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Biomedical subjects

J McGinness

Publications and source records attributed to J McGinness.

10 recordsLinked to original sources
PubMed1990

Avoiding neurotoxicity with lithium-carbamazepine combinations.

A therapeutic synergism has been well documented with carbamazepine (CBZ) and lithium in some patients who do not respond adequately to either drug alone. Because both of these drugs can induce neurotoxicity, concern has been expressed about their safety when combined. The serum levels for effective and safe dosage have been determined when these drugs are used alone. Unfortunately, this information does not give us automatic insight into the range of safe serum levels for each drug when these drugs are combined. We do not know whether the contribution of each drug to the neurotoxicity is the same. We have plotted the paired serum levels on a two-dimensional graph and quantitatively determined the region where we begin to encounter neurotoxicity. When we examine the available data on this graph, we see no evidence for synergistic neurotoxicity.

Carbamazepine↗
PubMed1985

Protective effects of O-(beta-hydroxyethyl)-rutosides (HR) against adriamycin-induced toxicity in rats.

Adriamycin (Adriablastine), administered weekly at the dose of 5 mg/kg i.p. for 3 weeks in rats, produced a general decrease of vitality associated with a decrease of body weight, hypothermia, decreases of stroke volume and cardiac output. Hematocrit was decreased. Renal blood flow decreased whereas pulmonary blood flow increased. Mean blood pressure and heart rate remained unaffected. Biochemical evaluations revealed a decrease of blood urea and serum creatinine, which might be related to decreased food intake and protein metabolism. Morphological changes in the heart tissue could not be appreciated. Venoruton (HR), administered at the dose of 300 mg/kg p.o. daily for 28 days (5 days before and 23 days after the first injection of adriamycin), improved adriamycin-induced clinical signs and symptoms (loss of body weight, hypothermia and decreased general vitality). It tended to increase cardiac output and stroke volume.

Animals↗
PubMed1977

A superoxide-producing system in the conjunctival mucus thread.

In normal sterile eyes, the conjunctival mucus thread is capable of reducing the vital stain iodonitrotetrazolium (INT). The greatly increased amount of INT reduction in bacterial conjunctivitis has been used as a clinical test for this disorder. We find that native superoxide dismutase, but not the heat inactivated enzyme, inhibits INT reduction by the conjunctival mucus thread in vitro as well as in vivo in sterile rabbit eyes. Furthermore, 3,4-dihydroxybenzoic acid (DHBA), a scavenger of superoxide radical (O2-), inhibits INT reduction by the mucus thread. We conclude that INT reduction by the mucus thread is due to a superoxide radical-producing system similar to that apparently responsible for the tetrazolium-reducing properties of granulocytes and other phagocytes. This oxygen radical-producing system may serve as a defense against infection and possibly as a mediator of the conjunctival inflammatory response.

Animals↗
PubMed1974

Amorphous semiconductor switching in melanins.

Melanins produced synthetically and isolated from biological systems act as an amorphous semiconductor threshold switch. Switching occurs reversibly at potential gradients two to three orders of magnitude lower than reported for inorganic thin films, and comparable to gradients existing in some biological systems. Of a number of other biological materials tested, only cytochrome c acted similarly, but at the high potential gradients reported for thin film amorphous semiconductors.

Cytochrome c Group↗
PubMedDate not supplied

Neuronal DNA damage correlates with overexpression of interleukin-1beta converting enzyme in APPV717F mice.

Transgenic APPV717F mice, homozygous for a human minigene encoding the V717F familial Alzheimer's disease mutation, develop Abeta plaques similar to those seen in Alzheimer patients and show evidence of neuronal cell drop out in CA2-3 regions of the hippocampus at 8 months of age and older. Interleukin-1 (IL-1)beta (IL-1beta) converting enzyme (ICE) is a cysteine protease (caspase-1) that processes inactive (33 kDa) pro-IL-1beta to the active (17 kDa) inflammatory cytokine. We used immunohistochemistry, RT-PCR, and DNA cleavage (TUNEL) analysis to show progressive, age-associated increases in ICE mRNA levels, in the numbers of ICE-immunoreactive glia, and in the numbers of neurons showing evidence of DNA damage in APPV717F mice that commenced months prior to the appearance of Abeta plaques. Moreover, there were significant correlations between these parameters over an age range of 1-17 months. These findings are consistent with the idea that increases in ICE activity and expression contribute to neuronal injury in Alzheimer's disease.

Alzheimer Disease↗