Intracranial circulation: pulse-sequence considerations in three- dimensional (volume) MR angiography

The technique and feasibility of magnetic resonance (MR) angiography of intracranial vessels were studied in 35 healthy volunteers. Variations in image orientation, repetition time (TR), and flip angle were evaluated to determine their effects on flow-related enhancement. Gradient modifications--including echo time (TE), motion compensation, bandwidth, and field of view--were also studied in an effort to reduce motion-induced phase shifts. Results indicated that a FISP (fast imaging with steady precession) sequence with a TR of 50 msec, TE of 15 msec, velocity compensation in the read and section-select directions, acceleration compensation in the read direction, anisotropic volume, and a 1.25-mm partition thickness produced three-dimensional angiographic MR images that were accurate and reproducible in the depiction of the major intracranial vessels. Difficulties with field of view, persistent signal void secondary to higher-order motion, and spatial resolution remain major problems requiring additional study.     

Paediatric dacryocystorhinostomy

Of 258 cases of dacryocystorhinostomy performed on children in the period September 1981 to September 1991, 130 were for simple, unresolved congenital nasolacrimal duct obstruction. Other indications for surgery included punctal agenesis, lacrimal fistula, post-traumatic and post-inflammatory canalicular obstruction. Of 177 children without canalicular pathology, 171 (96%) were relieved of symptoms with one operation, without canalicular intubation. Of 81 cases with canalicular disease, 55 of 70 (79%) who underwent DCR plus canalicular intubation, and 10 of 11 who underwent DCR plus Lester-Jones tube, were substantially improved with one operation. No child required peroperative or postoperative blood transfusion. Dacryocystorhinostomy in childhood, in experienced surgical hands, is a safe procedure, achieving relief of symptoms in most cases, particularly in the absence of canalicular disease.     

Mechanisms responsible for the thermal sensitivity of adrenal microsomal monooxygenases.

Studies were done to determine the mechanism(s) responsible for the thermal lability of adrenal microsomal monooxygenases. Preincubation of guinea pig adrenal microsomal suspensions at 37 degrees C caused large time-dependent declines in benzo(a)pyrene (BP) hydroxylase and benzphetamine (BZ) demethylase activities. Similar preincubations with hepatic microsomes had little effect on enzyme activities. The decreases in adrenal enzyme activities were completely prevented by co-incubation of microsomes with cytosol, but were not diminished by reduced glutathione, ascorbic acid, or bovine serum albumin. Partial protection was afforded by EDTA, suggesting that lipid peroxidation might be involved, but malonaldehyde production was not demonstrable and MnCl2, a potent inhibitor of lipid peroxidation, did not affect the decline in enzyme activities. The decreases in the rates of BP and BZ metabolism were prevented by including NADPH or NADP+ in the preincubation medium. The preincubation conditions causing losses of adrenal enzyme activities did not affect cytochrome P-450 concentrations or substrate binding to cytochromes P-450, as indicated by type I difference spectra. NADH-cytochrome c reductase activity also was not affected, but there were decreases in NADPH-cytochrome c reductase activity that were proportionately similar to the declines in drug-metabolizing activities. Direct assessment of NADPH-cytochrome P-450 reductase revealed similarly large decreases in enzyme activity resulting from preincubation of adrenal microsomes. The results demonstrate a need for extra caution when doing preincubation experiments with adrenal microsomal preparations, and suggest that the thermal lability of adrenal monooxygenases is attributable to effects at the active site of NADPH-cytochrome P-450 reductase.     

Lung biopsy in chronic lymphocytic leukemia

Nine patients with chronic lymphocytic leukemia (CLL), with pulmonary involvement confirmed by biopsy, presented with progressive cough and/or shortness of breath and had interstitial infiltrates on chest radiographs. Biopsies showed a dense lymphocytic infiltrate that followed bronchovascular bundles. We considered CLL the predominant finding, and the cause of the patient's pulmonary disease, in eight cases; in one, a histologically nonspecific organizing pneumonia was the main lesion and CLL was an incidental finding. Culture results were available in six cases and were negative except in one case with presumed contaminants. A granulomatous reaction was present in five cases and was necrotizing in two, although culture results were negative. The only case with a recognizable organism had noninvasive fungal hyphae growing in many of the small airways. All of the patients' respiratory symptoms improved after chemotherapy and/or steroid therapy, and the chest radiographs also showed clearing.     

Inhibition of voltage-gated K channels in synaptosomes by sn-1,2-dioctanoylglycerol, an activator of protein kinase C

Tracer efflux studies were used to determine the effect of activation of protein kinase C on K channel function in rat brain synaptosomes. Hippocampal synaptosomes were treated with sn-1,2-dioctanoylglycerol (diC8), a synthetic diacylglycerol (DG) analog that activates protein kinase C. DiC8 inhibited depolarization-induced 86Rb efflux through voltage-gated K channels but did not affect the component of efflux corresponding to Ca-activated K channels. In time-course experiments, diC8 inhibited two components of 86Rb efflux: efflux through a rapidly inactivating, voltage-gated K channel (responsible for the "A" current) and that through a slowly inactivating, voltage-gated K channel (believed to be the "delayed rectifier"). Experiments with specific blockers of these voltage-gated K channels supported this observation. Inhibition of K-stimulated 86Rb efflux by diC8 was time dependent: at least 15 sec of preincubation was required before the effect could be observed. The effect of diC8 was concentration dependent: 50 microM diC8 produced a half-maximal inhibition of K-stimulated 86Rb efflux. The idea that the inhibition of synaptosome K channels by diC8 resulted from activation of C kinase was supported by pharmacological evidence. The action of diC8 was mimicked by 1-oleoyl-2-acetylglycerol, another DG analog that activates protein kinase C, but not by deoxy-diC8, a DG analog that does not activate C kinase. Inhibition of C kinase by sphingosine or H-7 prevented the diC8 effect. These studies demonstrate that synaptosomes are a good model in which to study modulation of mammalian CNS K channels.(ABSTRACT TRUNCATED AT 250 WORDS)