Facial porokeratosis: A series of six patients

Porokeratosis is a disorder of epidermal keratinization characterized by annular plaques with an atrophic centre and hyperkeratotic edges, and includes a heterogeneous group of disorders that are mostly inherited in an autosomal dominant fashion. Facial porokeratosis is rare and is not well documented. We present six cases of facial porokeratosis seen over a period of 15 years in a hospital in Lima, Peru. In most of the cases, porokeratosis was found in younger women without any significant past medical history. Oral isotretinoin showed moderate improvement in two of our patients.     

Fluorescent Magnetic Bioprobes by Surface Modification of Magnetite Nanoparticles

Bimodal nanoprobes comprising both magnetic and optical functionalities have been prepared via a sequential two-step process. Firstly, magnetite nanoparticles (MNPs) with well-defined cubic shape and an average dimension of 80 nm were produced by hydrolysis of iron sulfate and were then surface modified with silica shells by using the sol-gel method. The Fe₃O₄@SiO₂ particles were then functionalized with the fluorophore, fluorescein isothiocyanate (FITC), mediated by assembled shells of the cationic polyelectrolyte, polyethyleneimine (PEI). The Fe₃O₄ functionalized particles were then preliminary evaluated as fluorescent and magnetic probes by performing studies in which neuroblast cells have been contacted with these nanomaterials.     

Purified and highly aggregated chimeric protein DIIIC-2 induces a functional immune response in mice against dengue 2 virus

It was previously reported that DIIIC-2 (a fusion protein composed of domain III of the envelope protein and the capsid protein from dengue 2 virus), as an aggregate antigen from a partially purified preparation, induced a functional protective immune response against dengue 2 virus in the mouse encephalitis model. In the present work, a purification procedure was developed for DIIIC-2, and soluble and aggregated fractions of the purified protein were characterized and evaluated in mice. The purification process rendered a protein preparation of 91 % purity, and the remaining 9 % consisted of fragments and aggregates of the same recombinant protein. After the in vitro aggregation process, upon addition of oligodeoxynucleotides, 80 % of the protein formed aggregates, whereas 20 % remained as soluble protein. An immunological evaluation revealed the proper immunogenicity of the aggregated purified protein in terms of induction of antiviral and neutralizing antibodies, cell-mediated immunity and protection upon dengue 2 virus challenge in the mouse encephalitis model. Based on these results, we can assert that the purified protein DIIIC-2 is functional and could be used for further scalable steps and preclinical studies in non-human primates.     

Dermal exposure to jet fuel suppresses delayed-type hypersensitivity: a critical role for aromatic hydrocarbons.

Dermal exposure to military (JP-8) and/or commercial (Jet-A) jet fuel suppresses cell-mediated immune reactions. Immune regulatory cytokines and biological modifiers, including platelet activating factor (PAF), prostaglandin E(2), and interleukin-10, have been implicated in the pathway of events leading to immune suppression. It is estimated that approximately 260 different hydrocarbons are found in jet fuel, and the exact identity of the active immunotoxic agent(s) is unknown. The recent availability of synthetic jet fuel (S-8), which is refined from natural gas, and is devoid of aromatic hydrocarbons, made it feasible to design experiments to address this problem. Here we tested the hypothesis that the aromatic hydrocarbons present in jet fuel are responsible for immune suppression. We report that applying S-8 to the skin of mice does not upregulate the expression of epidermal cyclooxygenase-2 (COX-2) nor does it induce immune suppression. Adding back a cocktail of seven of the most prevalent aromatic hydrocarbons found in jet fuel (benzene, toluene, ethylbenzene, xylene, 1,2,4-trimethlybenzene, cyclohexylbenzene, and dimethylnaphthalene) to S-8 upregulated epidermal COX-2 expression and suppressed a delayed-type hypersensitivity (DTH) reaction. Injecting PAF receptor antagonists, or a selective cycloozygenase-2 inhibitor into mice treated with S-8 supplemented with the aromatic cocktail, blocked suppression of DTH, similar to data previously reported using JP-8. These findings identify the aromatic hydrocarbons found in jet fuel as the agents responsible for suppressing DTH, in part by the upregulation of COX-2, and the production of immune regulatory factors and cytokines.     

Operational studies with Valent VectoLex WDG,Bacillus sphaericus,in three Florida Mosquito Control Districts

VectoLex WDG, Bacillus sphaericus (Valent BioSciences Corporation), was evaluated in 3 Florida Mosquito Control Districts under operational conditions. Application rates were 0.5 and 1.0 lb/acre and an untreated control in each district. Study sites included woodland ponds, residential areas such as catch basins, and commercial business retention ponds. Pretreatment and posttreatment assessments were made with a standard dipper at designated dipping stations. The most prevalent mosquitoes included Culex quinquefasciatus, Culex nigripalpus, Culex erraticus, Ochlerotatus infirmatus, Anopheles crucians, Anopheles quadrimaculatus, and Psorophora spp. VectoLex WDG was effective for 24-35 days posttreatment with one application.     

Dermal application of jet fuel suppresses secondary immune reactions

Applying military jet fuel (JP-8) to the skin of mice activates systemic immune suppression. In all of our previous experiments, JP-8 was applied to immunologically na?ve mice. The effect of jet fuels on established immune reactions, such as immunological memory, is unknown. The focus of the experiments presented here was to test the hypothesis that jet fuel exposure [both JP-8 and commercial jet fuel (Jet-A)] suppresses established immune reactions. Mice were immunized with the opportunistic fungal pathogen Candida albicans and, at different times after immunization (10 to 30 days), various doses of undiluted JP-8 or Jet-A were applied to their skin. Both the elicitation of delayed-type hypersensitivity (DTH) (mice challenged 10 days after immunization) and immunological memory (mice challenged 30 days after immunization) were significantly suppressed in a dose-dependent manner. Dermal exposure to either multiple small doses (50 microl over 4 days) or a single large dose (approximately 200-300 microl) of JP-8 and/or Jet-A suppressed DTH to C. albicans. The mechanism by which dermal application of JP-8 and Jet-A suppresses immunological memory involves the release of immune biologic response modifiers. Blocking the production of prostaglandin E(2) by a selective cyclooxygenase-2 inhibitor (SC 236) significantly reversed jet fuel-induced suppression of immunologic memory. These findings indicate, for the first time, that dermal exposure to commercial jet fuel (Jet-A) suppresses the immune response. In addition, the data reported here expand on previous findings by suggesting that jet fuel exposure may depress the protective effect of prior vaccination.