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F J Kelly

Publications and source records attributed to F J Kelly.

140 records · Page 8Linked to original sources

Pre- and postnatal growth and protein turnover in four muscles of the rat.

Developmental growth and associated changes in protein turnover and nucleic acid concentrations have been studied in four individual skeletal muscles. They have also been related to changes in the whole animal. The growth rates of both fast and slow muscle types progressively diminished from the fetus to old age. Similarly, the fractional rates of protein synthesis (measured in vivo) and breakdown in each muscle type declined with age; the changes in the former correlating with decreases in the ribosomal capacities of the muscles. Throughout, fast muscles possessed lower turnover rates. The mean half-lives of mixed proteins were 12.0, 14.4, 13.5, and 7.2 days in the extensor digitorum longus (EDL), gastrocnemius, diaphragm, and soleus muscles, respectively, 310 days postpartum. Muscle atrophy was found at 735 days, at which stage the decreased protein synthetic rate in the soleus was due to a fall in the ribosomal capacity, while that in the EDL was attributable to a decreased synthetic rate per ribosome.

Animals↗

Ozone and the lung: a sensitive issue.

Ozone is a powerful oxidant and toxic air pollutant. As a gaseous pollutant, its primary target tissue is the lung and breathing slightly elevated concentrations of ozone results in a range of respiratory symptoms. These include decreased lung function and increased airway hyper-reactivity in 10-20% of the healthy population. Moreover, those with conditions such as asthma and chronic obstructive pulmonary disease (COPD) generally experience an exacerbation of their symptoms. Together, these observations suggest that certain individuals are particularly susceptible to this oxidant gas. The primary goal of this review is to examine the basis of this increased sensitivity. Ozone is a highly reactive gas that is consumed by reactive processes on reaching the first interface in the lung, the lung lining fluid compartment. Reactions between ozone and antioxidants tend to dominate in this compartment and these are generally thought of as beneficial, or protective interactions. In those instances when ozone reacts with other substrates in lung lining fluid such as protein or lipid, secondary oxidation products arise which transmit the toxic signals to the underlying pulmonary epithelium. The rules that govern the balance between beneficial and detrimental interactions in the lung lining fluid compartment are not well established but these may contribute, in part, to sensitivity. On reaching the lung surface, secondary oxidation products arising from ozone initiate a number of cellular responses. These include cytokine generation, adhesion molecule expression and tight junction modification. Together, these responses lead to the influx of inflammatory cells to the lung in the absence of a pathogenic challenge. Moreover, lung permeability is increased and oedema develops. The nature and extent of these responses are variable and often not related within an individual. Thus, although an improved appreciation of the general mechanism of action of ozone has been attained in recent years, the basis for individual susceptibility is still unclear.

Animals↗

Gluthathione: in defence of the lung.

Oxidative stress is implicated in the pathology of numerous diseases of the lung. These include cystic fibrosis, chronic obstructive airway disease and asthma. All these conditions are characterised by an imbalance between the amounts of reactive oxygen species (ROS) and available antioxidant defences. In the lung, ROS arise from endogenous sources, such as the influx of inflammatory cells or exogenous sources, such as from air pollution and cigarette smoke. When ROS production increases the redox balance of the airways alters, and this can lead to bronchial hyperactivity and further inflammation. The lung, like many other tissues, has a range of antioxidant defences which help to maintain a balanced redox status. These antioxidants are present in the intracellular, the vascular and extracellular respiratory tract lining fluid (RTLF) compartments. The reduced glutathione (GSH) content of RTLF is particularly high and new findings are beginning to reveal the role that the RTLF GSH pool plays in defending the lung.

Adult↗

Plasma and red blood cell vitamin E status of patients on total parenteral nutrition.

Plasma and red blood cell (RBC) tocopherol isomer (alpha, beta, delta, and gamma) concentrations were measured prior to, and following total parenteral nutrition (TPN), with Intralipid. Before feeding, nine of 13 patients had plasma total tocopherol levels less than 0.6 mg/dl (normal range 0.63-1.24 mg/dl) and 10 of 13 had total RBC tocopherol levels less than 0.2 mg/dl (normal range (0.20-0.39 mg/dl). Following 7 days TPN plasma vitamin E status increased significantly (p less than 0.001). However, this was due mostly to increases in the circulating level of beta + gamma-tocopherols. RBC vitamin E status was also significantly increased (p less than 0.001) following TPN, however, this was again due to incorporation of non-alpha-tocopherols. In a second study a alpha-tocopherol supplement, Vitlipid N, (9.1 mg alpha-tocopherol/day) was included in the feed. In these patients, large increases in plasma concentrations of non-alpha-tocopherol isomers were accompanied by an apparent improvement in alpha-tocopherol status (0.64 vs 0.44 mg/dl after 7 days). However, RBC alpha-tocopherol concentration did not change appreciably in these patients following either 7 or 14 days feeding. It is concluded that RBC vitamin E status is markedly influenced by the available plasma tocopherol pool and that provision of a small supplement of alpha-tocopherol is not sufficient to compete with the high concentration of non-alpha-isomers present in Intralipid. TPN utilizing fat emulsions containing high levels of non-alpha-tocopherol isomers (even when accompanied by alpha-tocopherol supplements) does not improve alpha-tocopherol status.

Adult↗