Impact of chronic cough on quality of life

STUDY DESIGN: The biomechanical influence of in situ setting hydroxyapatite cement was examined for use in pedicle screw revision surgery. Pull-out testing of control and pedicle screws augmented with hydroxyapatite cement was performed in human cadaver vertebrae. OBJECTIVES: To determine the immediate effect of using hydroxyapatite cement to augment revision pedicle screws after failure of the primary pedicle screw fixation. SUMMARY OF BACKGROUND DATA: The potential problems associated with using polymethylmethacrylate to augment revision pedicular instrumentation have prompted the search for other solutions. The introduction of resorbable hydroxyapatite pastes may have provided new biocompatible solutions for pedicle screw revision. METHODS: Ten human cadaver vertebrae were instrumented with 6.0-mm pedicle screws in each pedicle. The screws were loaded to failure in axial tension (pull-out). The failed pedicles then were instrumented with 7.0-mm pedicle screws, either augmented with hydroxyapatite cement or nonaugmented, which also were loaded to failure. Finally, the nonaugmented 7.0-mm screw hole was reinstrumented with a hydroxyapatite cement-augmented, 7.0-mm pedicle screw and loaded to failure. RESULTS: The pull-out strength of the 7.0-mm, hydroxyapatite cement-augmented screws was 325% (P = 2.9 x 10(-5)) of that of the 6.0-mm control screws, whereas the strength of the 7.0-mm nonaugmented screws was only 73% (P = 2.0 x 10(-2)) of that of the 6.0-mm control screws. The 7.0-mm screws augmented with hydroxyapatite cement also were able to salvage 7.0-mm pull-out sites to 384% (P = 6.9E-5) of the pull-out strength of the 7.0-mm nonaugmented screws. CONCLUSIONS: Hydroxyapatite cement may be a mechanically viable alternative to polymethyl methacrylate for augmenting revision pedicular instrumentation and should be considered for future experimental, animal, and clinical testing.     

Defective transfer RNA-queuine modification in C3H10T1/2 murine fibroblasts transfected with oncogenic ras

tRNA isoacceptors for aspartic acid, asparagine, histidine, and tyrosine are modified in the anticodon wobble position with the deazaguanine analogue queuine. Queuine modification is defective in many tumors and transformed cell lines, and the extent of hypomodification correlates with staging and outcome in numerous human tumors. The molecular role of queuine modification in normal cells and the mechanisms of queuine hypomodification in tumors are unknown. We have characterized nontransformed C3H10T1/2 murine fibroblasts (C3H) and their ras-transfected counterparts (RasC4) with respect to the causes and effects of queuine hypomodification. RasC4 cells are hypomodified for queuine compared with C3H cells, despite increase tRNA-guanine ribosyltansferase activity. Excess exogenous queuine can cause repletion of tRNA queuine levels in RasC4 cells. Queuine modification of both C3H and RasC4 cells can be decreased by treatment with 7-methylguanine. This treatment does not affect growth in monolayer culture but enhances anchorage-independent growth of RasC4 cells greatly. These cell lines may be useful systems for the study of queuine function in normal cells and the causes and consequences of hypomodification for queuine in tumors.     

Cerebrospinal fluid shunts

Arginine-insulin stimulation and IV glucose suppression (AIGT) tests were used to evaluate release of insulin and growth hormone. Adult patients responded normally. Hypopituitary patients showed no hGH response. One third of short normal patients showed abnormal hGH responses to glucose suppression. Two thirds of the short normal patients showed poor insulin responses to either amino acid or glucose stimulation. Such patients might have abnormalities in release mechanisms for insulin and suppression mechanisms for hGH and this might contribute to their growth failure.     

Tetrahydroisoquinolinecarboxylic acids and catecholamine metabolism in adrenal medulla explants

In a study of the relationship of the tetrahydroisoquinolinecarboxylic acids (TIQCAs) to catecholamine metabolism, we have investigated their effects on cultured rat adrenal medulla explants. Medullae were incubated in medium containing norlaudanosolinecarboxylic acid (NLCA) or 3',4'-deoxynorlaudanosolinecarboxylic acid (DNLCA) (0.5 mM) in the presence and absence of [3H]tyrosine. By paired-ion reverse-phase high pressure liquid chromatography, tissue epinephrine (EPI), norepinephrine (NE), dopamine (DA) and TIQCA were resolved. Endogenous concentrations were measured with electrochemical detection, and radioactivity was assayed by collecting appropriate effluents. Tissue levels of the TIQCAs reached saturating levels of 0.36 mM by about 20 hr. DNLCA elicited a significant decrease (60%) in endogenous DA, NE and EPI at 40 hr, whereas only DA was depressed at 30 hr. NLCA had little effect after 30 or 40 hr. When tissues were maintained in the presence of alpha-methyltyrosine (0.5 mM) for 40 hr, catecholamine levels were depressed to an extent similar to that observed with DNLCA. Incubation with [3H]tyrosine in the presence of TIQCAs revealed inhibition of tyrosine uptake and suggested a reduction in the rate of catecholamine synthesis. These results are consistent with previous data on the inhibition of tyrosine 3-monooxygenase by DNLCA in vitro.     

Postural changes in plasma renin activity and responses to vasoactive drugs in a case of Shy-Drager syndrome

A male aged 47 years with gross autonomic insufficiency as part of the Shy-Drager syndrome is described. He did not sweat normally when warmed, and his circulatory responses to mental arithmetic, the Valsalva manoeuvre, and head-up tilt were abnormal indicating severe sympathetic failure. During head-up tilt there was a rise in plasma renin activity and plasma aldosterone. It is argued that plasma renin activity is not dependent on sympathetic nervous activity and may be mediated by renal baroreceptors. These rises may help sustain the blood pressure in such patients during repeated head-up tilts. Infusions of L-noradrenaline and angiotension produced greater hypertension, and injections of isoprenaline greater hypotension than in controls. Although it is difficult to exclude the possibility that one factor in this may be hypersensitivity of receptors in blood vessel walls, the principal factor is likely to be the absence of those baroreflexes of which the efferent pathways are in the sympathetic nervous system.