Risk factors for secondary dilatation of the aorta after acute type A aortic dissection.

OBJECTIVES: Prompt diagnosis of subsequent dilatation of the dissected aorta is crucial to reduce late mortality in these patients. This study focuses on risk factors for dilatation of the aorta after type A aortic dissection (AADA) affecting a normal-sized or slightly dilated aorta. METHODS: Overall 531 CT scans were analysed. Patients were included in the study if at least 3 CT scans were available after operative repair. 64 patients (59.8%) out of 107 patients full-field the inclusion criteria. Volumetric analyses of the aorta were performed. Patients were divided in 3 groups: group A included 26 patients (40.6%) without progression of the aortic diameter, group 2, 27 patients (42.2%) with slight progression and group 3, 11 patients (17.2%) with important progression, requiring surgery in 9 patients (81.8%). Risk-factors for progression of the aortic size were analysed and compared between the groups. RESULTS: Patients from group 3 were younger 57.7+/-13.4 vs. 61.9+/-11.6 in group 1 (P<0.05) and were more frequent female (45.4 vs. 23.1%; P<0.05). Dissection of the supraaortic branches (100 vs. 80.8%; P<0.05), the presence of preoperative cerebral, visceral or peripheral malperfusion (54.6 vs. 26.9%; P<0.05) and contrast enhancement in the false lumen during the follow-up (72.7 vs. 57.7%; P=0.07) were additional risk factors for late aortic dilatation in these patients. CONCLUSIONS: Acute type A aortic dissection in younger patients, involving the supraaortic branches and/or combined with malperfusion syndrome favour secondary dilatation. A close follow-up is mandatory to prevent acute complications of the diseased downstream aorta following repair of a AADA.     

Bovine mesenteric vein graft (ProCol) in critical limb ischaemia with tissue loss and infection.

OBJECTIVES: Poor results have been reported following infrainguinal reconstructions using heterogenous grafts. The objective of this study was to assess the use of bovine mesenteric vein (ProCol) graft in patients with critical limb ischaemia (CLI), tissue loss/infection and no autologous vein available for reconstruction. METHODS: Prospective analysis of 32 patients with CLI and tissue loss/infection, in whom reconstruction with ProCol was undertaken between October 1999 and May 2002. RESULTS: The primary patency rate was 16% at 1 month. After thrombectomy, the secondary patency rate was 50% at 1 month and 26% at 14 months. No graft infections were seen. Aneurysmal dilatation of the graft occurred in 2 (6%). Limb salvage at 14 months was 47%. CONCLUSION: In patients with critical limb ischaemia, tissue loss/infection and no available vein, the ProCol graft may be an alternative. However, primary patency is a problem. In situations without tissue loss/infection, where the risk of graft infection is less, prosthetic material may be a better alternative.     

Extension of the “Elephant Trunk” Technique in Complex Aortic Pathology: The “Bidirectional” Option

Background. The “elephant trunk” technique, using a free-floating vascular prosthesis, was originally described to facilitate a subsequent operation on the downstream aorta. We developed an additional refinement of this technique, called the “bidirectional elephant trunk.” This option may represent an interesting tool in more complex aortic operations, especially when the descending aorta has to be replaced first in patients with concomitant pathology of the ascending aorta or of the aortic arch.

Methods. The initial operation is performed through a left thoracotomy. The proximal elephant trunk is created by invaginating the future aortic arch graft into the descending aortic graft. The proximal anastomosis between the doubled graft and the proximal descending aorta is performed first. During construction of the distal anastomosis, a distal elephant trunk may be inserted likewise. If the aortic arch and ascending aorta have to be replaced later, this second step is performed through a median sternotomy. The free-floating arch graft is pulled out of the proximal descending aorta with a nerve hook, unfolded, and used for total arch replacement.

Results. This technique was used successfully in 3 patients without mortality. No major complications were observed excepted persistent hoarseness in a patient with preoperative paresis of the recurrent nerve. No perfusion problems due to the unfolding of the free-floating graft occurred during the second operation.

Conclusions. The bidirectional elephant trunk technique is an interesting option that may be suitable for patients presenting with a complex pathology of the whole thoracic aorta when the descending segment has to be replaced first.     

Pericarditis constrictiva after aortic valve replacement simulating tricuspid stenosis.

Pericarditis constrictiva after cardiac surgery is rare and may occasionally lead to congestive heart failure. The case of a 29-year-old patient is described who presented with pericarditis constrictiva after aortic valve replacement with localized tamponade, causing functional tricuspid stenosis. Pericardiectomy as the treatment of choice was curative.     

Monoclonal antibodies against carcinoembryonic antigen (CEA) used in a solid-phase enzyme immunoassay. First clinical results

A solid-phase enzyme immunoassay using both mouse monoclonal and goat polyclonal antibodies against carcinoembryonic antigen (CEA) was developed. The assay detects 0.6 to 1.2 ng of CEA per ml of serum and has 3 incubation steps which can be performed in 1 day. Polystyrene balls coated with polyclonal goat anti-CEA antibodies are first incubated with heat-extracted serum samples. Bound CEA is then detected by addition of mouse monoclonal antibodies, followed by goat IgG anti-mouse IgG1 coupled to alkaline phosphatase. Results with this enzyme immunoassay using monoclonal antibodiies (M-EIA) have been compared with those obtained by the conventional inhibition radioimmunoassay (RIA) using goat antiserum. Three hundred and eighty serum samples from 167 patients with malignant or non-malignant diseases and from 134 normal individuals with or without heavy smoking habits were analyzed by the 2 assays. Excellent correlation between the results of the 2 assays was obtained, but the M-EIA, using monoclonal antibodies from a single hybridoma, did not discriminate better than the conventional RIA between CEA produced by different types of carcinoma and between CEA associated with malignant or non-malignant diseases. Follow-up studies of several patients by sequential CEA determinations with the 2 assays showed that the M-EIA was as accurate as the RIA for the detection of tumor recurrences.     

Stimulation and proliferation of CD4+ peripheral blood T lymphocytes induced by an anti-CD4 monoclonal antibody

There is experimental evidence that the CD4 molecule participates in the antigen-driven activation of T cells expressing this surface glycoprotein. Whether CD4, a member of the immunoglobulin supergene family, acts as a ligand-binding molecule and/or is directly involved in the activation pathway has yet to be established. In this study, we show that human CD4⁺ lymphocytes can be activated by exposure to the anti-CD4 monoclonal antibody (mAb) B66. Normal peripheral blood CD4⁺ cells were induced to proliferate and to synthesize interleukin 2 (IL2) by the antibody. The specificity of the antibody stimulatory activity was tested by using IL2-producing clones bearing either CD4 or CD8 on their surface. IL2 production was induced by mAb B66 in CD4+, but not CD8⁺, clones, whereas both types of clones responded to stimulation by the anti-CD3 mAb Leu-4. Despite its unique stimulatory activity, mAb B66 shared with other anti-CD4 antibodies the ability to inhibit the specific cytolytic activity of CD4⁺ effector cells. These results clearly indicate that cross-linking of surface CD4 molecules with appropriate antibodies can fully activate CD4⁺ lymphocytes. Whether the natural ligand for CD4 can trigger this activation pathway remains to be defined.     

The UTX gene escapes X inactivation in mice and humans

We recently have identified a ubiquitously transcribed mouse Y chromosome gene, Uty , which encodes a tetratricopeptide repeat (TPR) protein. A peptide derived from the UTY protein confers H-Y antigenicity on male cells. Here we report the characterization of a widely transcribed X-linked homologue of Uty , called Utx , which maps to the proximal region of the mouse X chromosome and which detects a human X-linked homologue at Xp11.2. Given that Uty is ubiquitously transcribed, we assayed for Utx expression from the inactive X chromosome (Xi) in mice and found that Utx escapes X chromosome inactivation. Only Smcx and the pseudoautosomal Sts gene on the mouse X chromosome have been reported previously to escape inactivation. The human UTX gene was also found to be expressed from Xi. We discuss the significance of these data for our understanding of dosage compensation of X-Y homologous genes in humans and mice.      

Tissue and lineage-specific variation in inactive X chromosome expression of the murine Smcx gene

To understand how gene expression patterns are established on the inactive X chromosome during development, we have studied the murine gene Smcx, which is expressed from both the active and inactive mouse X chromosomes. In all tissues assayed, Smcx only partially escapes X inactivation, with expression levels from the inactive X allele approximately 30-65% that of the active X allele. Additionally, inactive X expression levels differed between extraembryonic and embryonic tissues and among different tissues from newborn and adult mice. Imprinted extraembryonic tissue had the lowest levels of inactive X Smcx expression, whereas the highest levels were in heart. These data suggest that the chromosomal basis of X inactivation differs among tissues, perhaps reflecting differences in the timing or regulation of inactivation in these cell lineages.      

Expression of HLA-DR and common acute lymphoblastic leukemia antigens on glioma cells

The expression on several established human glioma cell lines of two well-defined differentiation antigens, HLA-DR and the common acute lymphoblastic leukemia antigen (CALLA) has been demonstrated. Rabbit anti-CALLA antiserum and monoclonal anti-la antibodies specifically lysed glioma cells in the presence of complement. Absorption of anti-CALLA antiserum and anti-Ia antibodies by glioma cells abolished their cytotoxicity against blasts isolated from a common acute lymphoblastic leukemia. Immunoprecipitation of solubilized glioma cells by monoclonal anti-Ia antibodies revealed two polypeptide chains of 28 and 33 kDa, whereas the anti-CALLA antiserum precipitated a single polypeptide chain of 100 kDa.     

The mouse Mid1 gene: implications for the pathogenesis of Opitz syndrome and the evolution of the mammalian pseudoautosomal region

We have recently reported isolation of the gene responsible for X- linked Opitz G/BBB syndrome, a defect of midline development. MID1 is located on the distal short arm of the human X chromosome (Xp22. 3) and encodes a novel member of the B box family of zinc finger proteins. We have now cloned the murine homolog of MID1 and performed preliminary expression studies during development. Mid1 expression in undifferentiated cells in the central nervous, gastrointestinal and urogenital systems suggests that abnormal cell proliferation may underlie the defect in midline development characteristic of Opitz syndrome. We have also found that Mid1 is located within the mouse pseudoautosomal region (PAR) in Mus musculus , while it seems to be X- specific in Mus spretus. Therefore, Mid1 is likely to be a recent acquisition of the M. musculus PAR. Genetic and FISH analyses also demonstrated a high frequency of unequal crossovers in the murine PAR, creating spontaneous deletion/duplication events involving Mid1. These data provide evidence for the first time that genetic instability of the PAR may affect functionally important genes. In addition, we show that MID1 is the first example of a gene subject to X-inactivation in man while escaping it in mouse. These data contribute to a better understanding of the molecular content and evolution of the rodent PAR.