Polynomial regression model fitted to deseasonalized data on the proportions of pulmonary tuberculosis cases among migrants at entry in Kuwait: 1997–2006

<p><b>Copyright information:</b></p><p>Taken from "Nonlinear pattern of pulmonary tuberculosis among migrants at entry in Kuwait: 1997–2006"</p><p>http://www.biomedcentral.com/1471-2458/8/264</p><p>BMC Public Health 2008;8():264-264.</p><p>Published online 30 Jul 2008</p><p>PMCID:PMC2527606.</p><p></p

Prevalence of IPIs by age groups.

<p>Prevalence of IPIs by age groups.</p

Kaplan-Meier survival curve i.e. probability estimates of not attaining a score of 6.0 on Expanded Disability Status Scale (EDSS) among cohorts with young-onset (YOMS) or late-onset (LOMS).

<p>Kaplan-Meier survival curve i.e. probability estimates of not attaining a score of 6.0 on Expanded Disability Status Scale (EDSS) among cohorts with young-onset (YOMS) or late-onset (LOMS).</p

Univariate analysis of factors associated with intestinal parasitic infection among children, 1 to 5 years of age, residing in Ghosia Colony, Karachi, Pakistan who provided a stool sample for this study.

$<p>n = 103.</p>∼<p>n = 91.</p>†<p>n = 202.</p>*<p>p≤0.05.</p>¶<p>p≤0.25.</p

Univariable associations of categorical demographic and clinical variables with time to reach EDSS 6.0 among multiple sclerosis (MS) patients stratified on late-onset (LOMS) or young-onset (YOMS) of disease.

<p>Univariable associations of categorical demographic and clinical variables with time to reach EDSS 6.0 among multiple sclerosis (MS) patients stratified on late-onset (LOMS) or young-onset (YOMS) of disease.</p

Multivariable Cox proportional-hazards model of variables associated with time to reach EDSS 6.0 in cohorts of patients with late-onset (LOMS) or young-onset (YOMS) of disease.

<p>Multivariable Cox proportional-hazards model of variables associated with time to reach EDSS 6.0 in cohorts of patients with late-onset (LOMS) or young-onset (YOMS) of disease.</p

Prevalence of intestinal parasitic infections among children, 1 to 5 years of age, residing in Ghosia Colony, Karachi, Pakistan (n = 218).

¥<p>If more than one intestinal parasite is identified in a sample, it is a multiple parasitic infection.</p>†<p>If only one intestinal parasite is identified in a sample, it is a single parasitic infection.</p>¶<p>Infection with the labeled parasite only.</p>*<p>Infection with multiple parasites including the labeled one.</p

Autophagy Activation Clears ELAVL1/HuR-Mediated Accumulation of SQSTM1/p62 during Proteasomal Inhibition in Human Retinal Pigment Epithelial Cells

<div><p>Age-related macular degeneration (AMD) is the most common reason of visual impairment in the elderly in the Western countries. The degeneration of retinal pigment epithelial cells (RPE) causes secondarily adverse effects on neural retina leading to visual loss. The aging characteristics of the RPE involve lysosomal accumulation of lipofuscin and extracellular protein aggregates called “drusen”. Molecular mechanisms behind protein aggregations are weakly understood. There is intriguing evidence suggesting that protein SQSTM1/p62, together with autophagy, has a role in the pathology of different degenerative diseases. It appears that SQSTM1/p62 is a connecting link between autophagy and proteasome mediated proteolysis, and expressed strongly under the exposure to various oxidative stimuli and proteasomal inhibition. ELAVL1/HuR protein is a post-transcriptional factor, which acts mainly as a positive regulator of gene expression by binding to specific mRNAs whose corresponding proteins are fundamental for key cellular functions. We here show that, under proteasomal inhibitor MG-132, ELAVL1/HuR is up-regulated at both mRNA and protein levels, and that this protein binds and post-transcriptionally regulates <i>SQSTM1/p62</i> mRNA in ARPE-19 cell line. Furthermore, we observed that proteasomal inhibition caused accumulation of SQSTM1/p62 bound irreversibly to perinuclear protein aggregates. The addition of the AMPK activator AICAR was pro-survival and promoted cleansing by autophagy of the former complex, but not of the ELAVL1/HuR accumulation, indeed suggesting that SQSTM1/p62 is decreased through autophagy-mediated degradation, while ELAVL1/HuR through the proteasomal pathway. Interestingly, when compared to human controls, AMD donor samples show strong SQSTM1/p62 rather than ELAVL1/HuR accumulation in the drusen rich macular area suggesting impaired autophagy in the pathology of AMD.</p></div

Transmission electron micrographs of ARPE-19 cells exposed to AICAR or/and MG-132 and aggregate quantification.

<p>(A) Representative transmission electron micrographs of ARPE-19 untreated control cells, cells exposed to AICAR 2 mM or/and MG-132 5 µM for 24 h. Aggregates are indicated by arrows. (B) Quantification of aggregates in ARPE-19 cells exposed to AICAR 2 mM or/and MG-132 5 µM for 24 h. Eight parallel samples were measured in all treatments. **p<0.01, Mann–Whitney.</p

Sections of foveomacular areas of age-matched control eyes for SQSTM1/p62, ubiquitin and ELAVL1/HuR.

<p>The extent of cytoplasmic immunopositivity for SQSTM1/p62, Bruch’s membrane immunopositivity for ubiquitin and the immunopositivity of nuclei of RPE cells for ELAVL1/HuR (foveomacular areas shown; A, B and C respectively) in the RPE cells (shown by arrows) was evaluated microscopically (no staining or positive staining). For SQSTM1/p62 there were only a few immunopositive cytoplasm’s randomly distributed through-out the RPE cell layer and the nuclei were negative. Bruch’s membrane (shown by arrowheads) was immunopositive for ubiquitin occasionally through-out the RPE cell layer in very small amounts while all of the nuclei were negative. Half of the nuclei showed minor immunopositivity for ELAVL1/HuR while the cytoplasm’s of RPE cells were negative. The foveomacular areas showed no difference in immunohistochemical stainings when compared to areas of perimacular and peripheral retina in all of the proteins studied. (Original magnifications of x 200 and in insets x 400).</p