There is uncertainty regarding whether patients with cancer should be screened for latent tuberculosis infection (LTBI). We performed a systematic review and meta-analysis to estimate the relative incidence of tuberculosis (TB) in cancer.We searched MEDLINE and Embase for studies published before December 21, 2016. We included studies that evaluated the incidence of TB in patients with solid cancers and haematological malignancies relative to a reference group (study control or general population). A pooled estimate of the incidence rate ratio (IRR) was obtained using standard meta-analysis methods.The search strategy identified 13 unique studies including 921 464 patients with cancer. The IRR of TB for adult patients with cancer was 2.61 (95% CI 2.12-3.22; I 2 =91%). In haematological cancers, the IRR was 3.53 (95% CI 1.63-7.64; I 2 =96%); and in solid cancers in adults, it was 2.25 (95% CI 1.96-2.58; I 2 =91%). The highest IRR was found in children with haematological malignancies or solid cancers (IRR 16.82,; I 2 =79%). Considering the limited duration of maximum immunosuppression in cancer and reduced cumulative lifetime risk of TB because of reduced life expectancy, children, but not adults, appear to be at a sufficient level of risk to warrant systematic screening for LTBI.

To investigate the apoptotic effects of detergent sclerosants sodium tetradecylsulphate (STS) and polidocanol (POL) on endothelial cells at sub-lytic concentrations. Human umbilical vein endothelial cells (HUVECs) were isolated and labelled with antibodies to assess for apoptosis and examined with confocal microscopy and flow cytometry. Isolated HUVECs viability was assessed using propidium iodide staining. Early apoptosis was determined by increased phosphatidylserine exposure by lactadherin binding. Caspase 3, 8, 9 and Bax activation as well as inhibitory assays with Pan Caspase (Z-VAD-FMK) and Bax (BI-6C9) were assessed to identify apoptotic pathways. Porimin activation was used to assess cell membrane permeability. Cell lysis reached almost 100 % with STS at 0.3 % and with POL at 0.6 %. Apoptosis was seen with both STS and POL at concentrations ranging from 0.075 to 0.15 %. PS exposure increased with both STS and POL and exhibited a dose-dependent trend. Active Caspase 3, 8 and 9 but not Bax were increased in HUVECs stimulated with low concentrations of both STS and POL. Inhibitory assays demonstrated Caspase 3, 8, 9 inhibition at low concentrations (0.075 to 0.6 %) with both STS and POL. Both agents increased the activation of porimin at all concentrations. Both sclerosants induced endothelial cell (EC) apoptosis at sub-lytic concentrations through a caspase-dependant pathway. Both agents induced EC oncosis.

Summary The respiration characteristics and energy metabolism of sheep lymphocytes collected from the popliteal lymph before and after antigenic challenge with Salmonella organisms have been studied at various O2 tensions. The O2 consumption of sheep lymphocytes could be related to the PO2 of the medium by the Michaelis‐Menten equation. In resting lymphocytes, Vmax (mean ± S.D.) was 1·70 ± 0·23 μmoles/h/2 × 108 cells), critical O2 concentration ([O2]crit) was 2·00 ± 0·20 μM and Km was 0·46 ± 0·11 μM. Significant chances occurred in the respiration characteristics of these cells following antigenic challenge of the nude. Both Vmax and Km reached maxima when the blast cell response in the lymph was at its peak. [O2]crit, however, did not change significantly over an immune response. Lymphocytes collected before antigenic challenge had mean rates of glucose uptake of 0·97 ± 0·29 μmoles/h/2 × 108 cells and lactate production of 1·31 ± 0·37 μmoles/h/2 × 108 cells. During the height of immune responses to Salmonella, lymphocytes showed an enhanced glucose uptake, lactate production and C‐1‐ and C‐6‐labelled glucose metabolism. The rates of energy metabolism of sheep lymphocytes varied with changes in the PO2 of the gas phase from 21% to 0% O2. The rates of glucose uptake and lactate production increased while the rates of 14CO2 production from C‐1‐ and C‐6‐labelled glucose decreased as the PO2 decreased.