Sporadic Creutzfeldt-Jakob disease with glial PrPRes nuclear and perinuclear immunoreactivity

Proteinase K-resistant prion protein (PrPRes ) nuclear and perinuclear immunoreactivity in oligodendrocytes of the frontal cortex is found in one case of otherwise typical sporadic Creutzfeldt-Jakob disease (sCJD) type VV2a. The PrP nature of the inclusions is validated with several anti-PrP antibodies directed to amino acids 130-160 (12F10), 109-112 (3F4), 97-102 (8G8) and the octarepeat region (amino acids 59-89: SAF32). Cellular identification and subcellular localization were evaluated with double- and triple-labeling immunofluorescence and confocal microscopy using antibodies against PrP, glial markers, and histone H3. Based on review of the literature and our own experience, this is a very odd situation that deserves further validation in other cases. Keywords: Creutzfeldt-Jakob disease; astrocytes; oligodendrocytes; prion

Reactivity of neonicotinoid insecticides with carbonate radicals

The reaction of three chloronicotinoid insecticides, namely Imidacloprid (IMD), Thiacloprid (THIA) and Acetamiprid (ACT), with carbonate radicals (CO·₃⁻) was investigated. The second order rate constants (4 ± 1) × 10⁶, (2.8 ± 0.5) × 10⁵, and (1.5 ± 1) × 10⁵ M⁻¹ s⁻¹ were determined for IMD, THIA and ACT, respectively. The absorption spectra of the organic intermediates formed after CO·₃⁻ attack to IMD is in line with those reported for α-aminoalkyl radicals. A reaction mechanism involving an initial charge transfer from the amidine nitrogen of the insecticides to CO·₃⁻ is proposed and further supported by the identified reaction products. The pyridine moiety of the insecticides remains unaffected until nicotinic acid is formed. CO·₃⁻ radical reactivity towards IMD, ACT, and THIA is low compared to that of HO• radicals, excited triplet states, and ¹O₂, and is therefore little effective in depleting neonicotinoid insecticides.Instituto de Investigaciones Fisicoquímicas Teóricas y AplicadasLaboratorio de Estudio de Compuestos Orgánico

Mutation analysis of the LCE3B/LCE3C genes in Psoriasis

<p>Abstract</p> <p>Background</p> <p>An association between a common deletion comprising the late cornified envelope LCE3B and LCE3C genes (LCE3C_LCE3B-del) and Psoriasis (Ps) has been reported. The expression of these LCE genes was induced after skin barrier disruption and was also strong in psoriatic lesions. The damage to the skin barrier could trigger an epidermal response that includes the expression of genes involved in the formation of skin barrier.</p> <p>Methods</p> <p>We determined the LCE3C_LCE3B-del genotype in 405 Ps patients and 400 healthy controls from a Northern Spain region (Asturias). These patients and controls were also genotyped for the rs4112788 single nucleotide polymorphism, in strong linkage disequilibrium with the LCE3C_B cluster. The LCE3B and LCE3C gene variant was determined in the patients through SSCA, DHPLC, and direct sequencing.</p> <p>Results</p> <p>Allele and genotype frequencies did not differ between patients and controls for the rs4112788 and LCE3C_LCE3B-del polymorphisms. However, del/del homozygotes were significantly higher among patients with chronic plaque type Ps who did not develop arthritis (p = 0.03; OR = 1.4; 95%CI = 1.03-1.92). The analysis of the coding sequence of LCE3B and LCE3C in the patients who had at least one copy of this showed that only one patient has a no previously reported LCE3B variant (R68C).</p> <p>Conclusion</p> <p>Our work suggested that homozygosity for a common LCE3C_LCE3B deletion contributes to the risk of developing chronic plaque type Ps without psoriatic arthritis. Our work confirmed previous reports that described an association of this marker with only skin manifestations, and supported the concept of different genetic risk factors contributing to skin and joint disease.</p