Effect of chronic suppurative otitis media on distortion product otoacoustic emission input-output functions in conventional and ultra-high frequencies.

BACKGROUND: Detection and valid measurements of distortion product otoacoustic emissions are not influenced by cochlear status alone, but also by middle-ear status. There is a need to understand the use of ultra-high frequency distortion product otoacoustic emissions in cases of abnormal distortion product otoacoustic emission findings for conventional frequencies related to the middle-ear condition. METHOD: The present study investigated distortion product otoacoustic emission input-output functions in conventional and ultra-high frequencies in: 37 adults with chronic suppurative otitis media (clinical group) and 37 adults with normal hearing sensitivity (control group). RESULTS: There were significant reductions in distortion product otoacoustic emission amplitude and mean signal-to-noise ratio in the clinical group compared to the control group, especially for conventional frequencies. CONCLUSION: There was a significant reduction in the rate of ears with measurable distortion product otoacoustic emissions in the clinical group, especially for conventional frequencies. The effect of chronic suppurative otitis media was more pronounced in the conventional frequency range compared to the smaller effect seen in the ultra-high frequency range.

The elm1 kinase functions in a mitotic signaling network in budding yeast.

In budding yeast, the Clb2 mitotic cyclin initiates a signaling network that negatively regulates polar bud growth during mitosis. This signaling network appears to require the function of a Clb2-binding protein called Nap1, the Cdc42 GTPase, and two protein kinases called Gin4 and Cla4. In this study, we demonstrate that the Elm1 kinase also plays a role in the control of bud growth during mitosis. Cells carrying a deletion of the ELM1 gene undergo a prolonged mitotic delay, fail to negatively regulate polar bud growth during mitosis, and show defects in septin organization. In addition, Elm1 is required in vivo for the proper regulation of both the Cla4 and Gin4 kinases and interacts genetically with Cla4, Gin4, and the mitotic cyclins. Previous studies have suggested that Elm1 may function to negatively regulate the Swe1 kinase. To further understand the functional relationship between Elm1 and Swe1, we have characterized the phenotype of Deltaelm1 Deltaswe1 cells. We found that Deltaelm1 Deltaswe1 cells are inviable at 37 degrees C and that a large proportion of Deltaelm1 Deltaswe1 cells grown at 30 degrees C contain multiple nuclei, suggesting severe defects in cytokinesis. In addition, we found that Elm1 is required for the normal hyperphosphorylation of Swe1 during mitosis. We propose a model in which the Elm1 kinase functions in a mitotic signaling network that controls events required for normal bud growth and cytokinesis, while the Swe1 kinase functions in a checkpoint pathway that delays nuclear division in response to defects in these events.

Effect of vitamin E deficiency on lipid composition of CNS-myelin in the rat.

Vitamin E deficiency in the rat is accompanied by a decrease in total lipids and in cholesterol and an elevation in the lysolecithin content of CNS-myelin.

Phospholipase A2 of rat liver mitochondria in vitamin E deficiency.

1. There is a more than 2-fold increase in phospholipase A(2) activity (EC 3.1.1.4) of liver mitochondria isolated from vitamin E-deficient rats compared with that in normal rats. 2. alpha-Tocopherol in lipoprotein-bound form is more effective than free alpha-tocopherol in restoring the enzyme activity to normal.

Possible interrelationship between vitamins E and b12 in the disturbance in methylmalonate metabolism in vitamin E deficiency.

1. The disturbance in 2-methylmalonate metabolism resulting in its increased urinary excretion observed in vitamin E deficiency is not caused by increased formation of methylmalonate from propionate as is evident from the activity of the enzyme propionyl-CoA carboxylase (EC 6.4.1.3), but can be traced to an impairment in the conversion of methylmalonate into succinate by the vitamin B12-requiring enzyme, methylmalonyl-CoA mutase (EC 5.4.99.2) in rat liver. 2. It is shown that the decrease in the activity of methylmalonyl-CoA mutase in vitamin E deficiency is not a consequence of a secondary vitamin B12 deficiency. Peroxidative destruction of the coenzyme in vitamin E deficiency was also ruled out. The results suggest a defect in the conversion of cyanocobalamin into its coenzyme form.

Radiation induced alterations in the endotoxin of S. typhimurium.

The lipopolysaccharide (LPS) of S. typhimurium has been shown to be significantly detoxified after in vivo irradiation at 500 krad. Radiation is thus a useful method for converting endotoxin into toxoid. The structural alterations in the detoxified LPS are shown to be mainly in the lipid A molecule, resulting in the loss of beta-hydroxymyristic acid.

Radiovaccine of S. typhimurium cells.

Gamma-irradiation of S. typhimurium cells up to a dose of 500 krad significantly reduces their toxicity. However, the antigenicity of these cells is not altered, which suggests that these cells could be used as a vaccine. The protection offered by the irradiated cells is comparable to that of formalin-treated cells. The radio-vaccine, however, offers an additional advantage of significant detoxification of the endotoxin, thereby minimizing side effects. The lipopolysaccharide extracted from the irradiated S. typhimurium cells offered cross-protection against other Salmonella species tested.

Effect of protein deficiency on absorption, transport and distribution of alpha-tocopherol in the rat.

The absorption, transport and distribution of alpha-[3H]tocopherol were greatly decreased in protein deficiency. This was reflected in the subcellular distribution of alpha-[3H]tocopherol in livers of protein-deficient rats. The ratio, bound:free for alpha-[3H]tocopherol, also decreased in both serum and liver cytosol. After protein refeeding, absorption, transport and distribution patterns of alpha-[3H]tocopherol for the protein-deficient rats were restored to patterns similar to those of control animals.

Study of protein synthesis in rat liver mitochondria use of cycloheximide.

1. The effects of short-term and long-term administration of cyclohexidine on rat liver mitochondrial protein synthesis have been examined and were found to be different. 2. Long-term administration of cycloheximide resulted in inhibition of total cellular protein synthesis including that of mitochondria while, at short-term intervals, 8-10% of mitochondrial protein synthesis was cycloheximide-resistant. 3. The inhibitory effect was also reflected in terms of protein synthesizing ability of mitochondria in vitro, the inhibition becoming apparent at 40 min and showing progressive increase with time. 4. The observed inhibition of mitochondrial protein synthesis by cycloheximide was not due to either inhibition of energy metabolism or alteration of amino-acid pool. 5. Cycloheximide did not enter mitochondria or sonic preparation under conditions in vitro. On the other hand, after administration of [3H]cycloheximide, significant quantities of the label were found to be associated with mitochondria and mitoribosomes. 6. These results indicated that cycloheximide reached the site of action in mitochondria under conditions in vivo but was unable to do so in vitro. 7. The results are discussed to elucidate the possible mechanisms involved in the inhibition of truly mitochondrial protein synthesis by cyclohexamide.