[An analysis of the status quo of ground-level ozone pollution research].

Objective: To analyze the research status of ground-level ozone pollution, explore research trends and hot spots, and provide references for future research on air pollution. Methods: Papers on ground-level ozone pollution research published before December 31, 2019 had been retrieved in SCI-E database of the "Web of Science Core Collection" in January 2020. The retrieval strategies were set as follows: TS= ( ("Tropospheric Ozone" OR "Low Level Ozone" OR "Ground Level Ozone") AND ("Air pollution*" OR "Air quality") ) . The survey included 2084 articles. By using bibliometric research and visual analysis tools, the research status of global ground-level ozone pollution was revealed from the aspects of time, discipline, journal, financing, institution, country and key words. Results: Cumulative publications increased in a cubic function of y=0.05x(3)+0.80x(2)+0.74x+4.55 (R(2)=0.999, P<0.01) . The most studied subject was Environmental sciences ecology (1401 articles, 67.23%) . Atmospheric Environment was the journal with the most articles (332 articles, 15.93%) . The United States was the country with the most publications (44.67%, 931/2084) , while China ranked second (17.13%, 357/2084) . 80.39% (287/357) of Chinese papers had funding information. Among the top 10 research institutions, 7 and 2 were affiliated to the United States and China respectively. Source apportionment and human health were high frequency keywords that had appeared in the last 5 years. Conclusion: The research on ground-level ozone pollution is in a good period of development. The United States has a leading position in this area, and China has a good prospect in this field. Pollution source apportionment and human health effects are new research directions.

Transcriptome analysis of sheep follicular development during prerecruitment, dominant, and mature stages after FSH superstimulation.

Sheep is usually a monovular animal; superovulation technology is used to increase the number of offspring per individual and shorten generation intervals. To date, mature FSH superstimulatory treatments have been successfully used in sheep breeding, but much remains unknown about genes, pathways, and biological functions involved in follicular development. Therefore, in this study, we performed transcriptome profiling of small follicles (SFs; 2-2.5 mm), medium follicles (MFs; 3.5-4.5 mm), and large follicles (LFs; > 6 mm) in Mongolian ewes after FSH superstimulation. Furthermore, we identified differentially expressed genes and performed Kyoto Encyclopedia of Genes and Genomes pathway and Gene Ontology enrichment analyses in 3 separate pairwise comparisons. We found that ovarian steroidogenesis was significantly enriched in the SFs versus MFs analysis; the associated genes, cytochrome P450 family 19 (CYP19) and Hydroxy-delta-5-steroid dehydrogenase 3 beta- and steroid delta-isomerase 1 (HSD3B1), were significantly upregulated. Moreover, proline metabolism, glutathione metabolism, and PPAR signaling pathways were significantly enriched in the LFs versus SFs analysis; the associated genes, glutamate-cysteine ligase modifier subunit (GCLM) and cystathionine gamma-lyase (CTH), were significantly upregulated, whereas peroxisome proliferator-activated receptor gamma (PPARγ) was significantly downregulated. In summary, our study provides basic data and possible biological direction to further explore the molecular mechanism of sheep follicular development after FSH superstimulation.

[The role of combined BRAFV600E gene detection in the diagnosis of thyroid nodule determined as Bethesda â ¢ by fine-needle aspiration].

Objective: To analyze the malignant probability of thyroid nodules with the diagnosis of atypia of undetermined significance or follicular lesion of undetermined significance (AUS/FLUS) determined by fine-needle aspiration (FNA) and to explore the value of the combined application of BRAFV600E gene detection for the diagnosis of benign and malignant thyroid nodules. Methods: A total of 114 patients including 20 males and 94 females, aged 16-76 years old with thyroid nodules underwent FNA examination and surgical treatment in the Affiliated Cancer Hospital of Zhengzhou University from October 2018 to November 2019 were retrospectively analyzed. Postoperative histopathological results were used as the gold standard for the diagnosis of malignant thyroid nodules. The malignant rate of thyroid nodules with the diagnosis of AUS/FLUS was evaluated. Differential diagnostic efficacy of preoperative FNA combined with BRAFV600E gene detection for papillary thyroid carcinoma (PTC) was analyzed by McNemer test and diagnostic test evaluation method. Results: The mutation rate of BRAFV600E gene was 84.76% (89/105) in PTC. PTC accounted for 57.14% (12/21) of the patients with the diagnoses of AUS/FLUS determined by FNA. The specificity, sensitivity, positive predictive value and negative predictive value of BRAFV600E mutation examination for the diagnosis of malignant thyroid nodules determined preoperatively as AUS/FLUS were 9/9, 5/12, 5/5 and 9/16, respectively. BRAFV600E mutation examination could improve the detection rate of PTC in patients with AUS/FLUS (OR=0.438, 95%CI=0.251-0.763, P=0.016). Conclusion: FNA combined with BRAFV600E mutation examination can significantly improve the detection rate of malignant thyroid nodules diagnosed preoperatively as AUS/FLUS.

Characterization and Mutational Analysis of Two UDP-Galactose 4-Epimerases in Streptococcus pneumoniae TIGR4.

Current clinical treatments for pneumococcal infections have many limitations and are faced with many challenges. New capsular polysaccharide structures must be explored to cope with diseases caused by different serotypes of Streptococcus pneumoniae. UDP-galactose 4-epimerase (GalE) is an essential enzyme involved in polysaccharide synthesis. It is an important virulence factor in many bacterial pathogens. In this study, we found that two genes (galEsp1 and galEsp2) are responsible for galactose metabolism in pathogenic S. pneumoniae TIGR4. Both GalESp1 and GalESp2 were shown to catalyze the epimerization of UDP-glucose (UDP-Glc)/UDP-galactose (UDP-Gal), but only GalESp2 was shown to catalyze the epimerization of UDP-N-acetylglucosamine (UDP-GlcNAc)/UDP-N-acetylgalactosamine (UDP-GalNAc). Interestingly, GalESp2 had 3-fold higher epimerase activity toward UDP-Glc/UDP-Gal than GalESp1. The biochemical properties of GalESp2 were studied. GalESp2 was stable over a wide range of temperatures, between 30 and 70°C, at pH 8.0. The K86G substitution caused GalESp2 to lose its epimerase activity toward UDP-Glc and UDP-Gal; however, substitution C300Y in GalESp2 resulted in only decreased activity toward UDP-GlcNAc and UDP-GalNAc. These results indicate that the Lys86 residue plays a critical role in the activity and substrate specificity of GalESp2.

Transcriptional regulation of the vitellogenin gene through a fecundity-related single nucleotide polymorphism within a GATA-1 binding motif in the brown planthopper, Nilaparvata lugens.

Identifying the Single Nucleotide Polymorphisms (SNPs) with functions in insect fecundity promises to provide novel insight into genetic mechanisms of adaptation and to aid in effective control of insect populations. We previously identified several SNPs within the vitellogenin (Vg) promoter region between a high-fecundity population (HFP) and a low-fecundity population (LFP) of the brown planthopper, Nilaparvata lugens Stål (Hemiptera: Delphacidae). Here, we found that an A-to-T (HFP allele to LFP allele) transversion at nucleotide -953 upstream of Vg in a Nilaparvata lugens GATA-1 (NlGATA-1) binding motif is associated with the level of Vg transcription. We also characterized NlGATA-1, containing a double CX2 CX17 CX2 C zinc finger, which has been implicated in the activation of Vg gene expression. Knockdown of the NlGATA-1 gene results in a reduced basal level of expression of the Vg gene and fewer offspring of N. lugens in vivo, whereas overexpression of NlGATA-1 in cells increased Vg promoter activity. Moreover, upon cotransfection with NlGATA-1 expression vector, the luciferase activities of Vg reporter vectors with the A allele were significantly higher than those with the T allele. These findings support a mechanism in which a SNP within the promoter of Vg is associated with the level of Vg transcription by altering the binding activity of NlGATA-1 and subsequently affecting fecundity in N. lugens.

[FAT1 inhibits cell proliferation of esophageal squamous cell carcinoma through regulating the expression of CDK4/CDK6/CCND1 complex].

Objective: To explore the expression of FAT1 in esophageal squamous cell carcinoma (ESCC) tissues, and its effect on cell proliferation. Methods: The expression levels of FAT1 protein in human ESCC tissues and matched adjacent normal tissues were determined by immunohistochemistry (IHC). Lentivirus based knockdown of FAT1 was carried out in YSE2 and Colo680N cell lines and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assays was performed to examine the effect of FAT1 on the proliferation of these ESCC cells. Colony formation assay was used to detect the colony formation ability. Flow cytometry was performed to analyze the cell cycle and apoptosis. The expression levels of cell cycle markers in FAT1 knock out ESCC cell lines were detected by real-time quantitative reverse transcription polymerase chain reaction(qRT-PCR) and Western blot. Results: The relative expression of FAT1 in ESCC tissues was 66.97±21.53, significantly lower than 78.13±16.76 of adjacent normal tissues(P<0.05). Knockdown of FAT1 promoted cell proliferation and colony formation. In YSE2 cell, the division time in negative control (NC) group was (1 570±51) min, significantly longer than (1 356±31) min in shFAT1 group. In Colo680N cell, division time in NC group was (1 532±53) min, significantly longer than (1 290±30) min in shFAT1 group (P<0.05). Knockdown of FAT1 promoted G1-to S-phase transition and resulted in the upregulation of CDK4/CDK6/CCND1. Conclusion: FAT1 inhibits the proliferation and G1-to S-phase transition of ESCC cells through regulating the protein expression of CDK4/CDK6/CCND1 complex.

Active immunization of fatty acid translocase specifically decreased visceral fat deposition in male broilers.

Lipid accumulation of avian adipocytes is mainly dependent upon the fatty acid transmembrane uptake process mediated by membrane proteins, such as fatty acid translocase (FAT/CD36), fatty acid transport protein 1, and caveolin-2. To examine the effects of FAT/CD36 on spatial-specific fat deposition, 60 broiler chickens were randomly allocated to 2 groups by sex. Each male or female group contained 2 subgroups (n = 14-15) inoculated by intramuscular injection with chicken FAT/CD36 or BSA (control) immunogens at 34, 49, and 63 d. The subcutaneous and visceral fat deposits were measured, as were levels of plasma triglyceride and free fatty acid. Serum antibody titer was measured by ELISA. The mRNA expression levels of fatty acid transport-related genes in the adipose tissue of the male broilers were investigated to reveal the relationships among various fatty acid transporters. The results showed that active immunization with FAT/CD36 could significantly decrease the visceral fat of the male broilers by up to 40%, but it had no effect on subcutaneous fat stores of male broilers or on either site of fat deposition in female broilers. The concentration of plasma free fatty acids increased in the experimental groups for both male and female broilers. After the FAT/CD36 immunization, very low density lipoprotein receptor mRNA expression was upregulated in both the subcutaneous and visceral fat of male broilers, whereas peroxisome proliferator-activated receptor γ, FAT/CD36, and acyl-CoA binding protein mRNA expression levels were upregulated only in the visceral fat of male broilers. These results indicated a novel role of chicken FAT/CD36 in fat deposition, with sex- and spatial-specific effects.

[A biomechanical study of the human periodontal ligament]

The structures and mechanical properties of the normal human periodontal ligament(PDL) were investigated by VDA measuring system through the microscope.It was found that the mechanical properties of PDL is not linear.Its mechanical properties are depending on its fibrous properties,directions and components.The linear and index relationships of the tensile and compression stress-strain curve of PDL can be divided into 6 segments.The strain changes and moduli of every segment were calculated.The relationship between periodontal function and the variation law of stress-strain is investigated and its clinic value is shown.

Increased expression of specific protein tyrosine phosphatases in human breast epithelial cells neoplastically transformed by the neu oncogene.

Protein tyrosine phosphorylation/dephosphorylation is a fundamental mechanism in the regulation of cell proliferation and neoplastic transformation; this metabolic process is modulated by the opposing activities of protein tyrosine kinases and protein tyrosine phosphatases (PTPases). While the role of protein tyrosine kinases has been examined extensively in human breast tumorigenesis, the role of PTPases in this process is virtually unknown. To address this issue, an activated neu oncogene was introduced into an immortalized nontumorigenic human breast epithelial cell line (184B5). This resulted in a substantial increase in P185neu expression, which led to the formation of progressively growing carcinomas after such cells were inoculated into athymic nude mice. Importantly, a striking increase in the expression of specific PTPases, LAR and PTP1B, was observed in 3 independently neu transformed cell lines and their derived tumors. This elevation was verified at both the mRNA and protein levels. TC-PTP PTPase expression was only slightly increased in these neu transformed cells, and no expression of CD45 PTPase was observed. The level of neu expression, as well as the differential expression between P185neu and LAR/PTP1B, directly correlated with tumorigenicity. Furthermore, rat mammary carcinomas with elevated neu expression (neu-induced) also had sharply elevated LAR-PTPase expression when compared to rat mammary carcinomas with little or no neu expression (7,12-dimethylbenzanthracene induced); the level of expression of LAR PTPase was directly correlated with the level of neu expression. Thus, our results provide the first evidence that, in human breast carcinoma cells and in rat mammary carcinomas that have an induced increase in neu expression, a consistent and substantial increase in the expression of specific PTPases occurs. The relationship between P185neu-protein tyrosine kinase expression and specific PTPase expression may play a critical role in human breast tumorigenesis.

Comparative abilities of athymic nude mice and severe combined immune deficient (SCID) mice to accept transplants of induced rat mammary carcinomas: enhanced transplantation efficiency of those rat mammary carcinomas that have elevated expression of neu oncogene.

Grafts of primary carcinogen (DMBA)-induced mammary carcinomas from Sprague-Dawley rats have a poor transplantation efficiency in athymic nude mice. Further compromising these mice immunologically via whole-body irradiation and/or splenectomy, or the administration of hormonal growth factors (estrogen and progesterone) to these mice, did not significantly alter transplantation efficiency. Use of strains of mice that are more immune-impaired than the athymic nude mouse, i.e., the athymic nude-beige-XID mouse (T-cell and LAK-cell deficient) or mice with severe combined immune deficiency (SCID) (which lack functional T cells and B cells) also failed to improve transplantation efficiency. In contrast, transplantation efficiency was sharply increased when primary neu-induced rat mammary carcinomas from female Sprague-Dawley rats were used. These mammary carcinomas, unlike the DMBA-induced rat mammary carcinomas, have a very high level of expression of neu; transplantation of these tumors to either athymic nude mice or SCID mice was considerably more efficient. Thus, these data provide evidence that enhanced expression of neu confers heightened efficiency in the transplantation of primary rat mammary carcinomas to immune-deficient mice (athymic-nude or SCID). Increased neu expression was a greater determinant than more compromised immune states in the transplantation of these rat mammary carcinomas. This biological characteristic of neu expression in mammary carcinomas provides new, additional insight into the importance of this oncogene in mammary tumorigenic processes and may explain, at least in part, the reported inverse relationship between human breast carcinoma neu expression and patient prognosis.

Growth of MCF-7 human breast carcinoma in severe combined immunodeficient mice: growth suppression by recombinant interleukin-2 treatment and role of lymphokine-activated killer cells.

The severe combined immunodeficient (SCID) mouse, lacking functional T and B lymphocytes, has been considered by many groups to be a prime candidate for the reconstitution of a human immune system in a laboratory animal. In addition, this immuno-deficient animal would appear to have excellent potential as a host for transplanted human cancers, thus providing an exceptional opportunity for the study of interactions between the human immune system and human cancer in a laboratory animal. However, because this animal model is very recent, few studies have been reported documenting the capability of these mice to accept human cancers, and whether or not the residual immune cells in these mice (e.g. natural killer, NK, cells; macrophages) possess antitumor activities toward human cancers. Thus, the purpose of this study was (a) to determine whether or not a human breast carcinoma cell line (MCF-7) can be successfully transplanted to SCID mice, (b) to determine whether or not chronic treatment of SCID mice with a potent lymphokine (recombinant interleukin-2, rIL-2) could alter MCF-7 carcinoma growth, and (c) to assess whether or not rIL-2-activated NK cells (LAK cells) are important modulators of growth of MCF-7 cells in SCID mice. To fulfill these objectives, female SCID mice were implanted s.c. with MCF-7 cells (5 x 10(6) cells/mouse) at 6 weeks of age. Six weeks later, some of the mice were injected i.p. twice weekly with rIL-2 (1 x 10(4) U mouse-1 injection-1). Results clearly show that MCF-7 cells can grow progressively in SCID mice; 100% of the SCID mice implanted with MCF-7 cells developed palpable measurable tumors within 5-6 weeks after tumor cell inoculation. In addition, MCF-7 tumor growth was significantly (P less than 0.01) suppressed by rIL-2 treatment. rIL-2 treatment was non-toxic and no effect of treatment on body weight gains was observed. For non-tumor-bearing SCID mice, splenocytes treated in vitro with rIL-2 (lymphokine-activated killer, LAK, cells) or splenocytes derived from rIL-2-treated SCID mice (LAK cells) had significant (P less than 0.01) cytolytic activity toward MCF-7 carcinoma cells in vitro. In contrast, splenocytes (LAK cells) derived from tumor(MCF-7)-bearing rIL-2-treated SCID mice lacked cytolytic activities toward MCF-7 cells in vitro. No significant concentration of LAK cells in MCF-7 human breast carcinomas ws observed nor did rIL-2 treatment significantly alter growth of MCF-7 cells in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)

[Studies on constituents of ganoderma capense IV. The chemical structures of ganoine, ganodine and ganoderpurine].

Two novel pyrrole alkaloids--ganoine and ganodine and a novel purine alkaloid ganoderpurine have been isolated from the mycelium of Ganoderma capense (Lloyd)Teng (Polyporaceae) obtained by submerged fermentation. On the basis of spectroscopic data their structures were elucidated, ganoine is N-isopentyl-5-hydroxymethyl-pyrryl alldehyde. Ganodine is N-phenylethyl-5-hydroxymethyl-pyrryl aldehyde and ganoderpurine is N9-(alpha, alpha dimethyl-gamma-oxobutyl) adenine.