In situ immunopathological events in human cervical intraepithelial neoplasia and cervical cancer: Review

Neoplasia of the cervix represents one of the most common cancers in women. Clinical and molecular research has identified immunological impairment in squamous intraepithelial cervical lesions and cervical cancer patients. The in-situ expression of several cytokines by uterine epithelial cells and by infiltrating leukocytes occurs during the cervical intraepithelial neoplasia and cervical cancer. Some of these cytokines can prevent and others can induce the progression of the neoplasm. The infiltrating leukocytes also produce cytokines and growth factors relate to angiogenesis, chemotaxis, and apoptosis capable of modulating the dysplasia progression. In this review we analyzed several interleukins with an inductive effect or blocking effect on the neoplastic progression. We also analyze the genetic polymorphism of some cytokines and their relationship with the risk of developing cervical neoplasia. In addition, we describe the leukocyte cells that infiltrate the cervical uterine tissue during the neoplasia and their effects on neoplasia progression.     

Cyst and encystment in protozoan parasites: optimal targets for new life-cycle interrupting strategies?

Certain protozoan parasites use survival strategies to reside outside the host such as the formation of cysts. This dormant and resistant stage results from the complex process of encystment that involves diverse molecular and cellular modifications. The stimuli and changes associated with cyst biogenesis are a matter of ongoing studies in human and animal protozoan parasites such as amoeba and Giardia species because blocking every step in the encystment pathway should, in theory, interrupt their life cycles. The present review thoroughly examines this essential process in those protozoan parasites and discusses the possibility of using that information to develop new kinds of anti-parasite specific and life cycle-interrupting drugs, aimed at holding back the dissemination of these infections.     

Extensive netting in Albasini and Nandoni dams: a potential threat to fish as a sustainable food source in the Vhembe District,South Africa

Fish populations in Albasini and Nandoni dams are negatively affected by extensive netting practices. This observation was made by the authors following a number of fish health assessment surveys related to aquatic pollution in the Luvuvhu River catchment. A comparison between the number and size of fish collected over a period of ten years indicated decreases in the average size and a consistent low number of fish, despite similar extensive sampling efforts. Unregulated netting is a common practice in both dams. This may become a serious problem as fish from these two dams are an important source of protein for the local communities. The purpose of this note is to report that gillnets are illegally used in the system and on the effect this could have on the fish population. The authors suggest educational and awareness initiatives to inform local communities about the importance of utilising fish in a sustainable manner to ensure the livelihood of generations to come.     

A molecular phylogeny of <Emphasis Type="Italic">Dorylus</Emphasis> army ants provides evidence for multiple evolutionary transitions in foraging niche

Background  

Army ants are the prime arthropod predators in tropical forests, with huge colonies and an evolutionary derived nomadic life style. Five of the six recognized subgenera of Old World Dorylus army ants forage in the soil, whereas some species of the sixth subgenus (Anomma) forage in the leaf-litter and some as conspicuous swarm raiders on the forest floor and in the lower vegetation (the infamous driver ants). Here we use a combination of nuclear and mitochondrial DNA sequences to reconstruct the phylogeny of the Dorylus s.l. army ants and to infer the evolutionary transitions in foraging niche and associated morphological adaptations.     

Coilin interacts with Ku proteins and inhibits in vitro non-homologous DNA end joining

Coilin is a nuclear protein that plays a role in Cajal body formation. The function of nucleoplasmic coilin is unknown. Here we report that coilin interacts with Ku70 and Ku80, which are major players in the DNA repair process. Ku proteins compete with SMN and SmB′ proteins for coilin interaction sites. The binding domain on coilin for Ku proteins cannot be localized to one discrete region, and only full-length coilin is capable of inhibiting in vitro non-homologous DNA end joining (NHEJ). Since Ku proteins do not accumulate in CBs, these findings suggest that nucleoplasmic coilin participates in the regulation of DNA repair.

Structured summary

MINT-8052983:coilin (uniprotkb:P38432) physically interacts (MI:0915) with SmB′ (uniprotkb:P14678) by pull down (MI:0096)MINT-8052941:coilin (uniprotkb:P38432) physically interacts (MI:0915) with Ku70 (uniprotkb:P12956) by competition binding (MI:0405)MINT-8052765:coilin (uniprotkb:P38432) physically interacts (MI:0915) with Ku80 (uniprotkb:P13010) by pull down (MI:0096)MINT-8052971:coilin (uniprotkb:P38432) physically interacts (MI:0915) with SMN (uniprotkb:Q16637) by pull down (MI:0096)MINT-8052957:coilin (uniprotkb:P38432) physically interacts (MI:0915) with Ku80 (uniprotkb:P13010) by competition binding (MI:0405)MINT-8052894, MINT-8052908:coilin (uniprotkb:P38432) binds (MI:0407) to Ku80 (uniprotkb:P13010) by pull down (MI:0096)MINT-8052804:coilin (uniprotkb:P38432) physically interacts (MI:0915) with Ku80 (uniprotkb:P13010) by anti bait coimmunoprecipitation (MI:0006)MINT-8052925:coilin (uniprotkb:P38432) binds (MI:0407) to Ku70 (uniprotkb:P12956) by pull down (MI:0096)MINT-8052786:Ku80 (uniprotkb:P13010) physically interacts (MI:0914) with coilin (uniprotkb:P38432) and Ku70 (uniprotkb:P12956) by anti bait coimmunoprecipitation (MI:0006)MINT-8052776:coilin (uniprotkb:P38432) physically interacts (MI:0915) with Ku70 (uniprotkb:P12956) by pull down (MI:0096)     

How protozoan parasites evade the immune response

Protozoan pathogens such as Plasmodium, Leishmania, Trypanosoma and Entamoeba are responsible for several of the most widespread and lethal human diseases. Their successful survival depends mainly on evading the host immune system by, for example, penetrating and multiplying within cells, varying their surface antigens, eliminating their protein coat, and modulating the host immune response. Immunosuppression is sometimes caused directly by parasite products and sometimes involves antigenic mimicry, which often appears in association with parasitic diseases. However, one of the most sophisticated mechanisms of evasion is the selective activation of a subset of T helper cells.     

Modelling the compartmentalization of splicing factors

Splicing factor (SF) compartments, also known as speckles, are heterogeneously distributed compartments within the nucleus of eukaryotic cells that are enriched in pre-mRNA SFs. We derive a fourth-order aggregation-diffusion model that describes a possible mechanism underlying the organization of SFs into speckles. The model incorporates two hypotheses, namely (1) that self-organization of dephosphorylated SFs, modulated by a phosphorylation-dephosphorylation cycle, is responsible for the formation and disappearance of speckles, and (2) that an underlying nuclear structure plays a major role in the organization of SFs. A linear stability analysis about homogeneous steady-state solutions of the model reveals how the self-interaction among dephosphorylated SFs can result in the onset of spatial patterns. A detailed bifurcation analysis of the model describes how phosphorylation and dephosphorylation modulate the onset of the compartmentalization of SFs.     

Current versus historical population sizes in vertebrate species with high gene flow: a comparison based on mitochondrial DNA lineages and inbreeding theory for neutral mutations

Using inbreeding theory as applied to neutral alleles inherited maternally, we generate expected probability distributions of times to identity by descent for random pairs of mitochondrial genotypes within a population or within an entire species characterized by high gene flow. For comparisons with these expectations, empirical distributions of times to most recent common ancestry were calculated (by conventional mtDNA clock calibrations) from mtDNA haplotype distances observed within each of three vertebrate species--American eels, hardhead catfish, and redwinged blackbirds. These species were chosen for analysis because census population size in each is currently large and because both genetic and life-history data are consistent with the postulate that historical gene flow within these species has been high. The observed molecular distances among mtDNA lineages were two to three orders of magnitude lower than predicted from census sizes of breeding females, suggesting that rate of mtDNA evolution is decelerated in these species and/or that long-term effective population size is vastly smaller than present-day population size. Several considerations point to the latter possibility as most likely. The genetic structure of any species is greatly influenced by historical demography; even for species that are currently abundant, mtDNA gene lineages appear to have been channeled through fairly small numbers of ancestors.      

DNA fingerprints from hypervariable mitochondrial genotypes

Conventional surveys of restriction-fragment polymorphisms in mitochondrial DNA of menhaden fish (Brevoortia tyrannus/patronus complex) and chuckwalla lizards (Sauromalus obesus) revealed exceptionally high levels of genetic variation, attributable to differences in mtDNA size as well as in restriction sites. The observed probabilities that any two randomly drawn individuals differed detectably in mtDNA genotype were 0.998 and 0.983 in the two species, respectively. Thus, the variable gel profiles provided unique mtDNA "fingerprints" for most conspecific animals assayed. mtDNA fingerprints differ from nuclear DNA fingerprints in several empirical respects and should find special application in the genetic assessment of maternity.