The prevalence of sacroiliac joint CT and MRI findings is high in large breed dogs.

Sacroiliac joint (SIJ) disease has been described as one of the possible causes of lumbosacral (LS) region pain in dogs. However, published information is currently lacking for the computed tomographic (CT) and magnetic resonance imaging (MRI) characteristics of canine SIJ disease. The objectives of this retrospective, observational study were to describe and quantify CT and MRI SIJ findings in a sample of large breed dogs and test associations between the numbers of SIJ findings and other variables. Data archives for a veterinary teaching hospital were searched for large breed dogs (≥ 22.7 kg) that had CT or MRI scans of the LS and pelvic regions in 2015-2019. Dogs with a history of acute trauma or scans with incomplete SIJs were excluded. A veterinary student recorded medical record findings. A veterinary radiologist and graduate student recorded CT and MRI findings based on previously published criteria in dogs and humans. Fifty-three dogs were sampled (20 CT, 33 MRI). Categories of findings with the highest prevalence were subchondral erosion (100% CT, 100% MRI) and subchondral sclerosis (95% CT, 97% MRI). The total numbers of SIJ findings per dog were not associated with dog age, sex, weight, or concurrent findings in the LS or pelvic regions. The total number of MRI SIJ findings per dog differed between German Shepherds and Labrador Retrievers (P = 0.0237) as well as between Labrador Retrievers and other breeds (P = 0.0414). These results indicated that CT and MRI findings reported in humans with SIJ disease are common in large breed dogs.

Inhibition of dendritic cell apoptosis by Leishmania mexicana amastigotes.

Macrophages (Mφ) and dendritic cells are the major target cell populations of the obligate intracellular parasite Leishmania. Inhibition of host cell apoptosis is a strategy employed by multiple pathogens to ensure their survival in the infected cell. Leishmania promastigotes have been shown to protect Mφ, neutrophils, and dendritic cells from both natural and induced apoptosis. Nevertheless, the effect of the infection with Leishmania amastigotes in the apoptosis of these cell populations has not been established, which results are very important since amastigotes persist in cells for many days and are responsible for sustaining infection in the host. As shown in this study, apoptosis of monocyte-derived dendritic cells (moDC) induced by treatment with camptothecin was downregulated by infection with L. mexicana amastigotes from 42.48 to 36.92% as detected by Annexin-V binding to phosphatidylserine. Also, the infection of moDC with L. mexicana amastigotes diminished the fragmentation of DNA as detected by terminal deoxynucleotidyl transferase-mediated fluorescein-dUTP nick end labeling assay, and changes in cell morphology were analyzed by electron microscopy. The observed antiapoptotic effect was found to be associated with an 80% reduction in the presence of active caspase-3 in infected moDC. The capacity of L. mexicana amastigotes to delay apoptosis induction in the infected moDC may have implications for Leishmania pathogenesis by favoring the invasion of its host and the persistence of the parasite in the infected cells.

Análisis de la tendencia de la mortalidad por cirrosis hepática en Chile: Años 1990 a 2007 / Mortality trend from liver cirrhosis in Chile from 1990 to 2007

Background: There is a worldwide tendency towards a reduction in the rates of deaths due to cirrhosis. In Chile, a decrease in the number of hospital admissions due to this disease has been recorded. Aim: To assess general characteristics and temporal evolution of liver cirrhosis mortality in Chile between 1990 and 2007. Material and Methods: National death records and population databases were reviewed. Crude and age-adjusted mortality rates for alcoholic and non-alcoholic cirrhosis were calculated, evaluating their evolution in the study period and the relative risk by gender. Results: In the study period, 44,894 deaths caused by cirrhosis were recorded. Mortality rate was 16.6 deaths per 100,000 inhabitants. 54 percent of deaths were attributed to non-alcoholic cirrhosis. There was a reduction in mortality rates for both types of cirrhosis. Males accounted for 83 and 65 percent of deaths caused by alcoholic and non-alcoholic cirrhosis, respectively. The figures for relative risk of death were 5 and 1.9, respectively. Conclusions: Alcoholic cirrhosis was the preponderant cause among liver cirrhosis deaths. A decrease in mortality rates was observed in the study period. Improvements in disease treatment and control could possibly explain this trend.

[Mortality trend from liver cirrhosis in Chile from 1990 to 2007]. / Análisis de la tendencia de la mortalidad por cirrosis hepática en Chile: Años 1990 a 2007.

BACKGROUND: There is a worldwide tendency towards a reduction in the rates of deaths due to cirrhosis. In Chile, a decrease in the number of hospital admissions due to this disease has been recorded. AIM: To assess general characteristics and temporal evolution of liver cirrhosis mortality in Chile between 1990 and 2007. MATERIAL AND METHODS: National death records and population databases were reviewed. Crude and age-adjusted mortality rates for alcoholic and non-alcoholic cirrhosis were calculated, evaluating their evolution in the study period and the relative risk by gender. RESULTS: In the study period, 44,894 deaths caused by cirrhosis were recorded. Mortality rate was 16.6 deaths per 100,000 inhabitants. 54% of deaths were attributed to non-alcoholic cirrhosis. There was a reduction in mortality rates for both types of cirrhosis. Males accounted for 83 and 65% of deaths caused by alcoholic and non-alcoholic cirrhosis, respectively. The figures for relative risk of death were 5 and 1.9, respectively. CONCLUSIONS: Alcoholic cirrhosis was the preponderant cause among liver cirrhosis deaths. A decrease in mortality rates was observed in the study period. Improvements in disease treatment and control could possibly explain this trend.

Leishmania lipophosphoglycan (LPG) activates NK cells through toll-like receptor-2.

Toll-like receptors (TLRs) mediate the cellular response to conserved molecular patterns shared by microorganisms. We report that TLR-2 on human NK cells is upregulated and stimulated by Leishmania major lipophosphoglycan (LPG), a phosphoglycan belonging to a family of unique Leishmania glycoconjugates. We found that purified L. major LPG upregulates both mRNA and the membrane expression of TLR-2 in NK cells. Additionally, IFN-gamma and TNF-alpha production and nuclear translocation of NF-kappaB was enhanced. The activation effect was more intense with LPG purified from infectious metacyclic parasites than from noninfectious procyclic Leishmania. Since the difference between the molecules derived from these two stages of the parasite growth cycle lies exclusively in the number of phosphosaccharide repeat domains and in the composition of glycan side chains that branch off these domains, we propose that TLR-2 possibly distinguishes between phosphorylated glycan repeats on LPG molecules. The effect of LPG on cytokine production and on membrane expression of TLR-2 could be blocked with F(ab')2 fragments of the mAb against LPG (WIC 79.3). Confocal microscopy demonstrated the co-localization of LPG and TLR-2 on the NK cell membrane. Binding of LPG to TLR-2 in NK cells was demonstrated by immunoprecipitations done with anti-TLR-2 and anti-LPG mAb followed by immunoblotting with anti-LPG and anti-TLR-2, respectively. Both antibodies recognized the immune complexes. These results suggest that NK cells are capable of recognition of, and activation by, Leishmania LPG through TLR-2, enabling them to participate autonomously in the innate immune system and thereby increasing the effective destruction of the parasite.