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Biological ageing is characterised by prolonged cellular damage over the lifespan, which results from oxidative stress processes that are implicated in both the initiation and progression of age-related disorders such as Alzheimer’s disease (AD). Recently, the role of the plasma membrane redox system, which consists of at least three major components: the lipophilic antioxidants (Coenzyme Q (CoQ) and α-tocopherol), the intracellular cytosolic electron donor (NAD(P)H) and membrane-associated quinone reductases (cytochrome b5 reductase and NADH-quinone), in protecting against oxidative stress has come into focus. Research shows that this redox system plays a protective role during mitochondrial dysfunction by aiding in the alternative glycolytic ATP production pathway and reducing oxidative stress. The different aspects of the plasma membrane operate in tandem to protect the membrane from lipid peroxidation, preventing the formation of semiquinone free radicals and reactive oxygen species, and to ultimately limit oxidative stress while still maintaining cellular levels of each component. Past studies have made a link between the plasma membrane redox system and AD and have revealed that each aspect is affected during the disease. Moreover, research has revealed that manipulating the system components can protect cells from amyloid-β toxicity, suggesting a key role in cell survival. To date, the relationship of the plasma membrane redox system to the brain changes seen in AD has yet to be fully elucidated, and we will review the current literature here.

Single-molecule studies of protein–DNA interactions continue to yield new information on numerous DNA processing pathways. For example, optical microscopy-based techniques permit the real-time observation of proteins that interact with DNA substrates, which in turn allows direct insight into reaction mechanisms. However, these experiments remain technically challenging and are limited by the paucity of stable chromophores and the difficulty of acquiring statistically significant observations. In this protocol, we describe a novel, high-throughput, nanofabricated experimental platform enabling real-time imaging of hundreds of individual protein–DNA complexes over hour timescales.

Micronutrient deficiencies are widely prevalent in developing regions, especially in vulnerable groups such as HIV-infected pregnant women. Micronutrient supplementation is considered one of the most cost-effective strategies to reduce malnutrition and improve health outcomes.

In order to inhibit human leukocyte proteolytic activity as a means of arresting the inflammatory response in tissues in vivo, we have designed a novel antiprotease carrier named serumsomes™. Stabilized human serum was added to a flask containing a film of dried, purified lipids (phosphatidylcholine/dicetyl phosphate/cholesterol, 70:20:10) and hand-shaken for 10 min. Equal volumes of human neutrophils, and either serumsomes™ (in stabilized human serum) or stabilized human serum alone were mixed together. Following 2 h of incubation at 37°C, the total elastase content of the neutrophils was reduced to 60 ± 15% and 83 ± 7% of the original activity by serumsomes™ and stabilized human serum, respectively. Analysis of β-glucuronidase activity, a nonproteolytic lysosomal marker enzyme, revealed no diminution of activity during either of these incubations. These experiments demonstrate that human neutrophils are capable of interacting with serumsomes™ in vitro, selectively inhibiting the lysosomal protease elastase. By administering serumsomes™ in vivo, one may potentially preload blood leukocytes with serum antiproteases prior to their migration to inflammatory sites and thus possibly reduce the extent of tissue injury.

Impulse conduction in normal and pathologically altered myelinated nerves has been extensively reviewed by many workers (Paintal, 1978; Sunderland, 1978; Waxman, 1978; 1980). Conduction velocity of nerve impulses is of particular clinical importance in demyelinating disorders (Rogart & Ritchie, 1977; Rasminsky & Sears, 1973). Notwithstanding these data, many aspects of nerve conduction velocity, particularly the underlying mechanisms that determine it, are incompletely understood (Paintal, 1978; Waxman, 1980).

Steady electric fields are known to affect development, growth and repair of various tissues in vivo and in vitro. Confirmed effects include accelerated repair and regeneration of articular cartilage and bone fractures (Norton, 1974; Baker et al., 1974; Bassett et al., 1974); the induction and control of morphogenesis in amputated forelimb regeneration in adult frogs (Smith, 1974); orientation and acceleration of neurite growth in chick dorsal root ganglia in tissue culture (Jaffe & Poo, 1979) and in differentiating frog embryonic neuroblasts (Patel & Poo, 1982) and myoblasts (Hinkle et al., 1981). Because there are few reports of electric fields influencing mammalian central and peripheral nerves (Wilson et al., 1974; Wilson, 1981), our aim was to examine the effects of such fields on peripheral nerve regeneration and functional recovery in the cat.