Disappearing left atrial vegetation in an intravenous drug abuser

Isolated left atrial mural endocarditis is rare. We report a case where the diagnosis was made clinically and supported by blood cultures and transoesophageal echocardiography. Appropriate intravenous antibiotics were administered and serial transoesophageal echocardiograms helped in monitoring the decrease in size and final disappearance of the vegetation, thus avoiding the need for surgical intervention.     

Aldosterone and dexamethasone stimulate calcineurin activity through a transcription-independent mechanism involving steroid receptor-associated heat shock proteins

1. PD 81,723 has been shown to enhance binding of adenosine to A1 receptors by stabilizing G protein-receptor coupling ('allosteric enhancement'). Evidence has been provided that in the perfused hearts and isolated atria PD 81,723 causes a sensitization to adenosine via this mechanism. 2. We have studied the effect of PD 81,723 in guinea-pig isolated atrial myocytes by use of whole-cell measurement of the muscarinic K+ current (I[K(ACh)]) activated by different Gi-coupled receptors (A1, M2, sphingolipid). PD 81,273 caused inhibition of I[K(ACh)] (IC50 approximately 5 microM) activated by either of the three receptors. Receptor-independent I[K(ACh)] in cells loaded with GTP-gamma-S and background I[K(ACh)], which contributes to the resting conductance of atrial myocytes, were equally sensitive to PD 81,723. At no combination of concentrations of adenosine and PD 81,723 could an enhancing effect be detected. 3. The compound was active from the outside only. Loading of the cells with PD 81,723 (50 microM) via the patch pipette did not affect either I[K(ACh)] or its sensitivity to adenosine. We suggest that PD 81,723 acts as an inhibitor of inward rectifying K+ channels; this is supported by the finding that ventricular I(K1), which shares a large degree of homology with the proteins (GIRK1/GIRK4) forming I[K(ACh)] but is not G protein-gated, was also blocked by this compound. 4. It is concluded that the functional effects of PD 81,723 described in the literature are not mediated by the A1 adenosine receptor-Gi-I[K(ACh)] pathway.     

The influence of nicotine pretreatment on mesoaccumbens dopamine overflow and locomotor responses to D-amphetamine

In this retrospective cephalometric study of mandibular rotational change, we studied 60 cases. All patients were treated with full fixed appliances and exhibited an opening rotation of at least 1.5 degrees during treatment, as measured on the basis of the angle of the Y-axis to the sella-nasion line (SN). Our objective was to determine whether this opening rotation was sustained during retention. Paired t tests were used to test the hypothesis that the treatment change or opening rotation was stable and that these patients did not return to their original mandible-to-cranium relationship in the posttreatment period. Stepwise regression analysis was used to determine which (if any) changes in the independent variables during treatment could predict the subsequent behavior of the angle of the mandibular plane to the SN and the angle of the Y-axis to the SN during retention. During treatment, the mean increase in the angle of the Y-axis to the SN was 2.43 degrees. After an average posttreatment period of 54 months, this angle was reduced on average by only 0.73 degrees. Stepwise linear-regression analysis indicated that none of the treatment changes seen in the independent variables strongly predicted the ensuing closing rotation seen during retention. The correlation coefficient between the Y-axis angle and the mandibular-plane angle during treatment was 0.67. Mandibular opening rotations as a consequence of orthodontic treatment do not invariably return to the pretreatment value, and their negative effects--although sometimes small--cannot be discounted. Because the preponderant evidence of a closing rotation occurs in the terminal pubertal growth stages, the net effect may be even more significant.     

Single photon emission computed tomographic blood flow and magnetic resonance volume imaging of basal ganglia in Huntington''s disease

During oogenesis in Drosophila, germ cells appear in sequential clusters of 16 interconnected cells. The events surrounding the differentiation of these cells are not fully understood. Here we present genetic and morphological analysis of mutations in the gene stand still (stil). Through complementation analyses we have refined the location of this gene to cyological region 49B-C. Our analyses of ovaries from ethylmethane sulfonate (EMS)-induced mutant alleles of this gene suggest that mutations in the stil gene produce a wide range of phenotypic abnormalities, from the absence of germ cells in the most severe alleles, to egg chambers with cytoskeletal defects in the less severe alleles. Our results suggest a role for this gene in specifying or maintaining a cytoskeletal component, with consequences during oogenesis and possibly during germ line sex determination.     

Pain drawings in the assessment of nerve root compression: a comparative study with lumbar spine magnetic resonance imaging

STUDY DESIGN: Prospective comparative study of pain drawings with findings on lumbar spine magnetic resonance imaging. OBJECTIVES: To assess the ability of the pain drawing to predict the presence of nerve root compression. SUMMARY OF BACKGROUND DATA: Most research work has concentrated on the ability of the pain drawing to act as a screening method for psychological distress with less work directed at the influence the anatomic abnormality has on the pain drawing. METHODS: One hundred thirty-four consecutive outpatients attending for lumbar magnetic resonance imaging in the investigation of back and leg pain completed pain drawings and psychological testing immediately before the examination. The pain drawing was analyzed by previously reported criteria, and the magnetic resonance imaging was assessed independently for the presence of nerve compression by three radiologists. Multivariate stepwise discriminant analysis was used to identify patients with nerve compression on the basis of their pain drawing. RESULTS: Nerve compression was predicted by numbness in the anterolateral aspect of the foot. There was considerable overlap in the appearances of the pain drawings between patients with and without nerve compression, and the pain drawing correctly classified only 58% of patients with nerve compression. CONCLUSIONS: The pain drawing is not a good predictor of nerve compression on magnetic resonance imaging in a group of patients investigated for back and leg pain. It should be interpreted with caution and in light of the full clinical picture.     

Metastatic pulmonary artery sarcoma. Report of a case with diagnosis by fine needle aspiration

Spontaneously hypertensive rats (SHR) of 3 to 12 months of age learned and retrieved less information than normotensive Wistar-Kyoto rats (WKY), although no difference was found with animals from 18 and 24 months of age. The combined influence of hypertension and aging had an additive detrimental effect on cognitive functions. Notwithstanding these deficiencies in learning and memory, SHR have seldom been used as a model in the screening of drugs with therapeutic potential for treatment of disorders of cognitive processes. Moreover, the calcium channel blocker nimodipine has beneficial effects on learning in both aged and hypertensive animals and humans. However, no attempt has been made to investigate whether nimodipine can reverse the additive deleterious effects of aging and hypertension in the same subject. We recently reported that deteriorated animals (middle-aged and/or hypertensive) chronically treated with nimodipine (via osmotic minipumps) exhibit higher learning scores. This information indicates that nimodipine can reverse the impairing effects of either aging or hypertension on learning; the presence of the two conditions, however, produces a severe impairment that can be partially reversed by this drug. Therefore, we propose that mature and middle-aged SHR represent a model for the screening of potentially useful drugs in the treatment of learning disorders, probably associated with hypertension and/or aging. Nevertheless, it must be remembered that the SHR is a genetic model and the appearance of neural disturbances could be a parallel genetic phenomenon and not necessarily or exclusively related to hypertension per se.     

Mechanisms involved in the intrinsic isoniazid resistance of Mycobacterium avium

Isoniazid (INH), which acts by inhibiting mycolic acid biosynthesis, is very potent against the tuberculous mycobacteria. It is about 100-fold less effective against Mycobacterium avium. This difference has often been attributed to a decreased permeability of the cell wall. We measured the rate of conversion of radiolabelled INH to 4-pyridylmethanol by whole cells and cell-free extracts and estimated the permeability barrier imposed by the cell wall to INH influx in Mycobacterium tuberculosis and M. avium. There was no significant difference in the relative permeability to INH between these two species. However, the total conversion rate in M. tuberculosis was found to be four times greater. Examination of in vitro-generated mutants revealed that the major resistance mechanism for both species is loss of the catalase-peroxidase KatG. Analysis of lipid and protein biosynthetic profiles demonstrated that the molecular target of activated INH was identical for both species. M. avium, however, formed colonies at INH concentrations inhibitory for mycolic acid biosynthesis. These mycolate-deficient M. avium exhibited altered colony morphologies, modified cell wall ultrastructure and were 10-fold more sensitive to treatment with hydrophobic antibiotics, such as rifampin. These findings may significantly impact the design of new therapeutic regimens for the treatment of infections with atypical mycobacteria.