Agromyces chromiiresistens sp. nov., Novosphingobium album sp. nov., Sphingobium arseniciresistens sp. nov., Sphingomonas pollutisoli sp. nov., and Salinibacterium metalliresistens sp. nov.: five new members of Microbacteriaceae and Sphingomonadaceae from polluted soil.

There are many unidentified microbes in polluted soil needing to be explored and nominated to benefit the study of microbial ecology. In this study, a taxonomic research was carried out on five bacterial strains which were isolated and cultivated from polycyclic aromatic hydrocarbons, and heavy metals polluted soil of an abandoned coking plant. Phylogenetical analysis showed that they belonged to the phyla Proteobacteria and Actinobacteria, and their 16S rRNA gene sequence identities were lower than 98.5% to any known and validly nominated bacterial species, suggesting that they were potentially representing new species. Using polyphasic taxonomic approaches, the five strains were classified as new species of the families Microbacteriaceae and Sphingomonadaceae. Genome sizes of the five strains ranged from 3.07 to 6.60 Mb, with overall DNA G+C contents of 63.57-71.22 mol%. The five strains had average nucleotide identity of 72.38-87.38% and digital DNA-DNA hybridization of 14.0-34.2% comparing with their closely related type strains, which were all below the thresholds for species delineation, supporting these five strains as novel species. Based on the phylogenetic, phylogenomic, and phenotypic characterizations, the five novel species are proposed as Agromyces chromiiresistens (type strain H3Y2-19aT = CGMCC 1.61332T), Salinibacterium metalliresistens (type strain H3M29-4T = CGMCC 1.61335T), Novosphingobium album (type strain H3SJ31-1T = CGMCC 1.61329T), Sphingomonas pollutisoli (type strain H39-1-10T = CGMCC 1.61325T), and Sphingobium arseniciresistens (type strain H39-3-25T = CGMCC 1.61326T). Comparative genome analysis revealed that the species of the family Sphingomonadaceae represented by H39-1-10T, H39-3-25T, and H3SJ31-1T possessed more functional protein-coding genes for the degradation of aromatic pollutants than the species of the family Microbacteriaceae represented by H3Y2-19aT and H3M29-4T. Furthermore, their capacities of resisting heavy metals and metabolizing aromatic compounds were investigated. The results indicated that strains H3Y2-19aT and H39-3-25T were robustly resistant to chromate (VI) and/or arsenite (III). Strains H39-1-10T and H39-3-25T grew on aromatic compounds, including naphthalene, as carbon sources even in the presence of chromate (VI) and arsenite (III). These features reflected their adaptation to the polluted soil environment.

Longer duration of initial invasive mechanical ventilation is still a crucial risk factor for moderate-to-severe bronchopulmonary dysplasia in very preterm infants: a multicentrer prospective study.

OBJECTIVES: We aimed to evaluate the risk factors for moderate-to-severe bronchopulmonary dysplasia (BPD) and focus on discussing its relationship with the duration of initial invasive mechanical ventilation (IMV) in very preterm neonates less than 32 weeks of gestational age (GA). METHODS: We performed a prospective cohort study involving infants born at 23-31 weeks of GA who were admitted to 47 different neonatal intensive care unit (NICU) hospitals in China from January 2018 to December 2021. Patient data were obtained from the Sina-northern Neonatal Network (SNN) Database. RESULTS: We identified 6538 very preterm infants, of whom 49.5% (3236/6538) received initial IMV support, and 12.6% (823/6538) were diagnosed with moderate-to-severe BPD symptoms. The median duration of initial IMV in the moderate-to-severe BPD group was 26 (17-41) days, while in the no or mild BPD group, it was 6 (3-10) days. The incidence rate of moderate-to-severe BPD and the median duration of initial IMV were quite different across different GAs. Multivariable logistic regression analysis showed that the onset of moderate-to-severe BPD was significantly associated with the duration of initial IMV [adjusted odds ratio (AOR): 1.97; 95% confidence interval (CI): 1.10-2.67], late-onset neonatal sepsis (LONS), and patent ductus arteriosus (PDA). CONCLUSION: In this multicenter cohort study, the duration of initial IMV was still relatively long in very premature infants, and the longer duration of initial IMV accounts for the increased risk of moderate-to-severe BPD.

Association between pulmonary hemorrhage and CPAP failure in very preterm infants.

Background: Pulmonary hemorrhage (PH) in neonates is a life-threatening respiratory complication. We aimed to analyze the perinatal risk factors and morbidity with PH among very preterm infants in a large multicenter study. Methods: This was a multicenter case-control study based on a prospective cohort. Participants included 3,680 in-born infants with a gestational age at 24-32 weeks (birth weight <1,500 g) who were admitted between January 1, 2019, and October 31, 2021. All infants were divided into two groups, namely, the PH and no-PH groups, at a ratio of 1:2 according to the following factors: gestational age (GA), birth weight (BW), and the Score for Neonatal Acute Physiology with Perinatal extension II (SNAPPE II). Perinatal factors and outcomes were compared between the two groups by logistic regression analyses. Results: A total of 3,680 infants were included in the study, and the number of identified cases of PH was 262 (7.1%). The incidence was 16.9% (136/806) for neonates with extremely low BW (BW < 1,000 g) infants. The multivariate analysis showed that CPAP failure (OR 2.83, 95% CI 1.57, 5.08) was significantly associated with PH. PH was associated with a high likelihood of death (OR 3.81, 95% CI 2.67, 5.43) and bronchopulmonary dysplasia (BPD) (≥grade II) (OR 1.58, 95% CI 1.00, 2.48). Conclusions: In this multicenter case-control study based on a prospective cohort, PH to be common among VLBW infants. PH is associated with significant morbidity and mortality, and perinatal management, especially CPAP failure. Respiratory management strategies to decrease the risk of PH should be optimized.

The Integrated Analysis Identifies Three Critical Genes as Novel Diagnostic Biomarkers Involved in Immune Infiltration in Atherosclerosis.

Atherosclerosis (AS), a chronic inflammatory disease of the blood vessels, is the primary cause of cardiovascular disease, the leading cause of death worldwide. This study aimed to identify possible diagnostic markers for AS and determine their correlation with the infiltration of immune cells in AS. In total, 10 serum samples from AS patients and 10 samples from healthy subjects were collected. The original gene expression profiles of GSE43292 and GSE57691 were downloaded from the Gene Expression Omnibus database. Least absolute shrinkage and selection operator regression model and support vector machine recursive feature elimination analyses were carried out to identify candidate markers. The diagnostic values of the identified biomarkers were determined using receiver operating characteristic assays. The compositional patterns of the 22 types of immune cell fraction in AS were estimated using CIBERSORT. RT-PCR was performed to further determine the expression of the critical genes. This study identified 17 differentially expressed genes (DEGs) in AS samples. The identified DEGs were mainly involved in non-small cell lung carcinoma, pulmonary fibrosis, polycystic ovary syndrome, glucose intolerance, and T-cell leukemia. FHL5, IBSP, and SCRG1 have been identified as the diagnostic genes in AS. The expression of SCRG1 and FHL5 was distinctly downregulated in AS samples, and the expression of IBSP was distinctly upregulated in AS samples, which was further confirmed using our cohort by RT-PCR. Moreover, immune assays revealed that FHL5, IBSP, and SCRG1 were associated with several immune cells, such as CD8 T cells, naïve B cells, macrophage M0, activated memory CD4 T cells, and activated NK cells. Overall, future investigations into the occurrence and molecular mechanisms of AS may benefit from using the genes FHL5, IBSP, and SCRG1 as diagnostic markers for the condition.

Identification of ITGA3 as an Oncogene in Human Tongue Cancer via Integrated Bioinformatics Analysis.

Human tongue cancer (TC) is an aggressive malignancy with a very poor prognosis. There is an urgent need to elucidate the underlying molecular mechanisms involved in TC progression. mRNA expression profiles play a vital role in the exploration of cancer-related genes. Therefore, the purpose of our study was to identify the progression associated candidate genes of TC by bioinformatics analysis. Five microarray datasets of TC samples were downloaded from the Gene Expression Omnibus (GEO) database and the data of 133 TC patients were screened from The Cancer Genome Atlas (TCGA) head and neck squamous cell carcinoma (HNSC) database. The integrated analysis of five microarray datasets and the RNA sequencing data of TC samples in TCGA-HNSC was performed to obtain 1023 overlapping differentially expressed genes (DEGs) in TC and adjacent normal tissue (ANT) samples. Next, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was conducted to enrich the significant pathways of the 1023 DEGs and PI3KAkt signaling pathway (P=0.011) was selected to be the candidate pathway. A total of 23 DEGs with |log2 fold change (FC)| ≥1.0 in phosphatidylinositol 3-kinase-serine/threonine kinase (PI3K-Akt) signaling pathway were subjected to survival analysis of 125 eligible TC samples in TCGA database, indicating increased integrin-α3 gene (ITGA3) expression was significantly associated with poorer prognosis. Taken together, our study suggested ITGA3 may facilitate the development of TC via activating PI3K-Akt signaling pathway.

Knockdown of GRHL3 inhibits activities and induces cell cycle arrest and apoptosis of human colorectal cancer cells.

The Grainyhead-like 3 (GRHL3) is involved in epidermal barrier formation, neural tube closure and wound repair. Previous studies have suggested that GRHL3 has been linked to many different types of cancers. However, to date, its effects on human colorectal cancer (CRC) has not been clarified yet. Our microarray analysis has indicated predominant GRHL3 expression in CRC. The purpose of this study was to investigate the expression and significance of GRHL3 in CRC tumorigenesis using CRC tissues and paired paracancerous tissues, as well as using distinct CRC cell lines (HT29 and DLD1). We observed increased GRHL3 expression at both mRNA and protein levels in CRC tissues and CRC cell lines using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Moreover, silencing GRHL3 with siRNA could suppress CRC cell proliferation, viability and migration in vitro. We also found that knockdown of GRHL3 could promote cell cycle arrest at G0/G1 phase in HT29 cells and DLD1 cells, and induce cell apoptosis in HT29 cells. Together, our study revealed the down-regulation of GRHL3 in vitro could inhibit CRC cell activity and trigger cell cycle arrest at G0/G1 phase and apoptosis.

Inhibition of adhesion and metastasis of HepG2 hepatocellular carcinoma cells in vitro by DNA aptamer against sialyl Lewis X.

The sialyl Lewis X (SLex) antigen encoded by the FUT7 gene is the ligand of endotheliam-selectin (E-selectin). The combination of SLex antigen and E-selectin represents an important way for malignant tumor metastasis. In the present study, the effect of the SLex-binding DNA aptamer on the adhesion and metastasis of hepatocellular carcinoma HepG2 cells in vitro was investigated. Reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence staining were conducted to detect the expression of FUT7 at both transcriptional and translational levels. The SLex expression in HepG2 cells treated with different concentrations of SLex-binding DNA aptamer was detected by flow cytometry. Besides, the adhesion, migration, and invasion of HepG2 cells were measured by cell adhesion assay, and the Transwell migration and invasion assay. The results showed that the FUT7 expression was up-regulated at both mRNA and protein levels in HepG2 cells. SLex-binding DNA aptamer could significantly decrease the expression of SLex in HepG2 cells. The cell adhesion assay revealed that the SLex-binding DNA aptamer could effectively inhibit the interactions between E-selectin and SLex in the HepG2 cells. Additionally, SLex-binding DNA aptamers at 20 nmol/L were found to have the similar effect to the monoclonal antibody CSLEX-1. The Transwell migration and invasion assay revealed that the number of penetrating cells on the down-side of Transwell membrane was significantly less in cells treated with 5, 10, 20 nmol/L SLex-binding DNA aptamer than those in the negative control group (P<0.01). Our study demonstrated that the SLex-binding DNA aptamer could significantly inhibit the in vitro adhesion, migration, and invasion of HepG2 cells, suggesting that the SLex-binding DNA aptamer may be used as a potential molecular targeted drug against metastatic hepatocellular carcinoma.

SLC38A1 promotes proliferation and migration of human colorectal cancer cells.

Current studies have demonstrated that SLC38A1 proteins play a causal role in neoplastic cell transformation. The twofold aim of this study was to provide insight into whether a variance in the expression of SLC38A1 exists between human colorectal cancer and healthy human tissues and to determine how silencing or overexpressing the SLC38A1 gene could affect the proliferation, viability and migration of colorectal cancer cells. Immunohistochemical staining was used to analyze the expression of SLC38A1 in colorectal cancer tissues and adjacent normal mucosa in 77 patients who underwent surgical resection. The expression of SLC38A1 in colorectal cancer tissues and cell lines was detected using RT-PCR and Western blotting. Two colorectal cancer cell lines SW480 and HCT116 were used to examine whether silencing SLC38A1 with siRNA and overexpressing SLC38A1 with shRNA could affect cell viability and migration. As a result, the SLC38A1 protein was very low or undetectable in the normal colon mucosa. In contrast, strong staining of SLC38A1 protein was found in the cytoplasm in 79.2% colorectal cancer samples. More pronounced SLC38A1 expression in colorectal cancer tissues was significantly associated with tumor node metastasis (TNM) stage. Inhibition of SLC38A1 reduced tumour growth and suppressed proliferation and migration of SW480 cells. In contrast, overexpression of SLC38A1 had the opposite effects on HCT116 cells. SLC38A1 is overexpressed in colorectal cancer, which suggests that it is associated with tumour progression. These results encourage the exploration of SLC38A1 as a target for intervention in colorectal cancer.

miR-200c inhibits invasion and migration in human colon cancer cells SW480/620 by targeting ZEB1.

MicroRNAs are a class of ≈22-nt noncoding single-strand RNAs regulating gene expression postscriptionally. Metastasis caused poor prognosis in colorectal cancer patients and half of the patients developed metastatic lesions when admission. Here we investigated the possible roles of microRNAs in regulating metastasis in the paired colon cancer cells SW480 and SW620. Among those dysregulated microRNAs, miR-200c was speculated to inhibit metastasis by targeting ZEB1. Overexpression of miR-200c was concurrent with downregulation of ZEB1 mRNA and protein. Functional assays demonstrated that modulation of miR-200c with mimics or inhibitors changed potential of metastasis in SW480/620 cancer cells in vitro. Taken together, our study demonstrated that miR-200c inhibits metastatic ability by targeting ZEB1 in colon cancer cells SW480/620 and suggested that modulation of miR-200c could serve as therapeutic tool for inhibiting metastasis in colorectal cancer.

A meta-analysis of chemotherapy regimen fluorouracil/leucovorin/oxaliplatin compared with fluorouracil/leucovorin in treating advanced colorectal cancer.

BACKGROUND: We performed a meta-analysis to evaluate the efficacy and safety of Fluorouracil (FU)/Leucovorin (LV)/Oxaliplatin compared to FU/LV in treating advanced colorectal cancer. METHODS: Two independent researchers identified and extracted all relevant literature using MEDLINE and the Cochrane Library Database. The regimens included arm A (FU/LV) and arm B (FU/LV/Oxaliplatin) with no other chemotherapy agent. RESULTS: Five randomized controlled trials (RCTs) fulfilled the requirements. All RCTs showed superiority of FU/LV/Oxaliplatin to FU/LV when measuring RR (response rate) and PFS (progression-free survival); no significant improvement in OS (overall survival) was observed. This meta-analysis shows a better RR for the FU/LV/Oxaliplatin group (OR 4.02, 95% CI 2.37-6.82, p<0.00001). The incidence of grade 3/4 toxicities, including neutropenia, thrombocytopenia, vomiting, neurological toxicity, toxicity-related dose modification and discontinuation was higher in the FU/LV/Oxaliplatin group, while the incidence of anemia, nausea and diarrhea was not different. CONCLUSION: FU/LV/Oxaliplatin offers better efficacy (RR and PFS) than FU/LV in the treatment of advanced colorectal cancer. The incidence of grade 3/4 toxicities, i.e. neutropenia, thrombocytopenia, vomiting, neurological toxicity, is significantly higher in the FU/LV/Oxaliplatin than in the FU/LV group but these are manageable or reversible.

[Feasibility of muscle-derived cell autotransplantation as a treatment for post-prostatectomy urinary incontinence].

OBJECTIVE: To explore the feasibility of muscle-derived cell autotransplantation in the treatment of post-prostatectomy urinary incontinence. METHODS: Skeletal muscle-derived cells (MDC) were isolated and purified by replate technique from 6 female SD rats, and then transduced with adenovirus carrying Lac-Z gene. About 5 x 10(6) of the transduced cells were injected autologously into the bladder neck of the animals. Tissues were harvested after 5 and 15 days for histological examination and X-gal staining. RESULTS: At 5 and 15 days after the autologous MDC transplantation, histological examination revealed no apparent sign of inflammation and inflammatory cell invasion, and X-gal staining showed a large number of cells dyed blue, indicating the survival of the autologous cells. CONCLUSION: Autotransplanted MDCs can survive permanently. Autologous muscle stem cell injection can be an effective treatment for post-prostatectomy urinary incontinence.

[Experimental study of contralateral testicular changes after unilateral testicular torsion in rats].

OBJECTIVE: To study the changes of the contralateral testicular histology and germ cell apoptosis after unilateral testicular torsion (UTT) and to determine whether the contralateral testis is injured or not. METHODS: Sixty SD male rats were divided into control group (12 rats) and experimental group(48 rats). The former underwent sham operation of the left testis under general anaesthesia. The latter underwent left testis torsion(720 degrees) for 6 h, and then 4 of them were sacrificed and the other 44 were subdivided into the torsed testis untwisted group (22 rats) and the torsed testis removal group (22 rats), 7-8 rats were sacrificed and both testes (twisted and untwisted) were removed 1 day, 1 week and 4 weeks after surgery. All testes underwent histological and germ cell apoptosis examination. RESULTS: There were significant histological changes in the contralateral testis, and the germ cell apoptosis was increased greatly in the contralateral testis. CONCLUSIONS: UTT can cause contralateral testicular injury, whose mechanism may be related to reperfusion, and torsed testis removal can prevent or reduce damage to the contralateral testis.