Viscosity dynamics and the production of extracellular polymeric substances and soluble microbial products during anaerobic digestion of pulp and paper mill wastewater sludges.

The production processes of the pulp and paper industry often run in campaigns, leading to large variations in the composition of wastewaters and waste sludges. During anaerobic digestion (AD) of these wastes, the viscosity or the production of extracellular polymeric substances (EPS) and soluble microbial products (SMP) may be affected, with the risk of foam formation, inefficient digester mixing or poor sludge dewaterability. The aim of this study was to investigate how viscosity and production of EPS and SMP during long-term AD of pulp and paper mill sludge is affected by changes in organic loading rate (OLR) and hydraulic retention time (HRT).

Combining high-rate aerobic wastewater treatment with anaerobic digestion of waste activated sludge at a pulp and paper mill.

The activated sludge process within the pulp and paper industry is generally run to minimize the production of waste activated sludge (WAS), leading to high electricity costs from aeration and relatively large basin volumes. In this study, a pilot-scale activated sludge process was run to evaluate the concept of treating the wastewater at high rate with a low sludge age. Two 150 L containers were used, one for aeration and one for sedimentation and sludge return.

High-rate anaerobic co-digestion of kraft mill fibre sludge and activated sludge by CSTRs with sludge recirculation.

Kraft fibre sludge from the pulp and paper industry constitutes a new, widely available substrate for the biogas production industry, with high methane potential. In this study, anaerobic digestion of kraft fibre sludge was examined by applying continuously stirred tank reactors (CSTR) with sludge recirculation. Two lab-scale reactors (4L) were run for 800days, one on fibre sludge (R1), and the other on fibre sludge and activated sludge (R2).

Insulin signaling in type 2 diabetes: experimental and modeling analyses reveal mechanisms of insulin resistance in human adipocytes.

Type 2 diabetes originates in an expanding adipose tissue that for unknown reasons becomes insulin resistant. Insulin resistance reflects impairments in insulin signaling, but mechanisms involved are unclear because current research is fragmented. We report a systems level mechanistic understanding of insulin resistance, using systems wide and internally consistent data from human adipocytes.