Duodenal hematoma: the ring sign in MR imaging

Proper management of duodenal hematoma requires that an accurate diagnosis be made using noninvasive radiological methods. Conventional imaging may be nonspecific if there is no history of trauma or coagulopathy. Two cases of duodenal hematoma that were imaged by magnetic resonance (MR) and computed tomography (CT) are described. In both cases the hematoma had a well-defined concentric ring configuration on MR images, a finding which helped establish the diagnosis. MR imaging may provide tissue-specific characterization of duodenal hematomas.     

Overexpression Of GPR7 In Schwann Cells From Patients With Peripheral Neuropathies

The identification of regulated gene products that play a role in Schwann cell-axon contact after nerve injuries may have important implications for pain mechanisms and nerve repair processes. Schwann cell-intrinsic defects have been recently shown to cause neuropathies associated with pain (Gillespie et al., 2000). The 7TM GPR7, originally described by O'Dowd et al. (1995) as a likely G-protein coupled receptor, is a human orphan receptor expressed in the nervous system with sequence similarity to both somatostatin and opioid receptors. Using real time quantitative PCR^TM we evaluated the expression of GPR7 in sural nerve biopsies from patients with different kinds of peripheral neuropathies. We observed that GPR7 expression was significantly (p < 0.001) increased in sural nerves when an epineurial and endoneurial perivascular inflammatory infiltration was present. The overexpression was particularly noted in patients with painful peripheral neuropathies with an inflammatory, immuno and vasculitic etiology. In order to confirm changes in GPR7 expression at the protein level, we performed immunofluorescence staining on sections of neuropathic human sural nerves. A comparative analysis of rat injured sciatic nerves was also performed. We observed that GPR7 receptor is expressed by Schwann cells and that the amount of Schwann cell-staining in both human and rat nerve is increased in conditions of inflammatory neuropathy. In addition, we observed that the expression of GPR7 was significantly decreased in severe axonal neuropathies, suggesting that GPR7 expression is axon dependent. Immunofluorescence staining in rat cultured Schwann cells suggested that the expression GPR7 increased during Schwann-axon interaction. Taken together these results suggest that molecules such as GPR7 whose expression in Schwann cells varies under pathological conditions may play a role in the pathogenesis of human neuropathies. Altered GPR7 expression may disrupt myelination leading to progression of the neuropathy. Alternatively, GPR7 may play a role in Schwann cell-axon signaling and thereby influence axonal function in neuropathies leading to a painful phenotype.     

Cloning of glycoprotein IIIa cDNA from human erythroleukemia cells and localization of the gene to chromosome 17

Platelet aggregation requires the binding of adhesive proteins such as fibrinogen to the heterodimer of membrane glycoproteins IIb (GPIIb) and IIIa (GPIIIa). Human erythroleukemia (HEL) cells synthesize both GPIIb and GPIIIa. Using poly(A+) RNA purified from HEL cells, we constructed a cDNA library in the lambda gt10 phage vector. This library was screened with a 38mer oligonucleotide derived from a platelet GPIIIa peptide, and three overlapping cDNAs were isolated. The three inserts encompassed 3.5 kilobases (kb), including the entire coding region of mature GPIIIa (2,286 basepairs, bp) and 1.3 kb of 3' untranslated sequence. All 222 residues determined directly from platelet GPIIIa tryptic peptides exactly matched the HEL cell-deduced amino acid sequence. The HEL cell sequence matched a previously reported endothelial cell cDNA sequence except for eight nucleotides. Five of these nucleotide differences were silent changes consistent with genetic polymorphisms. The other three differences resulted in changes in the deduced amino acid sequence of GPIIIa; reexamination of the endothelial cell cDNA sequence in these three areas revealed that it is actually identical to the HEL cell sequence. The virtual identity of the endothelial and HEL cell cDNA sequences provides direct evidence that GPIIIa is a subunit common to cell-adhesion receptors present in more than one cell type. We localized the gene for GPIIIa to chromosome 17, the same chromosome to which we had previously mapped the gene for GPIIb.     

Deficiency of platelet membrane glycoprotein Ia associated with a decreased platelet adhesion to subendothelium: a defect in platelet spreading

A bleeding disorder with absent collagen-induced platelet aggregation and adhesion has been described in a patient whose platelets failed to express surface glycoprotein Ia. We studied the interaction of her platelets with subendothelium in an annular perfusion chamber and the interaction with purified human collagen type III in a rectangular perfusion system under flow conditions. Platelet adherence was almost completely absent both at low and high shear rates. The few platelets which adhered remained in the contact stage without subsequent spreading and aggregate formation. Addition of a monoclonal antibody, which was directed against the von Willebrand moiety of FVIII-VWF, to the blood, completely abolished platelet adherence at high shear rates and had a partial effect at low shear rates. These data indicate that von Willebrand factor plays a role in the initial attachment (contact stage) of platelets to subendothelium. We conclude that the bleeding disorder and excessively prolonged bleeding time in our patient are caused by a new specific defect of the platelet-vessel wall interaction.     

The detection and use of hemoglobin mutants in the direct analysis of human globin genes

Many human globin-chain mutants contain amino acid replacements that result from single base changes in the corresponding globin gene. Using recombinants, the coding sequences of each of the alpha-, beta-, Ggamma- , and Agamma-globin genes have now been determined. Those sequences of DNA that are cleaved by a number of specific restriction endonucleases have been identified and accurately positioned. Mutations at these sequences abolish the restriction site, and therefore, the pattern of DNA fragments containing hybridizing globin-gene sequences is altered compared to DNA from normal persons. This allows the identification of one of a pair of cross-hybridizing human globin-gene sequences, as is shown here for the two alpha-globin, the two gamma-globin, and the delta- and beta-globin genes.     

RESTORATION OF NITRIC OXIDE FUNCTION IN HUMAN HYPERLIPIDAEMIA, CONGESTIVE HEART FAILURE AND LIVER CIRRHOSIS

1. There is accumulating evidence for a range of abnormalities in the nitric oxide (NO) signalling cascade in human cardiovascular disorders. 2. In the present review we assess the literature detailing such evidence in early (hyperlipidaemia) and end-stage (heart failure) disease, with emphasis on the mechanisms by which the disturbances are thought to occur. 3. Strategies for the correction of disturbed NO signalling in these states are reviewed and include both prescribed pharmacological interventions, such as lipid-lowering therapy and novel uses of angiotensin-converting enzyme inhibitors, as well as non-pharmacological interventions, such as exercise and dietary supplementation with l -arginine and n-3 polyunsaturated fatty acids. 4. In addition to a decreased production/function of NO, the possible detrimental effects of a chronic elevation in NO production in patients with liver cirrhosis, together with a novel use of antibiotics to correct this perturbation, is outlined.