Effect of immunodeficiency on MPV shedding and transmission.

C57BL/6 (B6) mice briefly shed low levels of MPV, and transmission is inefficient. To determine whether deficits in B or T cells or in interferon γ on a B6 background increased the duration of MPV shedding or transmission, B-cell-deficient (Igh), interferon-γ-deficient (Ifnγ), B- and T-cell-deficient (Rag), and B6 mice were inoculated with MPV. At 1 and 2 wk postinoculation (wpi), 11% to 94% of mice shed MPV.

Transmission of mouse parvovirus to neonatal mice.

To investigate the infection of newborn mice with mouse parvovirus (MPV), a single MPV-infected mouse was added to each of 15 cages, each of which housed an uninfected breeding pair of Swiss Webster mice just before parturition. Seven litters were left with their parents, and the remaining 8 litters were fostered at postpartum day 1. All dams were shedding MPV at 1 and 2 wk after exposure.

Transmission of mouse parvovirus by fomites.

The goal of the current studies was to determine the risk of transmission of mouse parvovirus (MPV) by caging and husbandry practices. To determine whether MPV can be transmitted during cage changes in a biologic safety cabinet without the use of disinfectants, 14 cages of Swiss Webster mice were inoculated with MPV. Cages containing infected mice were interspersed among 14 cages housing naïve Swiss Webster mice.

The repressor element 1-silencing transcription factor is a novel molecular target for the neurotoxic effect of the polychlorinated biphenyl mixture aroclor 1254 in neuroblastoma SH-SY5Y cells.

Chronic exposure to polychlorinated biphenyls (PCBs), a class of ubiquitous environmental toxicants, causes neurocognitive anomalies. The transcription factor repressor element 1-silencing transcription factor (REST) plays a critical role in neuronal phenotype elaboration in both neural progenitor cells and non-neuronal cells. Here, we investigated the possible relationship between PCBs and REST in neuroblastoma SH-SY5Y cells.

Residues 762-801 of PLD1 mediate the interaction with PED/PEA15.

The interaction of Phospholipase D1 (PLD1) by its C-terminal domain D4 with PED/PEA15 has been indicated as a target for type 2 diabetes. PED/PEA15 is overexpressed in several tissues of individuals affected by type 2 diabetes and its overexpression in intact cells and in transgenic animal models impairs insulin regulation of glucose transport by a mechanism mediated by the interaction with D4 and the consequent increase of protein kinase C-alpha activity. Expression of D4 or administration of a peptide mimicking the PED/PEA15 region involved in this interaction to cells stably overexpressing PED/PEA15 reduces its interaction with PLD1, thereby lowering PKC-alpha activation and restoring normal glucose transport mediated by PKC-zeta.