硫酸铵对蓝铜矿硫化浮选的影响及基因机理分析

氧化铜矿物作为铜矿资源的重要组成部分,提高其开发利用技术对于铜矿资源的高效综合回收具有重要意义,蓝铜矿是重要的氧化铜矿物,但自然可浮性较差,通常采用硫化浮选。通过单矿物浮选试验,考察硫酸铵对蓝铜矿硫化浮选的影响。通过矿物表面丁基黄药吸附量分析药剂作用前后矿物表面元素种类和含量的变化,以及药剂在矿物表面吸附能的模拟计算,研究硫酸铵对蓝铜矿硫化浮选的活化机理。结果表明,硫酸铵用量为200 mg/L时使蓝铜矿硫化浮选回收率由44.15%(未添加时)增加至60.03%,矿物表面X射线光电子能谱分析表明,硫酸铵使蓝铜矿矿物表面铜和硫含量增加,碳和氧含量减少,改善矿物表面硫化效果,增加矿物表面疏水性和丁基黄药吸附量。Material studio模拟计算结果表明,硫酸铵降低了丁基黄药以及硫化剂在蓝铜矿表面的吸附能,增加了丁基黄药和硫化钠在矿物表面的吸附稳定性,对蓝铜矿的硫化浮选具有活化作用。

大豆PPR基因功能的研究进展

PPR基因家族是由35个氨基酸组成的序列单元经串联重复排列而成[1],其在大豆生长发育的不同阶段起到举足轻重的作用,主要参与调节大豆植株线粒体、叶绿体等细胞器的基因表达水平,通过影响光合作用,造成干物质积累、生物农艺性状、生育期异常,最终影响大豆的产量、籽粒品质等。对PPR基因结构特征、表达特点等方面及PPR基因在大豆生长发育过程中的作用机理进行较全面的综述,对提高我国大豆产量及品质有重大意义,也为进一步深入研究大豆PPR基因家族的功能提供理论基础。

甘油歧化生产1,3-丙二醇过程的代谢和基因调控机理研究进展

用生物转化法将可再生资源 (如淀粉、纤维素等 )转化为重要的化工原料是目前生物技术领域的一个重要课题。本文以甘油生物转化为 1 ,3 丙二醇过程为考察对象 ,系统综述了该过程代谢和基因调控的研究现状 ,并对今后的研究提出了一些建议。

剥苔基因分子机理的研究

目的从舌上皮细胞凋亡及凋亡相关基因bax、TGF-β3表达的角度研究剥苔(舌黏膜剥脱)的基因分子的病理生理机制。方法运用TUNEL技术、原位杂交、免疫组化和图像分析技术,进行定性和定量分析。结果与正常薄苔比较,剥苔细胞凋亡增加,同时凋亡相关基因bax表达水平升高,而TGF-β3表达水平降低。结论促凋基因bax表达上调可能是引起舌苔上皮细胞凋亡增加从而导致舌黏膜剥脱的重要病理机制。

微生物诱变分子机理及其在肉类工业中的应用

随着分子生物学、细胞生物学及分子遗传学等学科的迅猛发展,对微生物诱变分子机理的研究也日益完善。本文从微生物诱变分子机理出发,着重介绍了DNA损伤分子机理、基因突变分子机理和诱变剂的种类及遗传效应,同时,列举了诱变菌在肉类工业中的应用。

Characteristics and fate behavior of environmentally persistent free radicals in atmospheric particulate matter

Background,aim,and scope Environmentally persistent free radicals(EPFRs)have received significant attention due to their longer lifetime and stable existence in various environments.The strong environmental migration ability of particulate matter allows EPFRs to migrate over long-distance transport,thereby impacting the quality of the local atmospheric environment.Additionally,EPFRs can also adhere to atmospheric particles and interact with typical gaseous pollutants to affect atmospheric chemical reactions.EPFRs can produce some reactive organic species,promoting oxidative stress in the human body,damaging biological macromolecules and ultimately affecting the organism health.EPFRs are considered as a novel type of pollutant that affects human health.Despite their significance,there are few literatures available on the characteristics and fate behaviors of EPFRs up to date.Therefore,supplemental reviews are crucial for providing comprehensive understanding of EPFRs.Materials and methods This review summarizes the characteristics of EPFRs in particulate matter,outlines the generation mechanism and influencing factors of EPFRs,and the impacts of EPFRs on environmental quality and organism health.Results The content of EPFRs in particulate matter ranges from 1017 to 1020 spins∙g−1.Due to the strong mobility of atmospheric particulate matter,the long-term exposure to high levels of EPFRs may aggravate the impact of particulate matter on human health.The interaction between EPFRs and typical gaseous pollutants can alter their fate and influence atmospheric chemical reactions.EPFRs are mainly produced by transition metal elements and substituted aromatic hydrocarbons through electron transfer.Additionally,the chemical bond rupture of organic substances through heat treatment or ultraviolet radiation can also produce EPFRs,and heterogeneous reactions are capable producing them as well.The production of EPFRs is not only influenced by transition metal elements and precursors,but also by various environmental factors such as oxygen,temperature,light radiation,and relative humidity.Discussion EPFRs in atmospheric particulates matters are usually rich in fine particulates with obvious seasonal and regional variations.They can easily enter the human respiratory tract and lungs with inhalable particulates,thereby increasing the risk of exposure.Additionally,EPFRs in atmospheric particulates can interact with some typical gaseous pollutants,impacting the life and fate of EPFRs in the atmosphere,and alter atmospheric chemical reactions.Traditionally,EPFRs are generated by transition metal elements and substituted aromatic hydrocarbons undergoing electron transfer in the post-flame and cool-zone regions of combustion systems and other thermal processes to remove HCl,H2O or CO groups,ultimately produce semiquinones,phenoxyls,and cyclopentadienyls.Recent studies have indicated that EPFRs can also be generated under the conditions of without transition metal elemental.Organics can also produce EPFRs through chemical bond rupture during heat treatment or light radiation conditions,as well as through some heterogeneous reactions and photochemical secondary generation of EPFRs.The presence or absence of oxygen has different effects on the type and yield of EPFRs.The concentration,type,and crystal type of transition metal elements will affect the type,content,and atmospheric lifetime of EPFRs.It is generally believed that the impact of transition metal element types on EPFRs is related to the oxidation-reduction potential.The combustion temperature or heat treatment process significantly affects the type and amount of EPFRs.Factors such as precursor loading content,pH conditions,light radiation and relative humidity also influence the generation of EPFRs.EPFRs can interact with pollutants in the environment during their migration and transformation process in environmental medium.This process accelerates the degradation of pollutants and plays a crucial role in the migration and transformation of organic pollutants in environmental media.The reaction process of EPFRs may lead to the production of reactive oxygen species(ROS)such as∙OH,which can induce oxidative stress,inflammation and immune response to biological lung cells and tissues,leading to chronic respiratory and cardiopulmonary dysfunction,cardiovascular damage and neurotoxic effects,ultimately impacting the health of organisms.Conclusions The interaction mechanism between EPFRs in particulate matter and gaseous pollutants remains unclear.Furthermore,research on the generation mechanism of EPFRs without the participation of transition metals is not comprehensive,and the detection of EPFRs is limited to simple qualitative categories and lack accurate qualitative analysis.Recommendations and perspectives Further research should be conducted on the generation mechanism,measurement techniques,migration pathways,and transformation process of EPFRs.It is also important to explore the interaction between EPFRs in atmospheric particulate matter and typical gaseous pollutants.

微生物诱变分子机理及其在肉类工业中的应用

随着分子生物学、细胞生物学及分子遗传学等学科的迅猛发展 ,对微生物诱变分子机理的研究也日益完善。从微生物诱变分子机理出发 ,着重介绍了DNA损伤分子机理、基因突变分子机理和诱变剂的种类及遗传效应 ,同时 。

细菌耐药机制及其控制对策

随着抗菌药物在畜牧养殖业中的广泛应用,细菌的耐药性越来越引起人们的重视,其极大地影响食品安全,危害人类身体健康。作者就近年来国内外对细菌的耐药机制、基因机理及对耐药性的控制对策等方面作了阐明和综述。

细菌耐药机制及其控制

随着抗菌药物在畜牧养殖业中的广泛应用,细菌的耐药性越来越引起人们的重视,成为全球化的重大问题,极大地影响着食品安全,危害着人类身体健康。本文就近年来国内外对细菌的耐药机制、基因机理及对耐药性的控制对策等方面作了阐明和综述。

细菌耐药机制及其控制对策

随着抗菌药物在畜牧养殖业中的广泛应用,细菌的耐药性越来越引起人们的重视,细菌耐药性成为全球化的重大问题,其极大地影响着食品安全,危害着人类身体健康。此就近年来国内外对细菌的耐药机制、基因机理及对耐药性的控制对策等方面作了阐明和综述。

Features,Mechanisms and Applies of Post-transcriptional Gene Silencing in Transgenic Plants

Since transgene silencing was found in transgenic plants,many scholars have studied it extensively and considered that it has three functional mechanisms:post dependent gene silencing,transcriptional gene silencing,post transcriptional gene silencing.At the moment,people have mainly focused on the study of post transcriptional gene silencing and found its features:extensivity,conduction and peculiarity,also put forward some hypothesis for its mechanisms,for example,RNA threshold model,aberrant RNA model,inter or intra molecular base pairing model and so on.Furthermore,post transcriptional gene silencing is being applied in gene engineering of plants.Recently the people have found that post transcriptional gene silencing has bearing on capacity plants resisting virus.Many researchers have studied post transcriptional gene silencing,but there are some questions which need be solved in the future.This article summarizes progresses in features,mechanisms,applies of post transcriptional gene silencing about transgenic plants.

Expression of Integrin α4 in Osteosarcoma and Significance

Objective： To investigate the expression of integrin α4 in osteosaxcoma and significance. Methods- Forty-six patients with osteosarcoma （Enneking Ⅰ-Ⅲ） were analyzed for the expression of α4 integrin subunit using immunohistochemical method. Results： Twenty-nine （63.04%） of 46 samples demonstrated positive （＋-＋＋） integrin α4 expression. Loss expression of integrin α4 was observed in the patients with advanced Enneking stage （P=0.0040） and with metastatic disease at presentation （P=0.0158）. Integrin α4 expression correlated with cell differentiation, the level of malignancy and the invasive behavior of osteosaxcoma. Conclusion： The loss expression of integrin α4 subunit might be a predictor indicating the invasive potential of osteosarcoma and play a role in metastasis of osteosaxcoma patients.

Detection and Sequence Analysis of Escherichia coli Virulence Genes

[Objective] This study aimed to explore the pathogenic mechanism of E., cherichia coll. [Method] An E. coil strain isolated from raccoon dogs in vivo was studied, which had been identified, PCR was used to detect the gene of irp2 （301 bp） and fyuA （953 bp） related to E. coil virulence and PCR products were s, quenced. [Result] The genes of irp2 and fyuA were successfully amplified in boi strains isolated from raccoon dogs. Compared with the GenBank, the identity of tTr irp2 gene sequence and the fyuA gene sequence of the strain reached 98.5% 99.2% and 98.9%-100% respectively. Compared with each other, the identity of tt- two gene sequences of irp2 was 99.3%, and that between the two fyuA gene se quences was 98.9%. [Conclusion] This study provided scientific experimental data fi E. coil pathogenicity, prevention, diagnosis and treatment.

Genome-wide comparative analysis of type-A Arabidopsis response regulator genes by overexpression studies reveals their diverse roles and regulatory mechanisms in cytokinin signaling

Cytokinin is a critical growth regulator for various aspects of plant growth and development. In Arabidopsis, cytokinin signaling is mediated by a two-component system-based phosphorelay that transmits a signal from the receptors, through histidine phosphotransfer proteins, to the downstream response regulators （ARRs）. Of these ARRs, type-A ARR genes, whose transcription can be rapidly induced by cytokinin, act as negative regulators of eytokinin signaling. However, because of functional redundancy, the function of type-A ARR genes in plant growth and development is not well understood by analyzing loss-of-function mutants. In this study, we performed a comparative functional study on all ten type-A ARR genes by analyzing transgenic plants overexpressing these ARR genes fused to a MYC epitope tag. Overexpression of ARR genes results in a variety of cytokinin-associated phenotypes. Notably, overexpression of different ARR transgenes causes diverse phenotypes, even between phylogenetically closely-related gene pairs, such as within the ARR3-ARR4 and ARR5-ARR6 pairs. We found that the accumulation of a subset of ARR proteins （ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15） is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation. Moreover, similar to that of previously characterized ARR5, ARR6 and ARR7, stability of ARR16 and ARR17, possibly including ARR8 and ARR15, is regulated by cytokinin. These results suggest that type-A ARR proteins are regulated by a combinatorial mechanism involving both the cytokinin and proteasome pathways, thereby executing distinctive functions in plant growth and development.

Homologous recombination in DNA repair and DNA damage tolerance

Homologous recombination （HR） comprises a series of interrelated pathways that function in the repair of DNA double-stranded breaks （DSBs） and interstrand crosslinks （ICLs）. In addition, recombination provides critical support for DNA replication in the recovery of stalled or broken replication forks, contributing to tolerance of DNA damage. A central core of proteins, most critically the RecA homolog Rad51, catalyzes the key reactions that typify HR： homology search and DNA strand invasion. The diverse functions of recombination are reflected in the need for context-specific factors that perform supplemental functions in conjunction with the core proteins. The inability to properly repair complex DNA damage and resolve DNA replication stress leads to genomic instability and contributes to cancer etiology. Mutations in the BRCA2 recombination gene cause predisposition to breast and ovarian cancer as well as Fanconi anemia, a cancer predisposition syndrome characterized by a defect in the repair of DNA interstrand crosslinks. The cellular functions of recombination are also germane to DNA-based treatment modalities of cancer, which target replicating cells by the direct or indirect induction of DNA lesions that are substrates for recombination pathways. This review focuses on mechanistic aspects of HR relating to DSB and ICL repair as well as replication fork support.

Mechanisms inactivating the gene for E-cadherin in sporadic gastric carcinomas

AIM： To study the role of CDH1/E-cadherin （E-cad） gene alteration profiles including mutation, loss of heterozygosity （LOH）, promoter polymorphism and hypermethylation in mechanisms of CDH1 inactivation in gastric carcinoma （GC）. METHODS： Specimens were collected surgically from 70 patients with GC. Allelotyping PCR and detection of LOH, denaturing high pressure liquid chromatography and DNA sequencing, restriction fragment length polymorphism analysis, methylation specific PCR, and immunohistochemical staining were used. RESULTS： Promoter polymorphism was not a major mechanism of E-cad inactivation. Only one truncating mutation was found in a diffuse type tumor （3%）. Both LOH and promoter hypermethylation were major mechanisms of E-cad inactivation, but interestingly, there was a negative association between the fraction of allelic loss （LOH） in tumors and hypermethylation of CDH1. Therefore LOH and hypermethylation were two different tumorigenic pathways involved in GC. CONCLUSION： Given the findings that somatic mutation was extremely low and the relationship between LOH and hypermethylation was inverse, any two combinations of these three factors cannot fulfill the classical two-hit hypothesis of CDH1 inactivation. Thus, other mechanisms operating at the transcriptional level or at the post-translational level might be required to induce E-cadherin inactivation.

Phase I/II enzyme gene polymorphisms and esophageal cancer risk: A meta-analysis of the literature

AIM:Phase I/II enzymes metabolize environmental carcinogens and several functional polymorphisms have been reported in their encoding genes. Although their significance with regard to esophageal carcinogenicity has been examined epidemiologically, it remains controversial. The present systematic review of the literature was performed to clarify associations. METHODS: Eligible studies were case-control or cohort studies published until September 2004 that were written in any language. From PubMed and a manual review of reference lists in relevant review articles, we obtained 16 studies related to the CYP1A1 Ile-Val substitution in exon 7, CYP1A1 MspI polymorphisms, CYP2E1 Rsal polymorphisms, GSTM1 null type, GSTT1 null type and GSTP1 Ilel04Val. All were of case-control design. Summary statistics were odds ratios (ORs) comparing heterozygous-, homozygous-non-wild type or these two in combination with the homozygous wild type, or the null type with the non-null type for GSTM1 and GSTT1, A random effect model was used to estimate the summary ORs. A meta-regression analysis was applied to explore sources of heterogeneity. RESULTS: Individuals with the Ile-Val substitution in CYP1A1 exon 7 had increased esophageal cancer risk, with ORs (95%CI) compared with lie/lie of 1.37 (1.09-1.71), 2.52 (1.62-3.91) and 1.44 (1.17-1.78) for Ile-Val, Val/Val genotype and the combined group. No significant association was found between esophageal cancer risk and the other genetic parameters. CONCLUSION: A significant association exists between the CYP1A1 Ile-Val polymorphism and risk of esophageal cancer. Polymorphisms that increase the internal exposure to activated carcinogens may increase the risk of esophageal cancer.

Copy number changes of target genes in chromosome 3q25.3-qter of esophageal squamous cell carcinoma: TP63is amplified in early carcinogenesis but down-regulated as disease progressed

AIM: By using comparative genomic hybridization, gain of 3q was found in 45-86% cases of esophageal squamous cell carcinoma (EC-SCC). Chromosome 3q25.3-qter is the minimal common region with several oncogenes found within this region. However, amplification patterns of these genes in EC-SCC have never been reported. The possible association of copy number changes of these genes with pathologic characteristics is still not clear. METHODS: Real-time quantitative PCR (Q-PCR) was performed to analyze the copy number changes of 13 candidate genes within this region in 60 primary tumors of EC-SCC, and possible association of copy number changes with pathologic characteristics was analyzed by statistics. Immunohistochemistry (IHC) study was also performed on another set of 111 primary tumors of EC-SCC to verify the association between TP63 expression change and lymph node metastasis status. RESULTS: The average copy numbers (±SE) per haploid genome of individual genes in 60 samples were (from centromere to telomere): SSR3: 4.19 (±0.69); CCNL1: 5.24 (±0.67); SMC4L1: 2.01 (±0.16); EVI1: 2.02 (±0.12); hTERC. 5.28 (±0.54); SKIL 2.71 (±0.14); EIF5A2. 1.95 (±0.12); ECT2: 9.18 (±1.68); PIK3CA: 8.13 (±1.17); EIF4G1: 1.07 (±0.05); 557: 3.07 (±0.25); TP63: 2.51 (±0.22); TFRC. 2.42 (±0.19). Four clusters of amplification were found: SSR3 and CCLN1 at 3q25.31; hTERC and SKIL at 3q26.2; ECT2 and PIK3CA at 3q26.31-q26.32; and 55T, TP63 and TFRC at 3q27.3-q29. Patients with lymph node metastasis had significantly lower copy number of TP63 in the primary tumor than those without lymph node metastasis. IHC study on tissue arrays also showed that patients with lymph node metastasis have significantly lower TP63 staining score in the primary tumor than those without lymph node metastasis. CONCLUSION: This study showed that different amplification patterns were seen among different genes within 3q25.3-qter in EC-SCC, and several novel candidate oncogenes (SSR3, SMC4L1, ECT2, and SST) were identified. TP63 is amplified in early stage of EC-SCC carcinogenesis but down-regulated in advanced stage of disease.

Mechanism of metastasis by membrane type 1-matrix metalloproteinase in hepatocellular carcinoma

AIM To investigate the precise role of membrane type 1-matrix metalloproteinase （NTI-NNP） in hepatocellular carcinoma （HCC） metastasis. METHODS- Human HCC cells Hep3B with overexpression of MTT-MMP were established by stable transfection, and compared with control cells carrying the empty vector. Cells were examined in vivo for their differences in the metastatic ability of athymic nude mice, and analyzed in vito for their differences in invasion ability by invasion chamber coated with Matrigel, adhesion towards collagen I and migration through culture chamber. Cell proliferation and apoptosis in adherent and suspension status were evaluated by MTr and flow cytometry analysis. RESULTS We found that overexpression of MT1-MMP could increase intrahepatic metastasis in nude mice with orthotopic implantation of HCC cells （incidence of 100% [MT1-MMP transfectants] vs 40% [vector control transfectants], P〈0.05）. NT1-MMP could also enhance cell invasion through Natrigel （107.7 vs 39.3 cells/field, P〈0.001）, adhesion towards matrix （0.30 vs 0.12 absorbance unit at 540 nm, P〈0.001）, cell migration （89.3 vs 39.0 cells/field, P〈0.001）, and cell proliferation （24.3 vs 40.5 h/doubling, P〈0.001）. We also observed that NTI-NNP supported cell survival （71.4% vs 23.9%, P〈0.001） with reduced apoptosis （43.7% vs51.0%, P〈0.05） in an attachment-free environment. CONCLUSION： MT1-MMP overexpression could enhance metastasis. In addition to its active role in matrix degradation during tumor invasion, MT1-MMP enhances tumor cell survival upon challenge of detachment, which is important during metastasis when cells enter the circulation.

Expression of p57^(kip2) and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma

AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 patients with HCC and 10 liver tissues of normal persons was detected with Elivision immunohistochemical technique. RESULTS: The p57kip2 protein positive-expression rate in HCC was 56.25%, lower than that in normal tissues (100%, P<0.05). The reduced expression of p57kip2 protein correlated significantly with moderate or low differentiation of tumor cells (P = 0.007 <0.05), high clinical stage (P= 0.041 <0.05) and poor prognosis (P= 0.036 <0.05), but did not correlate significantly with metastasis, tumor size, level of AFP and age (P>0.05). The PCNA positive-expression rate was 56.25%, which was correlated significantly with the expression of p57kip2 (P= 0.025<0.05). The p53 positive-expression rate was 46.88%, which was not correlated significantly with the expression of p57kip2 (P>0.05). CONCLUSION: There is a marked loss or absence of p57kip2 expression and high expression of PCNA in HCC, which are involved in carcinogenesis and development of HCC. The p57kip2 and p53 may induce apoptosis via different mechanisms.