Fouling in membrane bioreactors used in wastewater treatment

and Introduction Abstract Study Design: Review and reinterpretation of existing literature. Objective: To suggest how intervertebral disc degeneration might be distinguished from the physiologic processes of growth, aging, healing, and adaptive remodeling. Summary of Background Data: The research literature concerning disc degeneration is particularly diverse, and there are no accepted definitions to guide biomedical research, or medicolegal practice. Definitions: The process of disc degeneration is an aberrant, cell-mediated response to progressive structural failure. A degenerate disc is one with structural failure combined with accelerated or advanced signs of aging. Early degenerative changes should refer to accelerated age-related changes in a structurally intact disc. Degenerative disc disease should be applied to a degenerate disc that is also painful. Justification: Structural defects such as endplate fracture, radial fissures, and herniation are easily detected, unambiguous markers of impaired disc function. They are not inevitable with age and are more closely related to pain than any other feature of aging discs. Structural failure is irreversible because adult discs have limited healing potential. It also progresses by physical and biologic mechanisms, and, therefore, is a suitable marker for a degenerative process. Biologic progression occurs because structural failure uncouples the local mechanical environment of disc cells from the overall loading of the disc, so that disc cell responses can be inappropriate or aberrant. Animal models confirm that cell-mediated changes always follow structural failure caused by trauma. This definition of disc degeneration simplifies the issue of causality: excessive mechanical loading disrupts a disc's structure and precipitates a cascade of cell-mediated responses, leading to further disruption. Underlying causes of disc degeneration include genetic inheritance, age, inadequate metabolite transport, and loading history, all of which can weaken discs to such an extent that structural failure occurs during the activities of daily living. The other closely related definitions help to distinguish between degenerate and injured discs, and between discs that are and are not painful.

What is intervertebral disc degeneration, and what causes it?

https://www.oarsijournal.com/article/S1063-4584(15)00877-8/pdf

Mechanics and biology in intervertebral disc degeneration: a vicious circle

In 2007, three times as many peer reviewed publications covering the biology and biotherapeutics of intervertebral disc (IVD) disease appeared in the literature than in 1997. This is testimony to the upsurge in interest in the IVD, mainly driven by the openings that modern molecular pathology has generated to investigate mechanisms of human disease and the potential offered by novel therapeutic technologies to use data coming from these studies to positively influence chronic discogenic back pain and sciatica. Molecular pathology has shown IVD degeneration, a major cause of low back pain, to be a complex, active disorder in which disturbed cytokine biology, cellular dysfunction and altered load responses play key roles. This has translated into a search for target molecules and disease processes that might be the focus of future, evidence-based therapies for back pain. It is not possible to describe the totality of advances that have been made in understanding the biology of the IVD in recent years, but in this review those areas of biology that are currently influencing, or could conceivably soon impinge on, clinical thinking or practice around IVD degeneration and discogenic back pain are described and discussed.

The cellular pathobiology of the degenerate intervertebral disc and discogenic back pain

Bioreactors for tissue mass culture: Design, characterization, and recent advances

Study design A review of the literature on disc nutrition. Objectives To summarize the information on disc nutrition in relation to disc degeneration. Summary of the background data The disc is avascular, and the disc cells depend on diffusion from blood vessels at the disc's margins to supply the nutrients essential for cellular activity and viability and to remove metabolic wastes such as lactic acid. The nutrient supply can fail due to changes in blood supply, sclerosis of the subchondral bone or endplate calcification, all of which can block transport from blood supply to the disc or due to changes in cellular demand. Methods A review of the studies on disc blood supply, solute transport, studies of solute transport in animal and human disc in vitro, and of theoretical modeling studies that have examined factors affecting disc nutrition. Results Small nutrients such as oxygen and glucose are supplied to the disc's cells virtually entirely by diffusion; convective transport, arising from load-induced fluid movement in and out of the disc, has virtually no direct influence on transport of these nutrients. Consequently, there are steep concentration gradients of oxygen, glucose, and lactic acid across the disc; oxygen and glucose concentrations are lowest in the center of the nucleus where lactic acid concentrations are greatest. The actual levels of concentration depend on the balance between diffusive transport and cellular demand and can fall to critical levels if the endplate calcifies or nutritional demand increases. Conclusions Loss of nutrient supply can lead to cell death, loss of matrix production, and increase in matrix degradation and hence to disc degeneration.

Nutrition of the intervertebral disc.

We inserted an electrode up the femoral neck into the femoral head of ten patients undergoing a metal-on-metal hip resurfacing arthroplasty through a posterior surgical approach and measured the oxygen concentration during the operation. In every patient the blood flow was compromised during surgery, but the extent varied. In three patients, the oxygen concentration was zero at the end of the procedure. The surgical approach caused a mean 60% drop (p < 0.005) in oxygen concentration while component insertion led to a further 20% drop (p < 0.04). The oxygen concentration did not improve significantly on wound closure. This study demonstrates that during hip resurfacing arthroplasty, patients experience some compromise to their femoral head blood supply and some have complete disruption.

The effect of hip resurfacing on oxygen concentration in the femoral head

We have undertaken an in vivo assessment of the tissue metabolism and cellular activity in torn tendons of the rotator cuff Cellular oxygen consumption was measured in 13 patients undergoing mini-open repair of small, medium, large and massive full-thickness tears Measurements were also taken from three control patients who were undergoing open stabilisation of the shoulder with grossly normal tendons The level of oxygen and nitrous oxide was measured amperometrically using silver needle microelectrodes at the apex of the tear and 15 cm from its edge With nitrous oxide indicating the degree of perfusion, oxygen consumption was calculated at each location to reflect cellular activity All of the torn tendons had lower levels of cellular activity than the control group This activity was lower still in the tissue nearest to the edge of the tear with the larger tears showing the lowest activity This indicated reduced levels of tissue metabolism and infers a reduction in tendon viability Our findings suggest that surgical repair of torn tendons of the rotator-cuff should include the more proximal, viable tissue, and may help to explain the high rate of re-rupture seen in larger tears

S.R. Smith

Papers

Nutrition of the intervertebral disc.

The effect of hip resurfacing on oxygen concentration in the femoral head

In vivo measurement of tissue metabolism in tendons of the rotator cuff: implications for surgical management.

Clinical Guidelines for the Physiotherapy Management of Whiplash Associated Disorder

An in line non-invasive optical system to monitor pH in cell and tissue culture.