycoprotein 120 in rats by exciting CB2R.

The occurrence and development of HIV-associated neurocognitive disorders (HAND) is related to synaptic injury and neuron loss, which gradually reduces the ability of learning and memory, and eventually leads to cognitive dysfunction. Human immunodeficiency virus type 1 (HIV-1) enveloped glycoprotein 120 (GP120) is the principal etiological agent of HIV-1-induced nerve damage and HAND. Our previous study demonstrated that GP120 can induce neuronal damage by increasing N-methyl-D-aspartic acid receptor (NMDAR) mediated excitatory postsynaptic currents (EPSCsNMDAR), In addition to neuroexcitotoxicity, the inflammatory response, oxidative stress, and neuronal apoptosis mediated by NMDAR overactivation are also involved in HAND. Because cannabinoids have known effects against neuroinflammation, stress response, and oxidative effects, we researched the effects of the cannabinoid receptor agonist Win55,212-2 [(R)-(+)-[2,3-dihydro-5-methyl-3 [(4-morpholinyl) methyl] pyrrolo [1,2,3-de]- 1,4-benzoxazinyl]-(1-naphthalenyl) methanone mesylate salt] on synaptic changes induced by GP120. In this study, we discovered that Win55,212-2 prevents GP120-induced neurological injury and cognitive dysfunction, and these effects are consistent with the neuroprotective effect of NMDAR blockers. In the Morris water maze (MWM) test, the results revealed that GP120 could induce learning and memory impairment in rats, while antagonizing NMDARs or activating CB2R could counteract GP120-induced cognitive dysfunction in rats; The results of TUNEL staining were consistent with the above results of MWM behavioral experiments. GP120 damaged hippocampal neurons in the CA1 region, while the NMDAR antagonist and cannabinoid 2 receptor (CB2R) agonist prevented GP120-induced effects. In molecular biology experiments, Our results showed that GP120 significantly upregulated the mRNA expressions of inflammatory factors IL-1ß, IL-6, TNF-α and CXCL10; Furthermore, GP120 significantly upregulated the protein expression level of pro-inflammatory cytokine IL-1ß and decreased the protein expression level of anti-inflammatory cytokine IL-10 as measured by ELISA. Additionally, in the GP120 group, the mRNA expression levels of pro-apoptosis factors such as Bax, CytC, and caspase-3, - 8 and - 9 were significantly increased while the expression level of anti-apoptotic factors Bcl-2 was significantly decreased (P < 0.05). Our studie also demonstrated that the mRNA expression levels of apoptotic pathway factors could be regulated by the p38 JNK MAPK pathway. But pretreatment with NMDAR antagonist memantine or CB2R agonist Win55,212-2 significantly reduced the expression levels of inflammatory factors and apoptotic factors. And the effects aroused by Win55,212-2 could be reversed by the CB2R antagonist AM630. These data suggest that the activation of the CB2R is neuroprotective against GP120-induced neurotoxicity, and CB2R agonist might play a potential therapeutic role in HAND.

[Methodological Evaluation of Microarray in the Detection of α-Thalassemia].

OBJECTIVE: To proceed the clinical evaluation of DNA microarray for thalassemia gene detection. METHODS: Peripheral blood samples of 166 thalassemia gene test subjects were collected and tested for thalassemia genes by microarray chip method and Gap-PCR method combined with PCR-reverse dot blot hybridization method according to double-blind control test. The specificity, sensitivity, positive predictive value, negative predictive value, and total coincidence rate of the microarray chip method were evaluated. When the two methods were inconsistent, multiplex ligation dependent probe amplification (MLPA) was used to verify the deletional α-thalassemia. RESULTS: Compared with Gap-PCR method, specificity, sensitivity, positive predictive value, negative predictive value, Youden index, and total coincidence rate of microarray chip method was 100% (70/70), 96.88% (93/96), 100% (93/93), 95.89% (70/73), 0.969, and 97.59% (162/166), respectively, while compared with PCR-reverse dot blot hybridization method was 100% (125/125), 100% (41/41), 100% (41/41), 100% (125/125), 1, and 100% (166/166), respectively. CONCLUSION: The microarray chip method for α-thalassemia gene detection shows the advantages of high specificity, sensitivity, and throughput.

[Application of DNA Microarray in Genetic Mutation Detection in Patients with Thalassemia].

OBJECTIVE: To perform dried blood spots thalassemia gene detection in patients with positive blood phenotypes by microarray technology, and evaluate its value in clinical detection. METHODS: DNA samples were extracted from dried blood spots of 410 patients. Microarray technology was used to detect 3 deletion and 3 non-deletion types of α-thalassemia and 19 ß-thalassemia point mutations which were common gene mutions in China. RESULTS: There were 357 positive cases in all the 410 tested samples with the positive rate 87.07%, among which 299 cases (72.93%) carried deletion or point mutations of α-thalassemia, 29 cases (7.07%) carried point mutations of ß-thalassemia and 29 cases (7.07%) carried gene mutations of complex αß-thalassemia syndrome. The mutations of α-thalassemia were involved with --SEA heterozygous deletion (177 cases, 59.2%), αCS heterozygote (60 cases, 20.07%) and several other genotypes. The common mutations of ß- thalassemia were involved with ßCD41-42 heterozygote (10 cases, 34.48%) and ßCD17 heterozygote (9 cases, 31.03%). The mutations of complex αß-thalassemia syndrome were mainly involved with --SEA/αα+ßCD17/ßN (7 cases, 24.14%), αCSα/αα + ßCD41-42/ßN (3 cases, 10.34%) and -α4.2/αα + ßCD17/ßN (3 cases, 10.34%). CONCLUSION: The most common genetic mutations are --SEA for α-thalassemia and CD41-42 for ß-thalassemia in Liuzhou, Guangxi Zhuang Autonomous Region. A and ß-thalassemia can be detected at the same time by microarray chip technology in a high throughput manner.

SDF2L1 Inhibits Cell Proliferation, Migration, and Invasion in Nasopharyngeal Carcinoma.

The purpose of this study was to explore the relationship between stromal cell-derived factor 2-like 1 (SDF2L1) and nasopharyngeal carcinoma (NPC). 12 NPC tissues and 12 chronic nasopharyngitis tissues were involved in our study. Quantitative real-time PCR (qRT-PCR) and Western Blot were utilized to detect the expression of SDF2L1. Besides, immunofluorescence analysis was utilized to determine the protein expression of 97 paraffin-embedded NPC tissues and 58 nasopharyngitis tissues. Biological functional experiment included Cell Counting Kit-8 (CCK-8) assay, cell clone formation assay, cell scratch migration assay, Transwell migration assay, and Transwell invasion assay. All data were analyzed by SPSS. Results showed that downexpression of SDF2L1 was prominently present in NPC tissues and cells. Furthermore, silencing the expression of SDF2L1 promoted NPC proliferation, migration, and invasion in vitro, while overexpression of SDF2L1 has the opposite effect. In conclusion, SDF2L1 may act as a cancer suppressor gene, play a crucial role in the occurrence and development of NPC, and be a new therapeutic target or prognostic indicator for NPC.

Analysis of rare thalassemia caused by HS-40 regulatory site deletion.

ABSTRACT Objectives: To investigate the effect of HS-40 regulatory site deletion on α-globin gene expression and its clinical significance. Methods: Venous blood samples of subjects were analyzed using a hematology analyzer and high- performance liquid chromatography; fetal cord blood was analyzed by a capillary electrophoresis analyzer. Gap-polymerase chain reaction (PCR), reverse dot blot (RDB), and multiple-link-dependent probe amplification (MLPA) were used for genotyping of thalassemia. Results: The proband was POLR3 K, HS-40 heterozygous deletion; the proband's wife was -SEA/αα; the fetus was POLR3 K, HS-40 heterozygous deletion combined with -SEA deletion; all of them had microcytic hypochromic anemia. Fetal umbilical cord blood electrophoresis revealed a suspected Hb Bart's band to be 88.4%, and the fetus was, thus, diagnosed as Hb Bart's fetus. The red blood cell parameters of the sporadic case showed that he had microcytic hypochromic anemia. Hemoglobin (Hb) electrophoresis analysis showed Hb H to be 5.3%, leading to a diagnosis of Hb H disease. Gap-PCR and RDB identified the genotype to be -α3.7/αα, ßA/ßA. MLPA detected heterozygous deletion or -α3.7 deletion on one allele and deletion of the HS-40 regulatory site on the other allele. Conclusion: The deletion of HS-40 regulatory site reduced expression of α-globin. HS-40 heterozygous deletion manifested as mild anemia, which was of microcytic hypochromic type. When compounded with -α3.7/αα, it manifested as Hb H disease; and when compounded with -SEA/αɑ, it manifested as Hb Bart's fetus.

[Analysis of beta-globin gene variants in Liuzhou area of Guangxi].

OBJECTIVE: To determine the composition and distribution of beta-thalassemia-associated genotypes in Liuzhou area of Guangxi, China. METHODS: From January to December 2017, 13 847 individuals who came for premarital examination, maternity examination or health check were recruited with informed consent. The subjects were analyzed by reverse dot blotting (RDB) for 17 common beta-thalassemia-associated variants among the Chinese population. Individuals with inconsistent results by blood test, electrophoresis, and RDB were subjected to Sanger sequencing to detect rare variants of the beta globin gene. RESULTS: In total 2098 individuals were found to harbor beta-thalassemia-associated variants, which included 2075 heterozygotes (98.90%), 12 compound heterozygotes (0.57%) and 11 homozygotes (0.52%). CD41-42 (48.43%) and CD17 (31.45%) were the most common variants. Three hundred and thirty eight-individuals were found to also carry heterozygous variants of the alpha globin gene, with the most common types being --SEA/aa, -a3.7/aa, aCSa/aa, -a4.2/aa. Through Sanger sequencing, rare genotypes such as beta-32/betaN, betaCD41-42/betaIVS-II-5 and betaCD30/betaN were detected. CONCLUSION: Liuzhou area has a high incidence of beta-thalassemia, but with a complex variant spectrum and clinical phenotypes different from other regions. Genetic counseling and prenatal diagnosis for the carrier population is crucial for the reduction of the related birth defects. Our result may provide valuable information for the prevention and control of beta-thalassemia in this area.

Pretreatment triglycerides-to-high density lipoprotein cholesterol ratio in postmenopausal women with endometrial cancer.

Raised triglycerides (TG) and reduced high density lipoprotein cholesterol (HDL-c) are components of metabolic syndrome. Both high TG and metabolic syndrome have been reported to be risk factors of endometrial cancer. Therefore, triglycerides-to-high density lipoprotein cholesterol ratio (TG/HDL-c ratio) may be a useful biological indicator in managing endometrial cancer. We aimed to explore the association between pretreatment TG/HDL-c ratio and endometrial cancer in postmenopausal women, and to evaluate its potential role in the disease. Pretreatment serum lipid profile and TG/HDL-c ratio were retrospectively analyzed for 167 postmenopausal women with endometrial cancer and 464 matched noncancer controls. Compared with controls, pretreatment TG/HDL-c ratio in endometrial cancer patients significantly elevated regardless of whether patients had diabetes or overweight/obesity (P < 0.05). Further analyses showed that pretreatment TG/HDL-c ratio increased significantly with advanced tumor stage. Interestingly, TG/HDL-c ratio of type I endometrial cancer patients was higher than those with type II endometrial cancer. A positive association was found between pretreatment TG/HDL-c ratio and tumor stage (adjusted r = 0.176, P = 0.027) in endometrial cancer group. Receiver operating characteristic curve analysis yielded the cut-off value of 1.52 for TG/HDL-c ratio to discriminate patients with cancer from controls (area under the curve, 0.689; sensitivity, 51.5%; specificity, 84.1%). Multivariate logistic regression model identified TG/HDL-c ratio ≥ 1.52 (odds ratio = 4.123; P < 0.001) as an independent predictor of endometrial cancer. TG/HDL-c ratio was positively associated with endometrial cancer clinical features, such as tumor stage and pathogenetic type. Accordingly, pretreatment TG/HDL-c ratio might be a potential marker for endometrial cancer.

Evaluation of the clinical value of hematological parameters in patients with urothelial carcinoma of the bladder.

This study aimed to evaluate the clinical significance of pretreatment red cell distribution width (RDW), monocyte/lymphocyte ratio (MLR), neutrophil/lymphocyte ratio (NLR), and platelet/lymphocyte ratio (PLR) in patients with urothelial carcinoma of the bladder (UCB).Hematological parameters of 127 consecutive patients with UCB and 162 healthy controls were retrospectively analyzed. Receiver operating characteristic curve was plotted to determine the optimal cut-off value of RDW, MLR, NLR, and PLR to predict UCB. Whether these parameters could be independent predictors of UCB and had an association with the demographics and clinical characteristics of patients were also assessed.Patients with UCB had higher pretreatment RDW, MLR, NLR, and PLR compared with the healthy controls. With the tumor progression, MLR, NLR, and PLR rose consistently, whereas no significant difference was observed in RDW across tumor stages. NLR and PLR were associated with tumor size and tumor grade, while MLR was correlated with tumor size only. The best threshold of RDW, MLR, NLR, and PLR to predict UCB was 13.50%, 0.26, 2.16, and 128.46, respectively. Multivariate logistic regression model identified NLR ≥ 2.16 (odds ratio [OR] = 2.914; P < .001) and PLR ≥ 128.46 (OR = 2.761; P < .001) as independent predictors of UCB. High NLR and PLR were also associated with tumor markers, such as carcinoembryonic antigen and α-fetoprotein.Pretreatment NLR and PLR could be significant independent predictors of UCB. These simple and readily available inflammatory markers therefore might be used to manage the disease.

Altered mean platelet volume in children with Henoch-Schonlein purpura and its association with disease activity.

Background Henoch-Schonlein purpura is a systemic small-vessel vasculitis that occurs mainly in children. A review of the literature has suggested a correlation between mean platelet volume and several inflammatory disorders. However, to the best of our knowledge, any potential correlation between mean platelet volume and Henoch-Schonlein purpura has not been reported in the literature. Therefore, our study aimed to evaluate the role of mean platelet volume concentrations in patients with Henoch-Schonlein purpura. Methods This study included 97 children with Henoch-Schonlein purpura and 120 healthy individuals as controls. Results Mean platelet volume concentrations were found to be significantly lower in Henoch-Schonlein purpura patients compared with healthy controls (8.1 ± 0.86 vs. 9.4 ± 0.81, P < 0.001). Similarly, significant negative correlations were observed between mean platelet volume and neutrophil count, platelet count and erythrocyte sedimentation rate in patients with Henoch-Schonlein purpura (r=-0.327, P = 0.001; r=-0.419, P < 0.001; r=-0.255, P = 0.012). Interestingly, mean platelet volume was significantly lower in the acute phase compared with the convalescent phase of Henoch-Schonlein purpura patients (7.8 ± 0.86 vs. 8.3 ± 0.77, P = 0.002). A cut-off value for mean platelet volume was 7.85 with area under the curve of 0.726 to identify acute phase vs. convalescent phase in patients with Henoch-Schonlein purpura. Mean platelet volume was independently associated with Henoch-Schonlein purpura in logistic regression analysis (odds ratio = 0.114, 95% confidence interval = 0.053-0.243, P < 0.001). Conclusions Our results suggest that mean platelet volume is inversely associated with disease in patients with Henoch-Schonlein purpura, and mean platelet volume may be a useful marker to identify active disease in Henoch-Schonlein purpura patients.

Is serum bilirubin associated with the severity of Guillain-Barré syndrome?

OBJECTIVE: Our aim was to assess the correlation between serum bilirubin levels and Guillain-Barré syndrome (GBS). PATIENTS AND METHODS: One hundred and one newly diagnosed patients with Guillain-Barré syndrome and 111 healthy age- and sex-matched individuals in the First Affiliated Hospital of Guangxi Medical University (Guangxi, China) from June 2012 to May 2017 were included in this study. Clinical characteristics and laboratory parameters of Guillain-Barré syndrome patients and healthy controls were retrospectively analysed. RESULTS: Serum bilirubin levels in Guillain-Barré syndrome patients were significantly lower as compared with those in healthy controls (p < 0.001); besides, log C-reactive protein and erythrocyte sedimentation rate were significantly higher. We found that there was a negative correlation between GBS disability scale scores and total bilirubin, direct bilirubin, indirect bilirubin (r = -0.541, P < 0.001; r = -0.403, P < 0.001; r = -0.526, P < 0.001), respectively. Among patients with GBS, serum total bilirubin, direct bilirubin, and indirect bilirubin levels were independently associated with Guillain-Barré syndrome disability scale scores in multiple linear regression analysis, respectively. CONCLUSIONS: We observed that serum bilirubin levels were lower in patients with Guillain-Barré syndrome, and suggested total bilirubin, direct bilirubin, and indirect bilirubin were independently and inversely associated with Guillain-Barré syndrome severity.

WWOX suppresses proliferation and induces apoptosis via G2 arrest and caspase 3 pathway in nasopharyngeal carcinoma cells.

BACKGROUND: WWOX plays crucial roles in various tumors. However, so far, minimal research into the role of WWOX in the development of nasopharyngeal carcinoma (NPC) has been reported. The present study investigates the effects of WWOX overexpression on cell proliferation, migration, and invasion in human NPC cell line CNE1. MATERIALS AND METHODS: A lentiviral vector carrying WWOX was transfected into CNE1 cells. The mRNA abundances of WWOX, MMP9, E-cadherin and WWOX protein were detected using quantitative RT-PCR and Western blotting in the transfected cells compared with the control cells (cells transfected using the empty vector and untransfected cells), respectively. Cell proliferation rates were assessed by plate colony formation assays and methyl thiazolyl tetrazolium (MTT). Cell migration and invasion were tested through wound healing assays and/or transwell migration and invasion assays. Cell cycle progression and apoptosis assays were performed by flow cytometry. The protein abundances of activated fragments of caspase-3, cleaved caspase-3 and AKT, phosphorylated p-AKT (Ser473) were measured using Western blotting. RESULTS: Overexpression of WWOX significantly inhibited cell proliferation, migration and invasion and induced apoptosis. Moreover, WWOX overexpression led to cell proliferation inhibition via induction of cell cycle arrest in G2/M phase. WWOX suppressed migration and invasion via downregulation of MMP9 and upregulation of E-cadherin. Meanwhile, WWOX could downregulate the phosphorylation of Akt protein kinase and upregulate cleavage of Caspase-3, contributing to inhibition of proliferation and promotion of apoptosis. CONCLUSION: WWOX gene may be a novel target for gene therapy in NPC.