Focal myositis.

Focal myositis is a rare, benign focal inflammation of muscle. The lesion often presents as a mass that may be mistaken for a soft tissue sarcoma. This report describes the MRI and histopathological features of a case and illustrates how the diagnosis may be suspected on the basis of the MR findings.

Effects of a stimulus-stimulus pairing procedure on conditioning vocal sounds as reinforcers.

Two experiments were conducted to investigate the effects of stimulus-stimulus pairing on conditioning vocal sounds as reinforcers. Four preschoolers with severe language and communication delays participated. In Experiment 1, an attempt was made to condition vocal sounds as a reinforcer by pairing a specific vocal sound with a reinforcing event (e.g., physical interaction). Results indicated that presentation of a stimulus-stimulus pairing was effective in conditioning the target vocal sounds as reinforcers, which increased the occurrence of vocalizations of those sounds by the participants. Experiment 2 compared the effects of the pairing procedure with those of echoic training. The pairing procedure was identical to that in Experiment 1. In the echoic training condition, the experimenter produced the target vocal sound and gave the participant an opportunity to echo. The same reinforcing stimulus (e.g., physical interaction) was provided contingent upon the occurrence of the target vocal sound emitted by the participant. Results showed that the pairing procedure was more effective than the echoic training. Findings from this study suggest that for these participants, who had no vocal imitation skills, the stimulus-stimulus pairing was an effective procedure for conditioning vocal sounds as reinforcers and increased the probability of occurrence of the vocalization without a direct reinforcement contingency.

Reduction of plasma clot stability by a novel factor XIIIa inhibitor from the Giant Amazon Leech, Haementeria ghilianii.

The blood-sucking leech, Haementeria ghilianii, has evolved a number of agents that attenuate haemostasis. Recently we have isolated a potent inhibitor of factor XIIIa, tridegin, in the salivary glands which is almost certainly involved in feeding. Addition of purified natural tridegin to plasma, prior to clotting with thrombin, results in clots that deform more readily as adjudged by the greatly reduced development of the storage modulus on application of a shear force. The increase in the storage modulus in developing plasma clots is a slow process and continues for many hours. The effect of tridegin is particularly great when the clots are permitted to age in this way, demonstrating the role of factor XIIIa in the process. The IC50 for this inhibition is 138 ng/ml. Clots formed in the presence of tridegin are also lysed more rapidly in vitro by the leech's own fibrinolytic enzyme, hementin (time for 50% lysis, 16.0 +/- 0.8 h versus 22.3 +/- 2.0 h, P < 0.05). The synergy with which these agents act together may provide lessons for therapy of thrombosis in man.

Direct evidence of monocyte recruitment to inflammatory bowel disease mucosa.

Alterations in phenotype and function of intestinal macrophages occur in inflammatory bowel disease (IBD) but it is unclear whether these changes result from the recruitment of circulating monocytes to the intestine or from proliferation of resident intestinal macrophages. We sought to demonstrate the arrival of blood monocytes, the precursors of macrophages, in IBD mucosa. Peripheral blood mononuclear cells were isolated from 23 patients with clinically active intestinal inflammation (13 Crohn's disease, eight ulcerative colitis, two infective colitis), then radiolabelled with 99mtechnetium (Tc)-stannous colloid (n = 13) or 111indium (In)-oxine (n = 10) before re-injection and abdominal scanning. Four patients had demonstrable intestinal monocyte uptake using [99mTc]-stannous colloid, while six [111In]-oxine-labelled monocyte scans were positive. Uptake sites correlated with actively inflamed regions. Patients demonstrating monocyte uptake had been treated with corticosteroids for a significantly (P < 0.02) shorter duration (median 3 vs 20 days) than those with negative scans. There was no significant difference between positive and negative scans for disease category, clinical or histological disease, activity, or radioisotope used. Biopsies of inflamed mucosa from two patients suffering ulcerative colitis who had positive scans showed a high proportion of CD14-positive macrophages, 4-9% of which contained autoradiographic grains. These results demonstrate that blood monocytes are recruited to the mucosa of actively inflamed bowel, and suggest that this process may be inhibited by corticosteroids. Moreover, the phenotype of the recently-arrived monocytes indicates their susceptibility to stimulation by lipopolysaccharide, and suggests a mechanism for the continuing inflammation in the bacterial product-rich milieu of IBD.

Changes in clot deformability--a possible explanation for the epidemiological association between plasma fibrinogen concentration and myocardial infarction.

This study examined the rheological properties of fibrin gels formed by adding thrombin to plasma samples from 99 subjects with fibrinogen concentrations ranging from 1.45 to 4.14 g/l. A highly significant (r = 0.757; P < 0.001) inverse correlation was observed between plasma fibrinogen concentration and the extent of clot deformability as estimated from the final value of the storage modulus (G') of the fibrin gel when obtained by rheological analysis. A similarly significant correlation (r = 0.844; P < 0.001) was obtained using samples from 47 subjects in which fibrin cross-linking was blocked by addition of 0.1 mM iodoacetamide to inactivate factor XIIIa. The characteristics of the relationship between G' and fibrinogen concentration in the plasma samples was comparable with that observed when the fibrin gel was formed by adding thrombin to purified fibrinogen. These results suggest that the increased risk of myocardial infarction associated with an elevated plasma fibrinogen concentration may, in part, be explained on the basis of a decreased deformability of the fibrin clot formed.

Effect of defined lipopolysaccharide core defects on resistance of Salmonella typhimurium to freezing and thawing and other stresses.

A family of mutants of Salmonella typhimurium with altered lipopolysaccharide (LPS) core chain lengths were assessed for sensitivity to freeze-thaw and other stresses. Deep rough strains with decreased chain length in the LPS core were more susceptible to novobiocin, polymyxin B, bacitracin, and sodium lauryl sulfate during growth, to ethylenediaminetetraacetic acid and sodium lauryl sulfate in resting suspension, and to slow and rapid freeze-thaw in water and saline, and these strains exhibited more outer membrane damage than the wild type or less rough strains. Variations in the LPS chain length did not dramatically affect the sensitivity of the strains to tetracycline, neomycin, or NaCl in growth conditions or the degree of freeze-thaw-induced cytoplasmic membrane damage. The deeper rough isogenic strains incorporated larger quantities of less-stable LPS and less protein into the outer membrane than did the wild type or less rough mutants, indicating that the mutations affected outer membrane synthesis or organization or both. Nikaido's model of the role of LPS and protein in determining the resistance of gram-negative bacteria to low-molecular-weight hydrophobic antibiotics is discussed in relation to the stress of freeze-thaw.

Cardiovascular effects of fentanyl during enflurane anesthesia in man.

The cardiovascular effects of three doses of intravenous fentanyl (50, 100, and 200 microgram) were determined in 42 adult patients undergoing intraabdominal surgical procedures with enflurane (2--3%) and nitrous oxide (50%) in oxygen. Fentanyl was administered a minimum of 40 minutes after induction of anesthesia and 30 minutes after initiation of the surgical procedure. Stroke volume, heart rate, cardiac output, mean arterial and central venous blood pressures, and peripheral arterial resistance were determined by computer analysis of the central aortic pulse-pressure curve according to the method of Warner. Measurements were made before and 2, 4, 6, 8, and 10 minutes after fentanyl. Fentanyl (50 microgram) produced increases in stroke volume and cardiac output as well as a decrease in peripheral arterial resistance but did not alter heart rate or mean arterial blood pressure. Fentanyl (100 microgram) did not significantly change any variable at any time. Fentanyl (1l (200 microgram) produced sustained decreases in stroke volume, cardiac output and mean arterial blood pressure and increased central venous pressure but did not alter heart rate or peripheral arterial resistance. The data indicate that fentanyl (50--100 microgram) stimulates or has no effect on cardiovascular dynamics during enflurane-nitrous oxide anesthesia but fentanyl (200 microgram) produces significant cardiovascular depression. Our findings suggest that small doses of intravenous fentanyl may be of benefit during enflurane-nitrous oxide but larger doses should probably be avoided.