Confirmation of a major QTL influencing oral morphine intake in C57 and DBA mice using reciprocal congenic strains.

C57BL/6 (B6) and DBA/2 (D2) mice exhibit disparate behavior when tested for voluntary morphine intake in a two-bottle choice drinking paradigm with B6 mice consuming 10 times more drug than D2 mice. Previous genetic mapping studies identified a locus, Mop2, on the proximal part of chromosome 10 that explained over half of the genetic variance in this mouse model of opioid self-administration. We constructed a set of reciprocal congenic strains between B6 and D2 mice in which the proximal portion of chromosome 10 has been introgressed from one strain onto the background of the other. We tested mice from this pair of reciprocal strains together with progenitor B6 and D2 mice in a two-bottle choice drinking paradigm with morphine and quinine. The results showed that introgression of chromosome 10 alleles from the B6 strain onto a D2 genetic background increased voluntary morphine intake four-fold compared to progenitor D2 mice. Preference for morphine was also increased significantly in D2.B6-Mop2 mice compared to progenitor D2 mice. Conversely, introgression of chromosome 10 alleles from the D2 strain onto a B6 genetic background decreased morphine intake by half compared to progenitor B6 mice in B6.D2 -Mop2 mice; however, high morphine preference was maintained in this congenic strain most likely due to strong quinine aversion. When quinine was eliminated from the control bottle, morphine preference in B6.D2-Mop2 mice was decreased significantly relative to B6 and D2.B6-Mop2 mice. Overall, these data confirm the existence of a gene(s) on chromosome 10 proximal to D10Mit124 that has a strong influence on the difference in morphine drinking behavior between B6 and D2 mice.     

Performance of the Vitek MS v2.0 System in Distinguishing Streptococcus pneumoniae from Nonpneumococcal Species of the Streptococcus mitis Group

The Vitek MS v2.0 matrix-assisted laser desorption ionization–time of flight mass spectrometry system accurately distinguished Streptococcus pneumoniae from nonpneumococcal S. mitis group species. Only 1 of 116 nonpneumococcal isolates (<1%) was misidentified as S. pneumoniae. None of 95 pneumococcal isolates was misidentified. This method provides a rapid, simple means of discriminating among these challenging organisms.     

Pulmonary Inflammation and Cell Death in Mice After Acute Exposure to Air Particulate Matter From an Industrial Region of Buenos Aires

Epidemiological studies have shown that air particulate matter (PM) can increase respiratory morbidity and mortality being the lungs the main target organ to PM body entrance. Even more, several in vivo and in vitro studies have shown that air PM has a wide toxicity spectra depending among other parameters, on its size, morphology, and chemical composition. The Reconquista River is the second most polluted river from Buenos Aires, and people living around its basin are constantly exposed to its contaminated water, soil and air. However, the air PM from the Reconquista River (RR-PMa) has not been characterized, and its biological impact on lung has yet not been assessed. Therefore, the present investigation was undertaken to study (1) RR-PMa morphochemical characteristic and (2) RR-PMa lung acute effects after intranasal instillation exposure through the analysis of three end points: oxidative stress, inflammation, and apoptosis. A single acute exposure of RR-PMa (1 mg/kg body weight) after 24 h caused significant (p < 0.05) enrichment in bronchoalveolar total cell number and polymorphonuclear (PNM) fraction, superoxide anion generation, production of pro-inflammatory cytokines TNF-α and IL-6, and induction of apoptosis. It was also observed that in lung homogenates, none of the antioxidant enzymes assayed showed differences between exposed RR-PMa and control mice. These data demonstrate that air PM from the Reconquista River induce lung oxidative stress, inflammation, and cell death therefore represents a potential hazard to human health.