Microplastic exposure disturbs sleep structure,reduces lifespan,and decreases ovary size in Drosophila melanogaster

The organ-specific toxicity resulting from microplastic(MP)exposure has been extensively explored,particularly concerning the gut,liver,testis,and lung.However,under natural conditions,these effects are not restricted to specific organs or tissues.Investigating whether MP exposure presents a systemic threat to an entire organism,impacting factors such as lifespan,sleep,and fecundity,is essential.In this study,we investigated the effects of dietary exposure to two different doses of MPs(1–5μm)using the terrestrial model organism Drosophila melanogaster.Results indicated that the particles caused gut damage and remained within the digestive system.Continuous MP exposure significantly shortened the lifespan of adult flies.Even short-term exposure disrupted sleep patterns,increasing the length of daytime sleep episodes.Additionally,one week of MP exposure reduced ovary size,with a trend towards decreased egg-laying in mated females.Although MPs did not penetrate the brain or ovaries,transcriptome analysis revealed altered gene expression in these tissues.In the ovary,Gene Ontology(GO)analysis indicated genotoxic effects impacting inflammation,circadian regulation,and metabolic processes,with significant impacts on extracellular structure-related pathways.In the brain,GO analysis identified changes in pathways associated with proteolysis and carbohydrate metabolism.Overall,this study provides compelling evidence of the systemic negative effects of MP exposure,highlighting the urgent need to address and mitigate environmental MP pollution.

Decoding the nexus:branched-chain amino acids and their connection with sleep,circadian rhythms,and cardiometabolic health

The sleep-wake cycle stands as an integrative process essential for sustaining optimal brain function and,either directly or indirectly,overall body health,encompassing metabolic and cardiovascular well-being.Given the heightened metabolic activity of the brain,there exists a considerable demand for nutrients in comparison to other organs.Among these,the branched-chain amino acids,comprising leucine,isoleucine,and valine,display distinctive significance,from their contribution to protein structure to their involvement in overall metabolism,especially in cerebral processes.Among the first amino acids that are released into circulation post-food intake,branched-chain amino acids assume a pivotal role in the regulation of protein synthesis,modulating insulin secretion and the amino acid sensing pathway of target of rapamycin.Branched-chain amino acids are key players in influencing the brain's uptake of monoamine precursors,competing for a shared transporter.Beyond their involvement in protein synthesis,these amino acids contribute to the metabolic cycles ofγ-aminobutyric acid and glutamate,as well as energy metabolism.Notably,they impact GABAergic neurons and the excitation/inhibition balance.The rhythmicity of branchedchain amino acids in plasma concentrations,observed over a 24-hour cycle and conserved in rodent models,is under circadian clock control.The mechanisms underlying those rhythms and the physiological consequences of their disruption are not fully understood.Disturbed sleep,obesity,diabetes,and cardiovascular diseases can elevate branched-chain amino acid concentrations or modify their oscillatory dynamics.The mechanisms driving these effects are currently the focal point of ongoing research efforts,since normalizing branched-chain amino acid levels has the ability to alleviate the severity of these pathologies.In this context,the Drosophila model,though underutilized,holds promise in shedding new light on these mechanisms.Initial findings indicate its potential to introduce novel concepts,particularly in elucidating the intricate connections between the circadian clock,sleep/wake,and metabolism.Consequently,the use and transport of branched-chain amino acids emerge as critical components and orchestrators in the web of interactions across multiple organs throughout the sleep/wake cycle.They could represent one of the so far elusive mechanisms connecting sleep patterns to metabolic and cardiovascular health,paving the way for potential therapeutic interventions.

Geroprotection from ergothioneine treatment in Drosophila melanogaster by improving intestinal barrier and activation of intestinal autophagy

Ergothioneine is a natural amino acid with powerful antioxidant activity.Previous studies have demonstrated that ergothioneine can increase the lifespan of Drosophila melanogaster and Caenorhabditis elegans,and enhance telomerase activity.In present study,the metagenomics sequencing and quantitative real-time polymerase chain reaction analysis were employed to characterize the composition and diversity of gut microbiome in aging flies.And the alterations in the gut barrier,gut morphology,and other gut physiological indicators of aging flies were evaluated.Here,the results showed that ergothioneine induced little variations in gut microbiota composition in flies at mid-life,and significant alterations in the gut microbiota populations were only observed in flies at late-life.And ergothioneine attenuated age-related gut injuries,including decreasing reactive oxygen species levels in intestinal enterocytes,reduction of intestinal cells death,and preservation of gut integrity in aging flies.Ergothioneine also improved the gut morphology by preserving the structure and shape of cell organelles and inducing the intestinal autophagy.And activation of intestinal autophagy also contributed to the longevity effect mediated by ergothioneine in an unidentified mechanism.

Exploiting fly models to investigate rare human neurological disorders

Rare neurological diseases,while individually are rare,collectively impact millions globally,leading to diverse and often severe neurological symptoms.Often attributed to genetic mutations that disrupt protein function or structure,understanding their genetic basis is crucial for accurate diagnosis and targeted therapies.To investigate the underlying pathogenesis of these conditions,researchers often use non-mammalian model organisms,such as Drosophila(fruit flies),which is valued for their genetic manipulability,cost-efficiency,and preservation of genes and biological functions across evolutionary time.Genetic tools available in Drosophila,including CRISPR-Cas9,offer a means to manipulate gene expression,allowing for a deep exploration of the genetic underpinnings of rare neurological diseases.Drosophila boasts a versatile genetic toolkit,rapid generation turnover,and ease of large-scale experimentation,making it an invaluable resource for identifying potential drug candidates.Researchers can expose flies carrying disease-associated mutations to various compounds,rapidly pinpointing promising therapeutic agents for further investigation in mammalian models and,ultimately,clinical trials.In this comprehensive review,we explore rare neurological diseases where fly research has significantly contributed to our understanding of their genetic basis,pathophysiology,and potential therapeutic implications.We discuss rare diseases associated with both neuron-expressed and glial-expressed genes.Specific cases include mutations in CDK19 resulting in epilepsy and developmental delay,mutations in TIAM1 leading to a neurodevelopmental disorder with seizures and language delay,and mutations in IRF2BPL causing seizures,a neurodevelopmental disorder with regression,loss of speech,and abnormal movements.And we explore mutations in EMC1 related to cerebellar atrophy,visual impairment,psychomotor retardation,and gain-of-function mutations in ACOX1 causing Mitchell syndrome.Loss-of-function mutations in ACOX1 result in ACOX1 deficiency,characterized by very-long-chain fatty acid accumulation and glial degeneration.Notably,this review highlights how modeling these diseases in Drosophila has provided valuable insights into their pathophysiology,offering a platform for the rapid identification of potential therapeutic interventions.Rare neurological diseases involve a wide range of expression systems,and sometimes common phenotypes can be found among different genes that cause abnormalities in neurons or glia.Furthermore,mutations within the same gene may result in varying functional outcomes,such as complete loss of function,partial loss of function,or gain-of-function mutations.The phenotypes observed in patients can differ significantly,underscoring the complexity of these conditions.In conclusion,Drosophila represents an indispensable and cost-effective tool for investigating rare neurological diseases.By facilitating the modeling of these conditions,Drosophila contributes to a deeper understanding of their genetic basis,pathophysiology,and potential therapies.This approach accelerates the discovery of promising drug candidates,ultimately benefiting patients affected by these complex and understudied diseases.

SARS-CoV2 Nsp3 protein triggers cell death and exacerbates amyloid β42-mediated neurodegeneration

Infection caused by the severe acute respiratory syndrome coronavirus 2(SARS-CoV2)virus,responsible for the coronavirus disease 2019(COVID-19)pandemic,induces symptoms including increased inflammatory response,severe acute respiratory syndrome(SARS),cognitive dysfunction like brain fog,and cardiovascular defects.Long-term effects of SARS-CoV2 COVID-19 syndrome referred to as post-COVID-19 syndrome on age-related progressive neurodegenerative disorders such as Alzheimer's disease remain understudied.Using the targeted misexpression of individual SARS-CoV2 proteins in the retinal neurons of the Drosophila melanogaster eye,we found that misexpression of nonstructural protein 3(Nsp3),a papain-like protease,ablates the eye and generates dark necrotic spots.Targeted misexpression of Nsp3 in the eye triggers reactive oxygen species production and leads to apoptosis as shown by cell death reporters,terminal deoxynucleotidyl transferase(TdT)dUTP Nick-end labeling(TUNEL)assay,and dihydroethidium staining.Furthermore,Nsp3 misexpression activates both apoptosis and autophagy mechanism(s)to regulate tissue homeostasis.Transient expression of SARS-CoV2 Nsp3 in murine neuroblastoma,Neuro-2a cells,significantly reduced the metabolic activity of these cells and triggers cell death.Misexpression of SARS-CoV2 Nsp3 in an Alzheimer's disease transgenic fly eye model(glass multiple repeats[GMR]>amyloidβ42)further enhances the neurodegenerative rough eye phenotype due to increased cell death.These findings suggest that SARS-CoV2 utilizes Nsp3 protein to potentiate cell death response in a neurodegenerative disease background that has high pre-existing levels of neuroinflammation and cell death.

Naringin ameliorates H_(2)O_(2)-induced oxidative damage in cells and prolongs the lifespan of female Drosophila melanogaster via the insulin signaling pathway

Naringin exists in a wide range of Chinese herbal medicine and has proven to possess several pharmacological properties.In this study,PC12,HepG2 cells,and female Drosophila melanogaster were used to investigate the antioxidative and anti-aging effects of naringin and explore the underlying mechanisms.The results showed that naringin inhibited H_(2)O_(2)-induced decline in cell viability and decreased,the content of reactive oxygen species in cells.Meanwhile,naringin prolonged the lifespan of flies,enhanced the abilities of climbing and the resistance to stress,improved the activities of antioxidant enzymes,and decreased malondialdehyde content.Naringin also improved intestinal barrier dysfunction and reduced abnormal proliferation of intestinal stem cells.Moreover,naringin down-regulated the mRNA expressions of inr,chico,pi 3k,and akt-1,and up-regulated the mRNA expressions of dilp2,dilp3,dilp5,and foxo,thereby activating autophagy-related genes and increasing the number of lysosomes.Furthermore,the mutant stocks assays and computer molecular simulation results further indicated that naringin delayed aging by inhibiting the insulin signaling(IIS)pathway and activating the autophagy pathway,which was consistent with the result of network pharmacological predictions.

The protective effects of Panax notoginseng in the treatment of inflammatory bowel disease:in silico and in vivo studies

Background:Panax notoginseng(PNE)is a prominent traditional Chinese medicine with extensive beneficial effects on the immune system.However,the precise mechanism of PNE in treating inflammatory bowel disease(IBD)remains unclear.Methods:We first used an extensive metabolomics approach utilizing UPLC-ESI-Q TRAP-MS/MS to identify the metabolite components of PNE aqueous extract.Moreover,the mechanism of PNE in treating IBD was investigated through in silico analysis including RNA-seq analysis,Network pharmacology and Molecular docking.Then a Drosophila toxin-induced intestinal inflammation model was employed to investigate further.Results:A total of 1,543 metabolites of PNE aqueous extract were characterized using UPLC-ESI-Q TRAP-MS/MS.In silico analyses showed that 97 IBD hub targets were targeted by 21 PNE ingredients.Kyoto Encyclopedia of Genes and Genomes results indicated that PNE may play an anti-IBD role through the Mitogen-activated protein kinase(MAPK)signaling pathway and other immune-related signaling pathways.Moreover,11 top hits compounds of PNE show a good affinity binding to IBD targets.The experimental results demonstrated that PNE can effectively improve the survival rate of adult Drosophila while also inhibit the excessive proliferation and differentiation of intestinal stem cells induced by sodium dodecyl sulfate.Furthermore,PNE notably lower the epithelial cell mortality,the accumulation of reactive oxygen species and the activation of oxidative stress-associated jun-Nterminal kinase(JNK)pathway.Conclusion:Our data suggests that PNE aqueous extract has a significant protective impact on the intestinal homeostasis of Drosophila.These findings establish a basis for utilizing PNE in clinical investigations and managing IBD.

Effects of Sodium Cyclohexyl Sulfamate on Growth and Development of Drosophila melanogaster

[Objectives]This study was conducted to investigate the effects of different concentrations of sodium cyclohexyl sulfamate on the growth and development of Drosophila melanogaster.[Methods]Different concentrations of sodium cyclohexyl sulfamate were added to the culture medium,and the effects of different concentrations of sodium cyclohexyl sulfamate on the development time and weight of D.melanogaster in various life stages were statistically analyzed.[Results]High concentration of sodium cyclohexyl sulfamate delayed the time of pupation and eclosion of D.melanogaster,which made D.melanogaster lose weight.The number of male D.melanogaster in the first generation was much larger than that of female individuals,which indicated that the effect of sodium cyclohexyl sulfamate on male D.melanogaster was greater than that of female individuals.In a word,high concentration of sodium cyclohexyl sulfamate significantly inhibited the growth and development of D.melanogaster.[Conclusions]This study provides some reference data for the research perspective of food additives and the safe use of sodium cyclohexyl sulfamate.

果蝇活动规律及其影响因素研究

以果蝇为研究对象,设置晴天、阴天、雨天等不同天气条件,苹果、香蕉、葡萄、杨梅、樱桃、蓝莓等不同水果果泥,诱剂处理,比较不同处理果蝇诱捕种类和数量,分析果蝇活动规律。结果表明,供试6种成熟水果中,香蕉、蓝莓果泥诱捕的果蝇数显著高于其他4种水果果泥(p<0.01),而绿如蓝牌果蝇诱剂诱捕数量显著高于香蕉果泥(p<0.01)。诱剂诱捕的果蝇种类主要有黑腹果蝇、斑翅果蝇、伊米果蝇、海德氏果蝇、筋果蝇等。晴天诱捕的雄果蝇数量明显高于阴天和雨天(p<0.01)。一天内,8:00—10:00和16:00—18:00诱捕果蝇数量较多,是果蝇活动的两个高峰期。

Humanization for neurological disease modeling:A roadmap to increase the potential of Drosophila model systems

Neuroscience and neurology research is dominated by experimentation with rodents.Around 75%of neurology disease-associated genes have orthologs in Drosophila mel-anogaster,the fruit fly amenable to complex neurological and behavioral investiga-tions.However,non-vertebrate models including Drosophila have so far been unable to significantly replace mice and rats in this field of studies.One reason for this situ-ation is the predominance of gene overexpression(and gene loss-of-function)meth-odologies used when establishing a Drosophila model of a given neurological disease,a strategy that does not recapitulate accurately enough the genetic disease condi-tions.I argue here the need for a systematic humanization approach,whereby the Drosophila orthologs of human disease genes are replaced with the human sequences.This approach will identify the list of diseases and the underlying genes that can be adequately modeled in the fruit fly.I discuss the neurological disease genes to which this systematic humanization approach should be applied and provide an example of such an application,and consider its importance for subsequent disease modeling and drug discovery in Drosophila.I argue that this paradigm will not only advance our un-derstanding of the molecular etiology of a number of neurological disorders,but will also gradually enable researchers to reduce experimentation using rodent models of multiple neurological diseases and eventually replace these models.

In vivo anti-aging properties on fat diet-induced high fat Drosophila melanogaster of n-butanol extract from Paecilomyces hepiali

The purpose of this study was to explore the potential of the development and application of Paecilomyces hepiali,a fungus with edible and medicinal value,as a foodborne antioxidant and anti-aging agent.Its n-butanol extract(PHE)from rice cultures was selected for anti-aging experiment because of significant free radical scavenging activity in vitro.In vivo,PHE could significantly prolong the mean lifespan,50%survival days,and the maximum lifespan of Drosophila on a high-fat diet.It is amazing that the mean lifespan increased from 19.1 days to 32.9 days,50%survival days increased from 15.7 days to 34.3 days,and the maximum lifespan extended from 44.7 days to 52.7 days,when the high-fat female Drosophila model was fed with 10μg/mL PHE.Further research showed that PHE reduced the accumulation of peroxide products and increased the activity of antioxidant enzymes.Then,through antioxidant activity tracking,dimerumic acid(compound 1,the IC_(50) value of 3.4μg/mL on DPPH free radicals scavenging activity),4,5-dihydroxy-3-methoxypentanoic acid(compound 2,new compound),and thymidine(compound 3)were isolated from PHE.It is worth mentioning that dimerumic acid,the major antioxidant compound of PHE(content up to 3%),was discovered in P.hepiali for the first time.It was concluded that PHE showed excellent anti-aging activity at a very low concentration on fat diet-induced high fat Drosophila melanogaster,and dimerumic acid may be its main material basis.These results indicated that PHE had the potential to be developed as antioxidant and anti-aging agent in the healthcare industry.

Signaling interactions among neurons impact cell fitness and death in Alzheimer's disease

The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may help prevent widespread cell death.Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role.As the disease progresses,dysregulation of signaling pathways that govern cell death contributes to neurodegeneration.Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated neurodegeneration.Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells.This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons.Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells.Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration.Generating genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease.These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.

Presenilin and Alzheimer’s disease interactions with aging,exercise and high-fat diet:A systematic review

Presenilin(Psn)protein is associated with organismal aging.Mutations in the Psn gene may lead to Alzheimer’s disease(AD),dilated cardiomyopathy(DCM),and many age-dependent degenerative diseases.These diseases seriously affect the quality of life and longevity of the population and place a huge burden on health care and economic systems around the world.Humans have two types of Psn,presenilin-1(PSEN1)and presenilin-2(PSEN2).Mutations in the genes encoding PSEN1,PSEN2,and amyloid precursor protein(APP)have been identified as the major genetic causes of AD.Psn is a complex gene strongly influenced by genetic and environmental factors.The effects of exercise,training,and a high-fat diet on the Psn gene expressed in the heart and its related pathways are not fully understood.Fortunately,relevant aspects of the mutational effects on Psn can be studied experimentally in easily handled animal models,including Drosophila,mice,and other animals,all of which share orthologous genes of Psn with humans.Many previous studies have linked aging,exercise training,and a high-fat diet to the Psn gene.This review discusses the interrelationship between aging,exercise training,and a high-fat diet on the Psn gene and its associated disease,AD.The aim is to understand the adverse effects of Psn gene mutations on the body and the diseases caused by AD,find ways to alleviate the adverse effects and provide new directions for the improvement of treatment strategies for diseases caused by Psn gene mutations.

Ontogenes and Their Role in Cellular Construction

The genes referred to as ontogenes are responsible for conditional mutations. Based on the results of the research of conditional mutations in D. melanogaster, we attempt to figure out the biological role of ontogenes. We conclude that ontogenes in the process of individual development control the construction of the living organisms of cells (cellular construction), which comprises the induction of cell division, determination of division plane, and the location of daughter cells after the division is completed. The process of morphogenesis consists of cellular construction and protein synthesis. Protein synthesis is controlled by protein-coding (Mendelian) genes. Mendelian genes are switched on by ontogenes. In terms of the two-component genome composed of Mendelian genes and ontogenes, we consider 1) the concept of biological character;2) interspecific incompatibility;3) ontogenesis;4) phylogenesis;and 5) mutagenesis. Ontogenes, which control cellular construction, possess the specific features unusual for Mendelian genes, namely, 1) the activity in germ line tissue;2) remote interaction;and 3) activity in a compacted state (heterochromatization). These specific features of ontogenes suggest that unlike the Mendelian genes with their chemical activity, ontogenes possess another type of activity (biophysical) involving induction of an electromagnetic field.

Mutation in Ontogene and Emergence of Secondary Chromosome Damages in Drosophila Germline Cells

The conditional mutations in drosophila were obtained by γ-irradiation and selected using the test for dominant lethality. The conditional mutations survive under permissive genetic conditions and, additionally, commence to display novel properties. One of such properties is a recessive lethality. Ten conditional mutations that displayed recessive lethality were mapped with the help of a standard set of deletions. Half mutations contained two and more lethal defects. The fact that a large number of the lethal defects are associated with one mutation suggests that γ-irradiation is the most unlikely cause of the defects. One of the conditional mutations carried four lethal regions and had a Small barrel (Smba) visual phenotype. The Smba phenotype in the Smba/ In(2LR) Cy strain is inherited according to a parental type and disappears in the Smba/In(2LR) Pm strain. Lethality in two of the four lethal regions also disappears in this strain. A separate experiment was conducted to clarify how these regions lost a lethal manifestation after the In(2LR) Cy chromosome in the Smba/In(2LR) Cy strain was replaced with the In(2LR) Pm chromosome. The process of disappearance of the Smba phenotype was also observed in three Smba/In(2LR) Cy substocks. These data suggest that the regions of multiple recessive lethality emerge in a secondary manner under the effect of the earlier formed radiation-induced mutation in ontogene. It is assumed that the recessive lethal regions are the ontogenes with an altered DNA conformation. The conformation in ontogenes is changed in the germline cells during a regular “editing” of the individual development program.

Analysis of the Constituents and Antisenile Function of Achyranthes bidentata Polysaccharides

Achyranthes bidentata polysaccharides (ABPS), water_soluble polysaccharides, isolated from the roots of Achyranthes bidentata Bl. of Amaranthaceae family, was divided into four parts, named as Con.1, Con.2, Con.3 and Con.4, respectively, by chromatography on DEAE_Sepharose fast_flow column and Sephadex G_100 column in order. Con.1 was the constituent of high molecular weight and the other three were all of low molecular weight. Micro_Kjeldahl analysis showed that Con.1 contained 3.95% of nitrogen and neither did the other three parts. The antisenile effects of the four parts of ABPS were studied with Drosophila melanogaster. Results showed that Con.1 has no antisenile effect and all the others could significantly increase the average body weight by 3.85%-5.47% and significantly prolonged the average lifespan by 2.61%- 3.16% of D. melanogaster at the concentration of 2 or 5 mg/g (ABPS/medium).

Insecticidal Activity of Crude Extract of Saponins isolated from Sapindus miukurossi Gatren

[Objective] The study aimed to provide the theoretical basis for the development of Saponins isolated from Sapindus mukurossi in the application of pesticides and lay the foundation for the development and utilization of Sapindus species resources in Yunnan province. [ Method] Saponine from S. mukurossi was extracted by the methods of dipping, feed mixed with pesticide, unlimited feeding, and conducted indoor toxicity determination on Plutella xylostella （Linnaeus）, Sitophilus zeamais motschulsky and Drosophila. [ Result] Saponin had no poisoning activity on maize weevil, while it had certain biological activity on diamondback moth and fruit fly, but it had high activity on fruit fly, when the concentration was 50 mg/ml, mortality was 100% at 72 h, LCso was 4.06 mg/ml at 72 h, LTso was 30.19 h when the concentration was 25.000 mg/ml. [Conclusion] Saponins from S. mukurossi could be develooed and utilized as the material for botanical eesticide.

Research on the Karyotype and Evolution of Drosophila melanogaster Species Group

Mitotic metaphase chromosomes of 34 species of Drosophila melanogaster species group were examined. Certain new karyotypes were described for the first time, and their evolutionary and interspecific genetic relationships among 8 subgroups of D. melanogaster species group were analyzed systematically. The results were as follows. The basic karyotype of elegans subgroup was type A. The karyotypes of eugracilis subgroup, melanogaster subgroup, and ficusphila subgroup were all type C. The karyotypes of takahashii subgroup and suzukii subgroup were both type C and type D. The montium subgroup had six kinds of karyotypes types B, C, C＇, D, D＇, and E. The ananassae subgroup had three kinds of karyotypes： types F, G, and H. Thus, the melanogaster species group was classified into five pedigrees based on the diversity of these karyotypes： 1） elegans; 2） eugracilis-melanogasterficusphila; 3） takkahashii-suzukii; 4） montium; 5） ananassae. The above-mentioned results in karyotypic evolution were consistent with those of DNA sequence analysis reported by Yang except for the elegans subgroup and this subgroup was considered as the ancestral subgroup. Karyotype analysis of the same drosophila from different isofemale lines indicated that the same Drosophila from different places showed karyotypic variation which might be due to different geographical environment and evolutionary degree or interaction between the two factors.

果蝇EZH2与乳腺癌分子分型及临床病理特征的关系

目的探讨果蝇Zeste基因增强子人类同源物2(EZH2)与乳腺癌分子分型及临床病理参数的关系。方法根据新型乳腺癌分子分型标准,将乳腺癌进行分子分型;免疫组织化学方法检测乳腺癌组织石蜡切片中EZH2的表达;采用χ~2检验分析EZH2表达与乳腺癌新型分子分型,以及临床病理参数之间的关系;采用KaplanMeier法分析EZH2表达与乳腺癌患者无病生存率(DFS)的关系。结果 13例管腔上皮A型乳腺癌患者中,3例为EZH2高表达(23.08%);10例管腔上皮B型乳腺癌患者中,5例为EZH2高表达(50.00%);7例人表皮生长因子受体2过表达型乳腺癌患者中,3例为EZH2高表达(42.86%);12例三阴性型乳腺癌患者中,10例为EZH2高表达(83.33%)。乳腺癌各分子亚型间EZH2表达的比较,差异有统计学意义(P<0.05)。EZH2高表达与EZH2低表达患者DFS比较,差异有统计学意义(P<0.05)。结论 EZH2可能是预测乳腺癌预后的指标之一。

Primary study on Nosema bombycis Infecting the Insect of Drosophila

[ Objective ] The aim of this study was to investigate the infectivity of Nosema bombycis to drosophila, which offered a new vision for systematical studies on the infection mechanism of Nosema bombycis, and also provided reference for the bio-control effect of Nosema bombycis. [ Method ] Nosema bombycis was used to feed wild type and mutant drosophila, and the morphological observation of Nosema bombycis in drosophila body fluid was also analyzed by calcofluor white M2R fluorescent staining. [ Result] Nosema bombycis could infect drosophila, and the number of Nosema bombycis in the infected mutant drosophila was higher than that in wild type drosophila. [ Conclusion ] Nosema bombycis can infect drosophila, which provides primary reference for studies on the infectivity of Nosema bombycis to other hosts and also lays a foundation for further study on the infection mechanism of Nosema bombycis.