Sick leave and disability pension among Swedish testicular cancer survivors according to clinical stage and treatment

<div><p><b>Purpose.</b> To investigate if testicular cancer survivors (TCSs) have a higher incidence of work loss compared with the population, accounting for stage, treatment and relapse.</p><p><b>Material and methods.</b> A cohort of 2146 Swedish TCSs diagnosed 1995–2007 (seminoma n = 926, non-seminoma n = 1220) was identified in the SWENOTECA (Swedish-Norwegian Testicular Cancer Group) register, and matched 1:4 to population comparators. Prospectively recorded work loss data (both before and after diagnosis) were obtained from national registers through September 2013. Adjusted relative risks (RR) and 95% confidence intervals (CI) of sick leave and/or disability pension were calculated annually and overall with Poisson- and Cox regression, censoring at relapse. The mean number of annual work days lost was also estimated.</p><p><b>Results.</b> TCSs were at a modestly increased annual risk of work loss up to the third year of follow-up (RR_{3rd year} 1.25, 95% CI 1.08, 1.43), attributed to a more pronounced risk among extensively treated patients (4 chemotherapy courses: RR_{3rd year} 1.60, 95% CI 1.19, 2.15; > 4 courses: RR_{3rd year} 3.70, 95% CI 2.25, 6.11). Patients on surveillance or limited treatment (radiotherapy, 1–3 chemotherapy courses) did not have an increased risk of work loss beyond the first year. TCSs receiving > 4 chemotherapy courses had higher mean number of annual days of work loss up to the 10th year post-diagnosis, and a five-fold risk of disability pension (RR 5.16, 95% CI 2.00, 10.3).</p><p><b>Conclusion.</b> Extensively treated TCSs, but not those on surveillance or limited treatment, are at increased risk of work loss long-term, not explained by relapse. These patients may benefit from early rehabilitation initiatives.</p></div

A role for pectin in the control of cell expansion

Uptake of nutrients and water depends on the growth of roots through elongation of individual cells near the. root tip. Many of the numerous components of Type I primary cell walls, those of dicotyledons and monocotyledons other than grasses (Poaceae), have been determined, and many hypotheses have been proposed for the control of cell expansion. This important aspect of plant growth still needs elucidation, however. A model is proposed in which pectin, which occurs as a calcium (Ca) pectate gel between the load-bearing cellulose microfibrils and xyloglucan (XG) chains, controls the rate at which cells expand. It is considered that the increasing tension generated by the expanding cell is transmitted to interlocked XG chains and cellulose microfibrils. The resulting deformation of the embedded Ca pectate gel elicits the excretion of protons from the cytoplasm, possibly via compounds such as cell wall-associated kinases, that weakens the Ca pectate gel, permitting slippage of XG molecules through the action of expansin. Further slippage is prevented by deformation of the pectic gel, proton diffusion, and the transfer of residual tension to adjacent XG chains. Evidence for this model is based on the effects of pH, Ca, and aluminum (Al) on root elongation and on the reactions of these cations with Ca pectate. This model allows for genetic selection of plants and adaptation of individual plants to root environmental conditions

Forest plots for association of rs2509049 with DLBCL, FL and all B-cell lymphomas.

<p>Squares indicate the ORs, with the sizes proportional to the weight of the study in the meta-analysis. Summary ORs with and without the inclusion of the BC population are indicated in bold and designated with a diamond extending the width of the CI. All p values are from a fixed effects model except those indicated with an asterisk (*) which are from a random effects model. <i>Q</i> values for analyses including the BC dataset for DLBCL, FL and All B cell groups are <i>Q</i>=0.876, <i>Q</i>=0.053 and <i>Q</i>=0.161 for combined sexes, and <i>Q</i>=0.344, <i>Q</i>=0.045 and <i>Q</i>=0.002 for females only, respectively. Abbreviations: OR, odds ratio; 95% CI, 95% confidence interval; DLBCL, diffuse large B-cell lymphoma; FL, follicular lymphoma; all B-cell, all B-cell lymphomas; SCALE, Scandinavian Lymphoma Etiology; SF, San Francisco; BC, British Columbia; NCI-SEER, National Cancer Institute - Surveillance, Epidemiology and End Results; NSW, New South Wales. Figure created with rmeta version 2.16.</p

Linkage Disequilibrium for 13 SNPs in 1115 cases and controls in the BC population.

<p>Chromosomal coordinates (Hg18) and Entrez genes are mapped relative to the 13 SNPs analyzed in this study. The linkage disequilibrium plot shows <i>r</i>² values; predicted haplotype blocks are outlined in black. Figure created with Haploview version 4.2.</p