Assessment of Mitochondrial Function in the AmE-711 Honey Bee Cell Line: Boscalid and Pyraclostrobin Effects.

There is a growing concern that chronic exposure to fungicides contributes to negative effects on honey bee development, life span, and behavior. Field and caged-bee studies have helped to characterize the adverse outcomes (AOs) of environmentally relevant exposures, but linking AOs to molecular/cellular mechanisms of toxicity would benefit from the use of readily controllable, simplified host platforms like cell lines. Our objective was to develop and optimize an in vitro-based mitochondrial toxicity assay suite using the honey bee as a model pollinator, and the electron transport chain (ETC) modulators boscalid and pyraclostrobin as model fungicides.

Using the Honey Bee (Apis mellifera L.) Cell Line AmE-711 to Evaluate Insecticide Toxicity.

One of the main contributors to poor productivity and elevated mortality of honey bee colonies globally is insecticide exposure. Whole-organism and colony-level studies have demonstrated the effects of insecticides on many aspects of honey bee biology and have also shown their interactions with pathogens. However, there is a need for in vitro studies using cell lines to provide greater illumination of the effects of insecticides on honey bee cellular and molecular processes.

An Insight Into the microRNA Profile of the Ectoparasitic Mite (Acari: Varroidae), the Primary Vector of Honey Bee Deformed Wing Virus.

The remarkably adaptive mite is the most important honey bee ectoparasite. mites are competent vectors of deformed wing virus (DWV), and the -virus complex is a major determinant of annual honey bee colony mortality and collapse. MicroRNAs (miRNAs) are 22-24 nucleotide non-coding RNAs produced by all plants and animals and some viruses that influence biological processes through post-transcriptional regulation of gene expression.

The Pathogen Profile of a Honey Bee Queen Does Not Reflect That of Her Workers.

Throughout a honey bee queen's lifetime, she is tended to by her worker daughters, who feed and groom her. Such interactions provide possible horizontal transmission routes for pathogens from the workers to the queen, and as such a queen's pathogen profile may be representative of the workers within a colony. To explore this further, we investigated known honey bee pathogen co-occurrence, as well as pathogen transmission from workers to queens.

Social-medication in bees: the line between individual and social regulation.

We use the term social-medication to describe the deliberate consumption or use of plant compounds by social insects that are detrimental to a pathogen or parasite at the colony level, result in increased inclusive fitness to the colony, and have potential costs either at the individual or colony level in the absence of parasite infection. These criteria for social-medication differ from those for self-medication in that inclusive fitness costs and benefits are distinguished from individual costs and benefits. The consumption of pollen and nectar may be considered a form of social immunity if they help fight infection, resulting in a demonstrated increase in colony health and survival.

Is the Brood Pattern within a Honey Bee Colony a Reliable Indicator of Queen Quality?

Failure of the queen is often identified as a leading cause of honey bee colony mortality. However, the factors that can contribute to "queen failure" are poorly defined and often misunderstood. We studied one specific sign attributed to queen failure: poor brood pattern.

Gamma irradiation inactivates honey bee fungal, microsporidian, and viral pathogens and parasites.

Managed honey bee (Apis mellifera) populations are currently facing unsustainable losses due to a variety of factors. Colonies are challenged with brood pathogens, such as the fungal agent of chalkbrood disease, the microsporidian gut parasite Nosema spp., and several viruses.

In vivo and in vitro infection dynamics of honey bee viruses.

The honey bee (Apis mellifera) is commonly infected by multiple viruses. We developed an experimental system for the study of such mixed viral infections in newly emerged honey bees and in the cell line AmE-711, derived from honey bee embryos. When inoculating a mixture of iflavirids [sacbrood bee virus (SBV), deformed wing virus (DWV)] and dicistrovirids [Israeli acute paralysis virus (IAPV), black queen cell virus (BQCV)] in both live bee and cell culture assays, IAPV replicated to higher levels than other viruses despite the fact that SBV was the major component of the inoculum mixture.

Naphthol AS-E Phosphate Inhibits the Activity of the Transcription Factor Myb by Blocking the Interaction with the KIX Domain of the Coactivator p300.

The transcription factor c-Myb is highly expressed in hematopoietic progenitor cells and controls the transcription of genes important for lineage determination, cell proliferation, and differentiation. Deregulation of c-Myb has been implicated in the development of leukemia and certain other types of human cancer. c-Myb activity is highly dependent on the interaction of the c-Myb with the KIX domain of the coactivator p300, making the disruption of this interaction a reasonable strategy for the development of Myb inhibitors.

A cell line resource derived from honey bee (Apis mellifera) embryonic tissues.

A major hindrance to the study of honey bee pathogens or the effects of pesticides and nutritional deficiencies is the lack of controlled in vitro culture systems comprised of honey bee cells. Such systems are important to determine the impact of these stress factors on the developmental and cell biology of honey bees. We have developed a method incorporating established insect cell culture techniques that supports sustained growth of honey bee cells in vitro.

Temperature and Time Requirements for Controlling Bed Bugs (Cimex lectularius) under Commercial Heat Treatment Conditions.

Developing effective alternative approaches for disinfesting bed bugs from residential spaces requires a balance between obtaining complete insect mortality, while minimizing costs and energy consumption. One method of disinfestation is the application of lethal high temperatures directly to rooms and contents within a structure (termed whole-room heat treatments). However, temperature and time parameters for efficacy in whole-room heat treatments are unknown given the slower rate of temperature increase and the probable variability of end-point temperatures within a treated room.

2-Methoxyestradiol suppresses osteolytic breast cancer tumor progression in vivo.

2-Methoxyestradiol (2ME(2)), a physiologic metabolite of 17beta-estradiol (estrogen), has emerged as a promising cancer therapy because of its potent growth-inhibitory and proapoptotic effects on both endothelial and tumor cells. 2ME(2) also suppresses osteoclast differentiation and induces apoptosis of mature osteoclasts, and has been shown to effectively repress bone loss in an animal model of postmenopausal osteoporosis. Given these observations, we have examined whether 2ME(2) could effectively target metastasis to bone, osteolytic tumors, and soft tissue tumors.

Local irradiation in combination with bevacizumab enhances radiation control of bone destruction and cancer-induced pain in a model of bone metastases.

Skeletal metastases are a major source of morbidity for cancer patients. The purpose of this study was to evaluate the effects of megavoltage irradiation and antiangiogenic therapy on metastatic bone cancer. A tumor xenograft model was prepared in C3H/Scid mice using 4T1 murine breast carcinoma cells.

Osteoclasts direct bystander killing of bone cancer.

Primary and metastatic bone cancers are difficult to eradicate and novel approaches are needed to improve treatment and extend life. As bone cancer grows, osteoclasts, the principal bone-resorbing cells of the body, are recruited to and activated at sites of cancer. In this investigation, we determined if osteoclast lineage cells could function as a cell-based gene delivery system to bone cancers.

Biology of bone cancer pain.

Bone cancer pain is a devastating manifestation of metastatic cancer. Unfortunately, current therapies can be ineffective, and when they are effective, the duration of the patient's survival typically exceeds the duration of pain relief. New, mechanistically based therapies are desperately needed.

Novel cytosine deaminase fusion gene enhances the effect of radiation on breast cancer in bone by reducing tumor burden, osteolysis, and skeletal fracture.

Background: Painful breast carcinoma metastases in bone are a common manifestation of malignant disease. Eradication of these tumors can be evasive, and as a result, skeletal morbidity increases with disease progression.

Experimental Design: The treatment potential of cytosine deaminase (CD) gene therapy combined with radiation treatment was evaluated in vitro and in vivo using a 4T1 murine breast carcinoma model.

Radiation treatment decreases bone cancer pain through direct effect on tumor cells.

The most used treatment for bone cancer pain is radiation; however, the mechanism responsible for analgesia after irradiation is unknown. The mechanistic influence of a single, localized 10-, 20- or 30-Gy dose of radiation on painful behaviors, osteolysis, histopathology and osteoclast number was evaluated in mice with painful femoral sarcomas. Dramatic reductions in pain behaviors (P < 0.

Direct and bystander killing of sarcomas by novel cytosine deaminase fusion gene.

Soft tissue and bone sarcomas of the extremities can be difficult to eradicate, and standard treatment may require limb amputation. New therapies to decrease tumor size could improve the effectiveness of treatment and decrease the frequency of limb amputation. Cytosine deaminase (CD)-based gene therapy has been shown to be effective in decreasing growth of solid tumors when animals with CD-expressing tumor cells are treated with 5 fluorocytosine (5FC), an inert prodrug that is converted to 5-fluorouracil (5FU) by CD.