Acceptable levels of digital image compression in chest radiology.

The introduction of picture archival and communications systems (PACS) and teleradiology has prompted an examination of techniques that optimize the storage capacity and speed of digital storage and distribution networks. The general acceptance of the move to replace conventional screen-film capture with computed radiography (CR) is an indication that clinicians within the radiology community are willing to accept images that have been 'compressed'. The question to be answered, therefore, is what level of compression is acceptable. The purpose of the present study is to provide an assessment of the ability of a group of imaging professionals to determine whether an image has been compressed. To undertake this study a single mobile chest image, selected for the presence of some subtle pathology in the form of a number of septal lines in both costphrenic angles, was compressed to levels of 10:1, 20:1 and 30:1. These images were randomly ordered and shown to the observers for interpretation. Analysis of the responses indicates that in general it was not possible to distinguish the original image from its compressed counterparts. Furthermore, a preference appeared to be shown for images that have undergone low levels of compression. This preference can most likely be attributed to the 'de-noising' effect of the compression algorithm at low levels.

Computerised tomography does not predict N2 disease in patients with lung cancer.

BACKGROUND: Mediastinal node involvement in primary lung cancer determines the staging and prognosis of the patient, and as these nodes can be seen on the computerised tomography (CT) scan of the chest it is a temptation to diagnose malignant involvement if the nodes appear enlarged. However, initial experience with mediastinal node mapping at lung resection demonstrated this extrapolation to be unreliable and misinterpretation of enlarged nodes on CT may lead to misdiagnosis and prejudice the patient's management. AIM: To demonstrate that the sensitivity, specificity, and accuracy of the CT to detect malignant mediastinal nodes is too low to use size of node on CT as representative of malignant involvement. METHODS: One hundred and fifty-three sequential patients with resectable lung cancer were studied with preoperative CT. Two radiologists determined the preoperative T and N status from these studies with nodes of 1.5 cm or larger diagnosed abnormal. These results were compared to the results of subsequent node mapping performed after lung resection. RESULTS: Sensitivity was found to be 26%, specificity to be 81% and overall accuracy 69%--too low to justify the diagnosis of N2 disease on size of 1.5 cm or larger. CT is not a valid means of diagnosing malignant involvement of mediastinal nodes.

Synthesis of N-nicotinoyl-tryptamine (tryptamide).

N-Nicotinoyl-tryptamine was synthetized by acylation of tryptamine with mixed nicotinic anhydride. The synthesis of tryptamine via DL-tryptophan decarboxylation in cyclohexanol, in the presence of tetraline oxidation products as the catalyst, was described as well.

Synthesis and gastric antisecretory properties of allenic 16-phenoxy-omega-tetranor prostaglandin E analogs.

In order to improve the modest oral activity of PGE2 as an inhibitor of gastric acid secretion, analogs were prepared and tested orally in histamine-challenged rats. Insertion of a double bond at C-4, resulting in the 4,5-allene analog of PGE1, gave a small increase in activity. Introduction of the omega-tetranor-16-phenoxy lower sidechain, a modification known to enhance activity in the PGF series, gave an eight-fold increase in activity. The analog having both modifications (enprostil, 2) showed a six hundred-fold increase in oral antisecretory activity over PGE2, which may reflect a potentiation effect. Modification of enprostil at C-1 (various esters) and at C-11 (11-methyl, 11-deoxy) generally resulted in compounds of high activity while modifications at other sites generally resulted in significant reductions in activity.

Gastric antisecretory and antiulcer properties of enprostil, (+/-)-11 alpha, 15 alpha-dihydroxy-16-phenoxy-17,18,19,20-tetranor-9-oxoprosta- 4,5,13(t)-trienoic acid methyl ester.

Prostaglandins of the E series have been shown, both in animals and humans to produce gastrointestinal antisecretory and antiulcer effects. Enprostil, a modified allenic prostaglandin E was found to be a highly potent inhibitor of gastric HCl secretion in a variety of species. In rats, in which both the pylorus and esophagus were ligated, p.o. ED50 values and 95% CL for inhibiting acid secretion evoked by histamine, pentagastrin and carbachol were 9.9 (6.7-15), 40 (11-145) and 0.83 (0.78-0.89) micrograms/kg, respectively. In inhibiting histamine-evoked acid secretion, enprostil was more potent when administered p.o. than when injected into the duodenum or s.c. When enprostil was injected directly into the pouch of Heidenhein dogs, intense antisecretory activity occurred, ED50 = 0.9 (0.7-1.1) micrograms/kg, whereas, when given p.o. to the main stomach the ED50 was 6.6 (3.2-13.6) micrograms/kg. Administration of cimetidine either p.o. or to the pouch resulted in virtually identical ED50 values, viz., 2.9 and 3.1 mg/kg. Enprostil also inhibited dimaprit- and pentagastrin-induced acid secretion in cats with permanent gastric fistulae. The oral ED50 values for inhibiting acid secretion evoked by these two secretagogues were 2.5 (1.4-4.3) and 0.8 (0.5-1.5) micrograms/kg, respectively. Enprostil was extremely potent in preventing indomethacin plus "cold stress" ulcers in rats. When given orally the ED50 was 0.61 (0.31-1.22) and s.c. it was 22 (9.0-52) micrograms/kg. It was also highly potent in preventing cysteamine-induced duodenal ulcers when given p.o., ED50 = 20 (17-23) micrograms/kg. Thus, enprostil is a highly potent antisecretory and antiulcer agent. It appears to act topically; directly at gastric mucosal sites.

Pulmonary dirofilariasis diagnosed by computerised tomography scan controlled percutaneous needle aspiration.

The use of computerised tomography has enabled a small lesion to be successfully aspirated with a percutaneous needle. The tissue obtained was characteristic of Dirofilaria immitis; thus a thoracotomy was unnecessary.

Synthesis and central nervous system properties of 2-[(alkoxycarbonyl)amino]-4(5)-phenyl-2-imidazolines.

A series of 2-[( alkoxycarbonyl )amino]-4(5)-phenyl-2-imidazolines was prepared and evaluated for central nervous system (CNS) effects (antidepressant, anticonvulsant, muscle relaxant, and depressant) in animal models. Some separation of those CNS activities was achieved through substitutions on the phenyl and imidazoline moieties. Halo-substituted phenyl compounds were among the most potent antidepressants in this series, while imidazole N-alkylation produced compounds with increased depressant effects (loss of righting reflex, mouse behavior). Comparison of in vitro and in vivo data for pairs of 2-[(methoxycarbonyl)amino]-4(5)-phenyl-2-imidazolines and their parent, 2-amino-4(5)-phenyl-2-imidazolines, suggests that the title compounds were prodrugs for the 2-amino-4(5)-phenyl-2-imidazolines in inhibition of norepinephrine reuptake.

Synthesis and antihypertensive activity of 4'-substituted spiro[4H-3,1-benzoxazine-4,4'-piperidin]-2(1H)-ones.

A series of 4'-substituted spiro[4H-3,1-benzoxazine-4,4'-piperidin]-2(1H)-ones was prepared and evaluated for antihypertensive activity in the spontaneously hypertensive rat (SHR). The basic ring system was prepared in one step by condensation of dilithiated (tert-butoxycarbonyl)aniline (3) with (tert-butoxycarbonyl)piperidinone. Deprotection afforded 6, which was condensed with expoxides or alkyl halides to furnish the title compounds. The most active compound was dl-erythro-4'-[2-(1,4-benzodioxan-2-yl)-2-hydroxyethyl]spiro [4H-3,1-benzoxazine-4,4'-piperidin]-2(1H)-one (9), and various modifications of this compound were made in order to elucidate the structure-activity relationships in the series. Preliminary indications are that 9 may act by both central and peripheral mechanisms.

A model for evaluation of postural hypotension induced by drugs in conscious restrained normotensive rats.

A rat model was developed for use in evaluating postural hypotensive activity of a compound. Conscious normotensive rats were restrained on a tilt board with special restrainers to avoid blocking limb circulation. Dose response curves were explored to delineate the potential postural hypotensive activity of a compound. In response to a 2-min 90 degree head-up tilt, only a negligible changes in blood pressure was observed in the control state. The conscious rat was therefore able instantaneously to compensate for postural change. This ability, however, was blocked by guanethidine. The compound induced a dose-related hypotension and a further, dose-dependent drop in blood pressure on tilt. Hydralazine, on the other hand, induced only dose-dependent hypotension, but no change in blood pressure response from control tilts. Since these findings appear to be in accord with human clinical data, this rat model may be suitable for use in evaluating potential postural hypotensive activity of compounds.

The anti-inflammatory and analgesic profile of 6,11-dihydrodibenzo-[b.e.]-thiepin-11-one-3-acetic acid (tiopinac).

Tiopinac displayed marked anti-inflammatory activity when given p.o. in rat models of acute and chronic inflammation. It inhibited carrageenan-induced paw edema (40 x phenylbutazone), and cotton-pellet-induced granuloma (0.8 x indomethacin). In an 18-day test, tiopinac prevented the development of adjuvant-induced arthritis (10-15 x naproxen) and had similar activity versus pre-induced arthritis. Tiopinac exhibited antiphlogistic activity in adrenalectomized rats. It did not have corticosteroid activity. Depending upon the type of analgesic test used, the potency of tiopinac varied. When given p.o. it inhibited phenylquinone-induced writhing in the mouse and rat (respectively 16 and 10 x aspirin). In contrast, tiopinac had approximately 10 times the potency of indomethacin in increasing the pain threshold when yeast-inflamed paws were compressed. The pain threshold of the noninflamed paw was not increased. Tiopinac was highly active versus pain induced by flexing the adjuvant arthritic-inflamed paw (greater than or equal to 1000 x aspirin). It was inactive in the mouse hot-plate test in which opiate-like agents are active. Tiopinac, p.o., lowered yeast-induced pyrexia (130 x aspirin). Tiopinac did not have significant cardiovascular or CNS activity. Whereas the Ed50 versus adjuvant arthritis in rats was 0.1 mg/kg/day p.o., rats tolerated up to 20 mg/kg/day p.o. in the 8-day cotton-pellet test. Lack of anorexia and emesis in dogs with up to 30 mg/kg p.o. and mild oral activity in producing gastric erosion in acute and subacute studies in rats suggests that tiopinac may have relatively little gastrointestinal irritating activity.

Inhibition of histamine-induced gastric secretion by flavone-6-carboxylic acids.

Twenty-five flavone-6-carboxylic acids were synthesized and tested as to their ability to inhibit histamine-induced gastric acid secretion in the rat. 3-Isopropoxy-4'-methoxyflavone-6-carboxylic acid (41) showed consistent oral activity while being devoid of any other noteworthy pharmacological effects. In vitro, this compound was found to be inactive as a histamine H2 antagonist, and its mode of action remains unknown.

Drug effects on plasma renin activity in the mouse.

To investigate the possible effects of newly synthesized beta-adrenergic blockers on plasma renin activity, an assay was developed using unanesthetized mice and radioimmunoassay. Renin activity was significantly increased by the administration of hydralazine (1 mg/kg, i.p.), furosemide (20 mg/kg, i.v.), and isoproterenol (0.1 mg/kg, s.c.). Unlike isoproterenol, norepinephrine (1 mg/kg, s.c.) and epinephrine (1 mg/kg, s.c.) were active but considerably less effective stimulants. The increase caused by isoproterenol was blocked by clonidine, pindolol, bunolol, atenolol, and l-propranolol, but not d-propranolol. The beta-blockers with intrinsic sympathomimetic activity such as pindolol were found to increase renin activity when given alone, but blocked an increase in renin activity when given prior to isoproterenol. In general, nonselective beta-blocking drugs possessing both beta 1- and beta 2-(vascular) blocking activity were found to be most effective in blocking plasma renin activity on oral administration.