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To analyze the clinical characteristics in patients with persistent positive pharyngeal swab of 2019 novel coronavirus Omicron variant and results of nucleic acid testing of anal swabs to provide basis for prevention and control measures.This study included 93 patients whose pharyngeal swab nucleic acid test were persistent positive and admitted to the ward of Daping Hospital in the National Exhibition and Convention Center (Shanghai) Makeshift Hospital from May 1 to May 24, 2022. The gender, age, underlying diseases, vaccination status, clinical symptoms, interval between infection onset and anal sampling, length of hospital stay, the nucleic acid test result of pharyngeal swabs and anal swabs and the time turning negative were collected and analyzed.The age of 93 patients ranged from 8 to 72 years old with a median of (46.0±16.0) years old. Among them, 30 cases (32.3%) were male and 63 cases (67.7%) were female. Sixty-five patients (69.9%) received 2-3 shots of vaccine, 2 patients (2.1%) received 1 shot, and 26 patients (28.0%) did not receive any vaccination. Twenty patients (21.5%) had underlying diseases, of which hypertension (13 cases, 14.0%) and type 2 diabetes mellitus (6 cases, 6.5%) were the most common. Twenty-four patients (25.8%) had asymptomatic infection and the rest (69 cases, 74.2%) had mild symptoms. Cough (50 cases, 53.8%) and sore throat (28 cases, 30.1%) were the most common clinical manifestations of the upper respiratory tract in these patients. Only 6 patients (6.5%) had gastrointestinal symptoms (including diarrhea in 5 patients and diarrhea with vomiting in 1 patient). Pharyngeal and anal swabs were collected simultaneously from all 93 patients at 8-16th days [(11.55±2.27) days] after 2019 novel coronavirus Omicron variant infection. The pharyngeal swabs were positive in 79 patients (85.0%) and the anal swabs were positive in 5 patients (5.4%). The time of pharyngeal swabs turning negative was (14.7±2.9) days, and that of anal swab turning positive was (14.2±1.9) days. The median length of hospital stay was (16.7±2.9) days.In patients with persistent positive nucleic acid of the 2019 novel coronavirus Omicron variant, there were more mild infection than asymptomatic. The upper respiratory tract symptoms such as cough and sore throat were the most. The likelihood of transmission of 2019 novel coronavirus Omicron variant through the digestive tract may be low. The correlation between gastrointestinal symptoms and 2019 novel coronavirus Omicron variant RNA in the digestive tract is uncertain.

Background Cryptorchidism is characterized by undescended or incomplete descent of the testes. The pathogenesis of cryptorchidism has not been fully elucidated. In addition, patients with cryptorchidism are at a higher risk of malignancy than normal individuals, and its etiology and underlying molecular mechanisms need to be further investigated. Methods Datasets GSE16191 and GSE25518 were downloaded from the Gene Expression Omnibus database to identify the common differentially expressed genes (DEGs). Gene enrichment analyses were performed using the WebGestalt database. A protein-protein interaction network of DEGs was constructed using the STRING database, of which hub genes were identified by Cytoscape software. The GEPIA database was used to validate the expression of the hub genes of cryptorchidism in testicular cancer, and then the protein level of genes was detected in the HPA database. The analysis of immune cell infiltration was conducted in the R package. The clinical significance of the selected genes was analyzed from four aspects: clinical correlation, overall survival (OS), recurrence-free survival (RFS), and receiver operating characteristic (ROC) curve. Results Of the 438 common DEGs identified, 134 were up-regulated and 304 were down-regulated. Biological functions analysis identified important signaling pathways, key functional modules, and co-expression networks in cryptorchidism. Nine hub genes (HNRNPM, SF1, U2SURP, SNRPA1, AQR, RBM39, PCBP2, RBM5, and HNRNPU) were identified in cryptorchidism, four (SF1, HNRNPM, RBM5, and AQR) of which were significantly expressed in testicular cancer. The high expression of the genes SF1 and HNRNPM predicted poor RFS in cancer patients. Moreover, genes AQR and HNRNPM may contribute to malignant transformation from cryptorchidism to cancer via the spliceosome pathway. Conclusion Our study revealed the potential molecular mechanisms under the pathogenesis of cryptorchidism and its carcinogenesis. The biomarkers identified in this study may provide a theoretical basis and new ideas for further mechanism research of cryptorchidism.

A encapsulation-adsorption-pyrolysis strategy for the construction of atomically dispersed Co-Te diatomic sites (DASs) that are anchored in N-doped carbon is reported as an efficient bifunctional catalyst for electrocatalytic hydrogen evolution reaction (HER) and oxygen reduction reaction (ORR). The as-constructed catalyst shows the stable CoN

Dendritic cells (DCs) are the most potent antigen-presenting cells, and are indispensable in the immune system. Prostaglandin E2 (PGE2) has been demonstrated to modulate the migration of DCs, but with inconsistent results. The present study, based on our previous research, used murine bone marrow-derived DCs to elucidate the potential regulatory mechanism of PGE2 on the migration of DCs. The results indicated that PGE2 served a dual role in regulating the migration of DCs in a dose-dependent manner. High concentrations of PGE2 inhibited cell migration, whereas low concentrations exhibited the opposite effect. Flow cytometry revealed that the expression of CC chemokine receptor type 7 on the DC surface was increased following treatment with low concentrations of PGE2 and slightly decreased by high concentrations of PGE2. The effect of PGE2 was indicated to be exerted via reorganizing the F-actin cytoskeleton using confocal micros-copy. Moreover, the regulatory effect of PGE2 on the migration of DCs was validated in vivo. Subsequent gene expression profile analyses using RNA-sequencing technology indicated that PGE2 induced alterations in the expression of multiple downstream genes and signaling pathway molecules associated with cell migration and the cytoskeleton. These findings may provide an improved understanding on the mechanism of DC migration under both pathological and physiological conditions. Moreover, the biological implications of these findings may provide a novel perspective of the immunological surveillance in the progression of different types of diseases.

The development of high atomic economic efficiency catalysts for hydrogen evolution reaction (HER) and oxygen reduction reaction (ORR) are important for the large-scale application of renewable energy technologies but still challenging. Herein, we reported a novel encapsulation-adsorption-pyrolysis strategy for the construction of atomically dispersed Co-Te diatomic sites (DASs) that are anchored in N-doped carbon (N-C) as efficient bifunctional catalyst for synergistic electrocatalytic HER and ORR. The as-constructed catalyst has stable and special CoN3C1-TeN1C3 coordination structures, Coδ+ has adsorption-activation function and the neighbouring Teδ+ acts as an electron donor adjusting the electronic structure of Coδ+, promoting the dissociation of H2O molecules and the adsorption of H and oxygen-containing intermediates in HER and ORR. This work provides numerous new opportunities to rational design and artificial synthesis of DASs catalysts for energy conversion.

ObjectiveTo investigate the clinical significance of abnormal human telomerase RNA gene component (hTERC) gene amplification tested by fluorescence in situ hybridization in cervical lesions.MethodsIn 373 patients with cytologic abnormalities, high-risk human papilomavirus (HR-HPV) was detected by the hybrid capture II method, and abnormal amplification of the hTERC gene in exfoliated cells was detected by fluorescence in situ hybridization.ResultsCell smear findings suggested atypical squamous cells in 148 patients, low-grade squamous intraepithelial lesion in 62 patients, and high-grade squamous intraepithelial lesion in 107 patients, squamous cell carcinoma in 56 patients, and cervical biopsy-revealed inflammation in 89 patients, cervical intraepithelial neoplasia (CIN) I in 36 patients, CIN II in 43 patients, CIN III in 129 patients, and infiltrating carcinoma in 76 patients. In the inflammation, CIN I, CIN II, CIN III, and infiltrating carcinoma groups, the infection rates of HR-HPV were 29.21%, 52.78%, 74.42%, 92.25%, and 93.42% (P < 0.01), respectively; the positive rates of hTERC gene amplification were 0.00%, 13.89%, 41.86%, 78.29%, and 89.47% (P < 0.01), respectively. With respect to advanced cervical lesions (≥CIN II), cytology (≥ low-grade squamous intraepithelial lesion), HR-HPV testing, and hTERC testing differed insignificantly in the negative predictive value (P > 0.05), but they differed significantly in the sensitivity, specificity, and positive predictive value (P < 0.01). Among the 3 methods, hTERC testing showed the highest specificity and positive predictive value, and HR-HPV testing showed the highest sensitivity. In 41 patients with untreated CIN I and CIN II, the sensitivity of detection of hTERC gene amplification to predict lesion progression was 88.89%, and the specificity was 93.75%.ConclusionDetection of abnormal amplification of the hTERC gene can assist in screening cervical lesions and identifying CIN I/II patients with a high progression risk.

This study investigated the roles of Rho protein in epidermal growth factor (EGF)-induced trophoblast cell migration and its mechanism. Using choriocarcinoma cell lines JEG-3 and JAR and first-trimester human chorionic villus explant cultures on matrigel, we examined EGF-mediated stimulation of trophoblast migration. EGF is shown to have a dose-dependent effect on trophoblast migration. A low concentration of EGF (1 ng/ml) has a stimulatory effect on cell migration, whereas high concentrations of EGF (100 ng/ml) shows an inhibitory effect. EGF (1 ng/ml) activates RhoA and RhoC, but not RhoB, through elevated protein levels and activity. EGF-induced migration was shown to be inhibited by either cell-permeable C3 exoenzyme transferase or selective RhoA or RhoC small interfering RNAs. The inhibition was not mitigated by the addition of EGF, suggesting that RhoA and RhoC play an important role in trophoblast migration and are obligatory for EGF action. Treatment of JEG-3 and JAR cells with RhoA small interfering RNA induced F-actin cytoskeleton disruption and cell shrinkage, which is consistent with the effect of C3 exoenzyme transferase, and this action was not mitigated by EGF treatment. RhoC small interfering RNA had no apparent effect on the F-actin arrangement, suggesting that RhoA but not RhoC takes part in the EGF-induced migration through F-actin rearrangement. These results indicate that RhoA and RhoC play more important roles than RhoB in EGF-mediated migration of trophoblast cells, and RhoA but not RhoC regulates this migration through F-actin cytoskeleton reorganization.

Analysis of fetal DNA in maternal plasma has recently been introduced for non-invasive prenatal diagnosis. We have now investigated the feasibility of polymerase chain reaction (PCR)/ligase detection reaction (LDR)/capillary electrophoresis for the detection of fetal point mutations, such as the beta-thalassemia mutation, IVS2 654(C --T), in maternal plasma DNA.The sensitivity of LDR/capillary electrophoresis was examined by quantifying the mutant PCR products in the presence of a vast excess of non-mutant competitor template, a situation that mimics the detection of rare fetal mutations in the presence of excess maternal DNA. PCR/LDR/capillary electrophoresis was applied to detect the mutation, IVS2 654(C --T), in an experimental model at different sensitivity levels and from 10 maternal plasma samples.Our results demonstrated that this approach to detect a low abundance IVS2 654(C --T) mutation achieved a sensitivity of approximately 1:10,000. The approach was applied to maternal plasma DNA to detect the paternally inherited fetal IVS2 654(C --T) mutation, and the results were equivalent to those obtained by PCR/reverse dot blot of amniotic fluid cell DNA.PCR/LDR/capillary electrophoresis has a very high sensitivity that can distinguish low abundance single nucleotide differences and can detect paternally inherited fetal point mutations in maternal plasma.

Objectives To characterize the H19 gene imprinting in the placental tissues of normal pregnancy and pre-eclampsia. Methods A total of 188 subjects at 5–9 weeks, 54 at 10–12 weeks, 50 at the second trimester, 65 at term of gestation, and 30 with pre-eclampsia at the third trimester were recruited. Their DNA and RNA were extracted from the placental tissues. The H19 genotypes for individuals were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and the H19 gene imprinting was identified by reverse transcription-PCR (RT-PCR) and the Rsa I-based RFLP. The levels of H19 RNA transcripts in the pre-eclampsia patients with the H19 heterozygote were measured by quantitative RT-PCR. The frequency of the H19 heterozygote, the H19 imprinting status among different trimesters of pregnancy and the clinical symptoms in the pre-eclampsia patients were analyzed. Results (1) About 40–46% of subjects at varying stages of normal pregnancy showed the H19 heterozygote, and 24 out of 87 (27.59%) heterozygous cases were at 5–9 weeks of gestation, but no single one in other stages displayed biallelic expression of the H19 gene. (2) Thirteen out of 30 pre-eclampsia patients were H19 heterozygous and six of these showed the biallelic expression of the H19 gene (loss of imprinting). (3) The pre-eclampsia patients with the biallelic expression of H19 tended to have severer hypertension although their H19 RNA transcription level was similar to that in those with monoallelic expression. Conclusions (1) The biallelic expression of the H19 gene exists in some cases at the early stage of normal pregnancy and changes into monoallelic expression near 10 weeks of gestation. The dynamic alternations in the patterns of the H19 gene imprinting may regulate the maintenance of normal pregnancy. (2) The loss of the H19 gene imprinting in the placental tissues of pre-eclampsia patients may be associated with severe hypertension, contributing to the pathogenic process of pre-eclampsia.

Increased circulating syncytiotrophoblast microparticles (STBMs) are often associated with preeclampsia (PE) but the molecular mechanisms regulating STBM shedding remain elusive. Experimental evidence has shown that actin plays a key role in STBM shedding and that Rho/ROCK is important in regulating actin rearrangement. To investigate the role of RhoB/ROCK-regulated actin arrangement in STBM shedding in PE, chorionic villous explants were prepared from placenta of patients with normotensive or PE pregnancies and BeWo cells were fused to imitate syncytiotrophoblasts. The oxygen–glucose deprivation (OGD) conditions were applied to imitate the pathophysiology of PE in vitro. The results showed that RhoB and ROCK were activated in the preeclamptic placenta, accompanied by increased actin polymerization and decreased outgrowing microvilli. In villous tissue cultures or BeWo cells, OGD activated RhoB, ROCK1 and ROCK2 and promoted STBM shedding and actin stress fibers formation. In BeWo cells, RhoB overexpression activated ROCK1 and ROCK2, leading to F-actin redistribution and STBM shedding and the OGD-induced actin polymerization and STBM shedding could be reversed by RhoB or ROCK knockdown. These results reveal that RhoB and ROCK play a key role in PE by targeting STBM shedding through actin rearrangement and that RhoB/ROCK intervention may be a potential therapeutic strategy for PE.

To investigate the clinical significance of abnormal human telomerase RNA gene component (hTERC) gene amplification tested by fluorescence in situ hybridization in cervical lesions.In 373 patients with cytologic abnormalities, high-risk human papilomavirus (HR-HPV) was detected by the hybrid capture II method, and abnormal amplification of the hTERC gene in exfoliated cells was detected by fluorescence in situ hybridization.Cell smear findings suggested atypical squamous cells in 148 patients, low-grade squamous intraepithelial lesion in 62 patients, and high-grade squamous intraepithelial lesion in 107 patients, squamous cell carcinoma in 56 patients, and cervical biopsy-revealed inflammation in 89 patients, cervical intraepithelial neoplasia (CIN) I in 36 patients, CIN II in 43 patients, CIN III in 129 patients, and infiltrating carcinoma in 76 patients. In the inflammation, CIN I, CIN II, CIN III, and infiltrating carcinoma groups, the infection rates of HR-HPV were 29.21%, 52.78%, 74.42%, 92.25%, and 93.42% (P0.01), respectively; the positive rates of hTERC gene amplification were 0.00%, 13.89%, 41.86%, 78.29%, and 89.47% (P0.01), respectively. With respect to advanced cervical lesions (≥CIN II), cytology (≥ low-grade squamous intraepithelial lesion), HR-HPV testing, and hTERC testing differed insignificantly in the negative predictive value (P0.05), but they differed significantly in the sensitivity, specificity, and positive predictive value (P0.01). Among the 3 methods, hTERC testing showed the highest specificity and positive predictive value, and HR-HPV testing showed the highest sensitivity. In 41 patients with untreated CIN I and CIN II, the sensitivity of detection of hTERC gene amplification to predict lesion progression was 88.89%, and the specificity was 93.75%.Detection of abnormal amplification of the hTERC gene can assist in screening cervical lesions and identifying CIN I/II patients with a high progression risk.

Objectives: It was the aim of this study to investigate the feasibility of polymerase chain reaction (PCR)/ligase detection reaction (LDR)/capillary electrophoresis for the detection of paternally inherited fetal CD17 (A→T) mutation of β-thalassemia in maternal plasma. Methods: The target DNA in maternal plasma was amplified by PCR and the mutant signal was detected by LDR. Unique LDR products were produced and separated by capillary electrophoresis. PCR/LDR/capillary electrophoresis was applied to detect CD17 (A→T) mutation in an experimental model at different sensitivity levels and from 3 maternal plasma samples. Results: The sensitivity of PCR/LDR/capillary electrophoresis for detecting low-abundance CD17 (A→T) mutation was 1:5,000 at least. The technique was applied in maternal plasma DNA for detecting paternally inherited fetal CD17 (A→T) mutation, and the results were concordant with that of PCR/reverse dot blot of amniotic fluid cell DNA. Conclusions: PCR/LDR/capillary electrophoresis has a very high sensitivity to distinguish low-abundance single nucleotide differences and probably detects paternally inherited fetal point mutations in maternal plasma.