ERCP and CT findings of ectopic drainage of the common bile duct into the duodenal bulb

OBJECTIVE: The purpose of this study was to evaluate ERCP and CT findings of ectopic drainage of the common bile duct into the duodenal bulb. CONCLUSION: Although rare, the diagnosis of ectopic drainage of the common bile duct into the duodenal bulb is important to prevent inadvertent damage during biliary tract or gastric surgery and to clarify the cause of chronic peptic ulcers.     

Quenched BODIPY dye-labeled casein substrates for the assay of protease activity by direct fluorescence measurement

We have prepared casein conjugates of two BODIPY dyes for use as fluorogenic protease substrates in homogeneous assays. Both conjugates are labeled to such an extent that the dyes are efficiently quenched in the protein, yielding virtually nonfluorescent substrate molecules. These fluorogenic substrates release highly fluorescent BODIPY dye-labeled peptides upon protease digestion, with fluorescence increases proportional to enzyme activity. These quenched substrates are suitable for the continuous assay of enzymatic activity using standard fluorometers, filter fluorometers, or fluorescence microplate readers using either fluorescein excitation and emission wavelengths to measure BODIPY FL casein hydrolysis or Texas Red wavelengths to detect proteolysis of BODIPY TR-X casein. Most current techniques for detecting protease activity, such as the fluorescein thiocarbamoyl casein (FTC-casein) protease assay, require extensive manipulation, including separation steps, and are therefore labor intensive and error-prone. In comparison, we found the BODIPY dye-labeled casein protease assays to be simple and precise and to have greater sensitivity and a broader dynamic range of detection than the FTC-casein assay. We were able to sensitively detect the activities of a wide variety of enzymes with these new substrates, including serine, acid, sulfhydryl, and metalloproteases. We also found the assay suitable for quantitating protease inhibitor concentrations and for real-time analysis of proteolysis.     

Substrate transport and cocaine binding of human dopamine transporter is reduced by substitution of carboxyl tail with that of bovine dopamine transporter

A chimeric dopamine transporter (DAT) cDNA encoding mutant human DAT (hDAT) protein in which the intracellular carboxyl-terminal tail is replaced by that of the bovine dopamine transporter (bDAT) was constructed. The chimeric hDAT cDNA was expressed in COS-7 cells, and [3H]dopamine and [3H]MPP+ uptake and [3H]CFT binding capacities were assessed. Substrate transport and ligand binding of bDAT were reduced by 32-43% as a result of substitution of the carboxyl tail in hDAT, suggesting that the functional characteristics of bDAT arise from differences in the carboxyl tail between human and bovine DAT. Thus, it appears that the sequences encoded within the carboxyl terminal of DAT would be one of the important determinants for its functions.     

Unified full wave solutions to interpret Apollo lunar surface data

Bistatic radar experiments carried out by Tyler and Howard during the Apollo 14, 15, and 16 missions provide a very useful dataset with which to compare theoretical models and experimental data. Vesecky et al. (1988) report that their model for near grazing angles compares favorably to experimental data. However, for angles of incidence around 80°, all the analytical models considered by Vesecky et al. predict values for the quasi-specular cross sections that are about half the corresponding values taken from the Apollo 16 data. In this work, questions raised by this discrepancy between the reported analytical and experimental results are addressed. The unified full wave solutions are shown to be in good agreement with the bistatic radar data taken during Apollo 14 and 16 missions. Using the full wave approach, the quasi-specular contributions to the scattered field from the large scale surface roughness as well as the diffuse Bragg-like scattering from the small scale surface roughness are accounted for in a unified self-consistent manner. Since the full wave computer codes for the scattering cross sections contain ground truth data only, it is shown how it can be readily used to predict the rough surface parameters, based on the measured data     

Spinal cholinergic and monoamine receptors mediate the antinociceptive effect of morphine microinjected in the periaqueductal gray on the rat tail, but not the feet

The antinociceptive effects of morphine (5 micrograms) microinjected into the ventrolateral periaqueductal gray were determined using both the tail flick and the foot withdrawal responses to noxious radiant heating in lightly anesthetized rats. Intrathecal injection of appropriate antagonists was used to determine whether the antinociceptive effects of morphine were mediated by alpha 2-noradrenergic, serotonergic, opioid, or cholinergic muscarinic receptors. The increase in the foot withdrawal response latency produced by microinjection of morphine in the ventrolateral periaqueductal gray was reversed by intrathecal injection of the cholinergic muscarinic receptor antagonist atropine, but was not affected by the alpha 2-adrenoceptor antagonist yohimbine, the serotonergic receptor antagonist methysergide, or the opioid receptor antagonist naloxone. In contrast, the increase in the tail flick response latency produced by morphine was reduced by either yohimbine, methysergide or atropine. These results indicate that microinjection of morphine in the ventrolateral periaqueductal gray inhibits nociceptive responses to noxious heating of the tail by activating descending neuronal systems that are different from those that inhibits the nociceptive responses to noxious heating of the feet. More specifically, serotonergic, muscarinic cholinergic and alpha 2-noradrenergic receptors appear to mediate the antinociception produced by morphine using the tail flick test. In contrast, muscarinic cholinergic, but not monoamine receptors appear to mediate the antinociceptive effects of morphine using the foot withdrawal response.     

Structural characterization of a new galactofuranose-containing glycolipid antigen of Paracoccidioides brasiliensis

An acidic glycolipid (Band 1), purified from P. brasiliensis by a combination of ion exchange chromatography, HPLC, and HPTLC, was found to be reactive with sera of all patients with paracoccidioidomycosis (PCM). Monosaccharide analysis of Band 1 yielded mannose and galactose in a 2:1 ratio, while mild acid hydrolysis and mild periodate oxidation/NaB3H4 reduction indicated the presence of a terminal galactofuranose. Preliminary analysis of 1H-NMR and MS data suggests that the structure of the glycan is Galf beta 1-->6(Manp alpha 1-->3)Manp beta 1-->2Ins (Ins = myo-inositol). Removal of the galacto-furanose decreased by 60-80% the reactivity of sera from PCM patients with Band 1, suggesting that this residue is immunodominant. With the presumed absence of galactofuranose in mammalian hosts, compounds containing this residue may be useful targets for therapy of several parasitic and fungal diseases.     

Influence of the major histocompatibility complex on age at onset of chronic lymphoid leukaemia

Goodpasture syndrome is an often fatal autoimmune disease associated with glomerulonephritis and/or pulmonary hemorrhage. The clinical manifestations of this disease correlate well with the presence of circulating antiglomerular basement membrane (GBM) autoantibodies. The primary target antigen in glomerular and alveolar basement membranes is thought to be the alpha 3 chain of type IV collagen. Nearly all that is known about anti-GBM antibodies in humans comes from work on unbound circulating antibody. We recently had the unique and rare opportunity to obtain early postmortem antibody and tissues from a patient who died with catastrophic Goodpasture syndrome. The specificity of circulating, kidney-bound and lung-bound autoantibodies from this patient was evaluated against a variety of purified basement membrane constituents. The results indicate that the primary target for the circulating and tissue-bound autoantibodies is the NC1 domain of the alpha 3(IV) chain of type IV collagen. Additionally, all the antibodies recognize a cryptic epitope/s on the alpha 3(IV)NC1 hexamer. Furthermore, tissue-bound and circulating antibodies compete with one another for overlapping epitopes on the antigen. These findings demonstrate that circulating autoantibodies in Goodpasture syndrome are highly representative of those bound to organ tissues, strengthening the notion that pathogenic autoantibodies are targeted to the alpha 3(IV)NC1 collagen, and that previous reports of findings in the circulation may be applicable to tissue injury.