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This paper defines the term 'reading therapy' and discusses its early development in the United Kingdom and the USA. A review of the recent literature in the field is followed by some recommendations on the implementation of reading therapy in health and community care libraries.

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This article uses a thematic approach to describe 50 years of hospital libraries for patients under the National Health Service. The strengths and weaknesses of the patients' library movement in the United Kingdom are discussed, followed by a number of recommendations for future opportunities in this field.

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The Rhodobacter capsulatus sucA, sucB, and lpd genes, which encode the alpha-ketoglutarate dehydrogenase (E1o), the dihydrolipoamide succinyltransferase (E2o), and the dihydrolipoamide dehydrogenase (E3) components of the alpha-ketoglutarate dehydrogenase complex (KGD), respectively, were cloned, sequenced, and used for regulatory analyses. The KGD enzymatic activity was greater in cells grown under aerobic, respiratory growth conditions than under anaerobic, photosynthetic conditions. Similarly, the sucA gene was transcribed differentially, leading to a greater accumulation of sucA mRNAs under respiratory growth conditions than under photosynthetic conditions, although differential rates of mRNA decay could also contribute to the different amounts of sucA mRNAs under these two growth conditions. The sucA promoter was located about 4 kb upstream of the 5' end of the sucA gene, and transcripts greater than 9.5 kb hybridized to a sucA probe, suggesting the presence of an operon that produces a polycistronic mRNA. Thus, these genes seem to be expressed as an unstable primary transcript, and we speculate that posttranscriptional processes control the stoichiometry of KGD proteins.

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To prospectively evaluate the efficacy of ultrasonography in the diagnosis of ruptured silicone gel breast implants, 98 patients (192 implants) underwent preoperative breast ultrasonography prior to silicone gel breast implant removal. The prevalence of implant rupture confirmed at surgery in this group of patients was 62 of the 192 implants (32 percent). Of the 60 implants diagnosed as ruptured by ultrasonography, 46 were confirmed as having visible defects at surgery (true positive) for a positive predictive value of 77 percent. Of the 132 implants diagnosed as intact by ultrasonography, 116 were confirmed as intact at surgery (true negative) for a negative predictive value of 88 percent. Overall, the sensitivity of ultrasonography for implant rupture was 74 percent, and the specificity was 89 percent. These findings demonstrate that ultrasonography is an effective imaging modality for the diagnosis of silicone gel breast implant rupture. Compared with mammography, ultrasonography appears to offer superior sensitivity and specificity without radiation exposure or discomfort. Although magnetic resonance imaging has shown considerable promise in the diagnosis of implant rupture, ultrasonography provides comparable sensitivity at a fraction of MRI's cost.

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OBJECTIVE: The purpose of this study was to describe and illustrate the sonographic appearances of 19 ruptured silicone gel breast implants. MATERIALS AND METHODS: We retrospectively reviewed the sonograms of 16 patients with 19 ruptured silicone gel implants from two institutions. The ruptured implant was confirmed at surgery in 17 cases and by mammographic and clinical findings of a ruptured implant combined with biopsy findings of a silicone granuloma in two cases. Breast sonograms were available for review in all patients. The clinical presentation of each patient was recorded. The sonograms and mammograms were reviewed, and the findings were correlated with the surgical findings. In 16 of the 19 ruptured implants, mammographic findings suggested rupture, including lobulation of the contour of the implant and/or silicone extrusion into the breast parenchyma or axilla. In two ruptured implants, mammographic findings were normal, and in one case, no mammogram was available. In those three patients, palpable masses and clinical findings were suggestive of rupture. RESULTS: Sonography showed a unique echogenic appearance called echo-dense noise, in 17 of the 19 ruptured implants; in 10 of the 17, sonograms showed hypoechoic masses of extruded silicone also. In two ruptured implants, sonograms showed only the hypoechoic masses of extruded silicone gel. CONCLUSION: Our experience suggests that echogenic noise is a unique sonographic sign of ruptured silicone gel breast implants and may be caused by phase aberration related to the speed of sound being slower in silicone than in soft tissue.

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The expression of cytochrome c3 from Desulfovibrio vulgaris (Hildenborough) was examined in Escherichia coli transformed with either of two plasmids, pJ8 and pJ81. The former has an 840 bp insert of D. vulgaris DNA, containing the structural gene for cytochrome c3 (387 bp) and its promoter region. Plasmid pJ81 was generated from pJ8 by deoxyoligonucleotide-directed mutagenesis to direct the synthesis of a protein with an altered signal peptidase cleavage site [Ala(-1)----Asp(-1)]. Synthesis of the 14 kDa precursor, which was partly processed to the 12 kDa mature protein, was observed in cells of E. coli TG2(pJ8) by SDS gel electrophoresis and Western blotting. Analysis of spheroplasts revealed that the processed polypeptide was present in the periplasm while the precursor was found only in the membrane/cytoplasmic fraction. No processing was observed in E. coli TG2(pJ81) cells, due to the mutation of the signal peptide cleavage site. No insertion of haem into the E. coli product could be detected in E. coli TG2(pJ8) cells by post-electrophoretic protohaem fluorescence analysis. The sensitivity of the cytochrome c3 synthesized in E. coli TG2(pJ8) to digestion by chymotrypsin also indicated that the apoprotein was formed. The results indicate that E. coli is capable of synthesizing and exporting the cytochrome c3 polypeptide, but fails to insert the haems.

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We report data indicating that the Rhodobacter capsulatus puf operon promoter and the site for its oxygen regulation are located more than 700 base pairs upstream from the previously identified puf genes and have identified the nucleotide sequences that constitute these control signals. A model is proposed in which a polycistronic transcript at least 3.4 kilobases in length is initiated near the O2-regulated promoter and is processed posttranscriptionally by endonucleolytic cleavage at multiple sites, yielding discrete mRNA segments that are degraded at different rates. A newly identified gene (pufQ), which includes a hydrophobic domain having some similarity to domains of the products of the pufL and pufM genes, begins 313 nucleotides into the puf transcript and is located entirely within the most rapidly degraded segment of the transcript. A previously identified puf transcript segment encoding structural proteins for photosynthetic membrane complexes persists after degradation of the most 5' region of the transcript and is itself subject to segmentally specific degradation. Our results suggest a model in which differential expression of the multiple genes encoded by the puf operon is at least in part attributable to major differences in the rates of decay of the various segments of puf mRNA.

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Sodium tetradecyl sulfate (Sotradecol), which has been employed for sclerotherapy of varicose veins, was evaluated in dogs and humans as an agent for selective arterial embolization. In dogs, intraarterial injection of Sotradecol 3% into the proximally occluded renal, hepatic, splenic, and deep femoral arteries produced arterial occlusion and tissue destruction. Transcatheter embolization with Sotradecol was performed in 11 patients and was successful in 10; in the remaining patient, failure was attributed to rapid dilution by unobstructed blood flow in arteriovenous malformations of the neck. The authors conclude that Sotradecol is a safe and efficient agent for selective arterial embolization.

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The vaginal absorption of a sulphated polysaccharide (SAEP), the active substance of A-gen 53+, was studied in rabbits using the 35S-labelled product. After intra-vaginal administration of 35S-SAEP, measurements of 35S in urine, faeces, plasma and tissues of the reticulo-endothelial system indicated that the small proportion of the dose (ca. 5%) absorbed from the vagina was associated mainly with inorganic material (i.e. 35S-sulphate), present as an impurity in the 35S-dose.

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Peripancreatic venous abnormalities were demonstrated angiographically in 10 patients with islet cell tumor: six nonfunctioning, two gastrin-producing, one glucagon-producing, and one pancreatic polypeptide-producing. Venous involvement recognized included venous occlusion, venous encasement, and intraportal tumor growth. Seven patients had islet cell carcinoma with hepatic metastases while the other three had benign tumors. Three patients had arteriographic evidence of intraportal tumor growth with the "thread and streaks" sign, similar to that of portal venous extension of hepatocellular carcinoma.

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Single oral doses of 20 mg of the carbon-14 labelled form of the antianginal drug isosorbide 5-mononitrate (5-ISMN, Elantan) were essentially completely absorbed and excreted fairly rapidly in the urine. Means of 24, 52, 78, 93 and 96% dose were excreted during 6, 12, 24, 48 and 120 h, respectively. Concentrations of 14C reached peak levels at about 1-2 h when about 86% of the 14C was associated with the parent drug, 5-ISMN (peak mean level 430 ng/ml), and the remainder mainly with the pharmacologically-inactive denitrated product isosorbide. Because the plasma (and urinary) half-life of isosorbide was longer (about 8-9 h) than that of 5-ISMN (about 4.5 h), the proportions of the former in plasma increased relative to the latter. Concentrations of 14C in whole-blood and plasma were similar, implying that 5-ISMN diffused into blood cells. Concentrations of 5-ISMN in saliva and plasma were almost identical, presumably because of the almost negligible plasma protein binding of the drug (less than 5%). At least five metabolites of 5-ISMN were detected in urine - these were isosorbide (about 37% dose), conjugated material (about 25% dose) presumably mainly 5-ISMN-glucuronide, sorbitol (about 7% dose), the parent drug 5-ISMN (about 2% dose) and two unidentified metabolites (about 7 and 4% dose, respectively). The conjugated material was excreted in the urine relatively more rapidly than the denitrated product, isosorbide.

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Hepatic arteriography, venography, and histopathology were reviewed in 20 patients with hepatic venous occlusion. The hepatic histologic materials (14 patients) were carefully examined in retrospect and correlated with the angiographic findings. Hepatic arteriographic findings were usually nonspecific but revealed neoplasms in all six patients studied and collaterals in four. Collateral channels that were recognized angiographically in 15 patients were extrahepatic, intrahepatic-interlobar, and indeterminate. The intrahepatic type was found in the partial Budd-Chiari syndrome, whereas other patterns were present in both diffuse and localized forms of hepatic venous occlusive disease. Histologically, the centrilobular sinusoids were congested and distorted in association with parenchymal destruction and compression. Hepatic venography correlated poorly with histopathologic findings.

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Fifty-five patients (33 male and 22 female), 3 to 73 years in age, underwent aortic arch and selective upper extremity arteriography for the evaluation of forearm and hand ischemia from 1971 to 1980. Fifty-one patients had organic occlusive lesions (12 subclavian, 15 axillobrachial, 17 radial-ulnar, and 7 palmar-digital), including distal forearm and hand emboli, as a consequence of proximal occlusive disease in nine patients (5 subclavian, 2 axillobrachial, and 2 radial-ulnar). The remaining four patients had vasospastic disease. Major arteriographic findings of obstructive disease were defined by: morphology of lesions, symmetry or asymmetry of obstructions, segmental versus tandem lesion distribution, and the resultant pattern of collateral circulation. Vasodilatory pharmacoangiography with magnification technique frequently facilitated evaluation of digital and collateral vessels. Therapeutic interventions were dictated by clinical data heavily weighed by the arteriographic examination. Limited arteriographic studies would have been misleading in the evaluation of many patients.

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The renal arteries in three groups of four dogs were occluded to induce renal infarcts using Gelfoam, Gelfoam and steel coil, and barium suspension. Each agent was evaluated for its effect on renal renin output, arteriographic appearance, and the extent of renal infarct produced. Gelfoam embolization produced incomplete infarcts with hypertrophy of remaining viable tissue. Renal infarcts were more extensive with the combination of Gelfoam and coil than with Gelfoam alone. Barium embolization produced the most diffuse and extensive renal infarct. Renal vein plasma renin levels from the embolized kidney were significantly elevated in the Gelfoam-plus-coil dogs, but arterial pressures were significantly higher in only two of four of these dogs 10 weeks after embolization.

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Three cases of subclavian steal syndrome are presented, with emphasis on the venous phase following aortic arch injection. Dense opacification of the jugular vein on the involved side was seen, rather than a progressive decrease. In addition, patterns of venous flow in the neck were variable. Venous-phase angiography did not correlate with symptoms.

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Three biliary cystadenomas are reported. Two occurred in the left lobe of the liver and the third involved the right lobe and the medial segment of the left lobe. All three patients had gray scale sonography of the liver and two underwent hepatic angiography. The sonographic features were similar to those of cystadenoma of the ovary or pancreas, that is, multilocular cystic lesions with septations and papillary projections. Angiographically the lesions were hypovascular with a faint rim of contrast-material accumulation in the wall and septa of the mass.

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The diagnosis of multiple endocrine neoplasia type II (MEN-II) was made in 18 patients from 1966 through 1978 at the University of Michigan Medical Center. Eight patients had adrenal medullary disease. Seven had bilateral adrenal pheocyromocytomas (two with concomitant medullary hyperplasia) and one had a unilateral pheochromocytoma with contralateral medullary hyperplasia. No malignant or extraadrenal pheochromocytomas were found. Pheochromocytomas in patients with MEN-II are multiple and involve both adrenal glands. Adrenal venography is advocated as the primary diagnostic tool for localization of adrenal medullary disease in MEN-II patients.

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Three patients developed diffuse pulmonary fibrosis caused by exposure to aerosolized cobalt while working in the tungsten carbide tool industry. Two cases were severe and one of these has died of cor pulmonale. The third is mildly disabled. The pathophysiology is reviewed. Clinicians and radiologists should be aware of hard metal exposure as a cause of diffuse interstitial fibrosis.

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