Percutaneous endoscopic trigonoplasty in children: long-term outcomes and modifications in technique

PURPOSE: Long-term outcomes of a minimally invasive method of correcting vesicoureteral reflux are presented with a discussion of the modification in our original technique. PATIENTS AND METHODS: A total of 29 children (46 refluxing ureters), 14 months to 18 years old, underwent percutaneous endoscopic trigonoplasty (PET) between December 1994 and June 1996. Follow-up ranged from 19 to 37 months. Reflux was grade 1 in 2, grade 2 in 16, grade 3 in 19, grade 4 in 8, and grade 5 in 1. The technique was a Gil-Vernet method in the first 23 patients and Cohen reimplantation in the last 6 patients. RESULTS: Resolution of reflux was observed to decrease from 63% to 47% with long-term (30-37 months') follow-up using the Gil-Vernet technique. Resolution was greater with unilateral reflux than bilateral reflux (83% v. 27%, respectively). The Cohen technique resulted in resolution of reflux in 83%; however, the operating time nearly doubled when compared with the Gil-Vernet group. In both groups, failure was unrelated to grade of reflux, age, operative sequence, or bladder instability. CONCLUSIONS: Although showing an improvement in resolution of reflux over the Gil-Vernet PET procedure, the Cohen PET reimplant has a lower success rate than traditional open operative reimplants. The PET also requires more operating time and two operating surgeons. Despite some advantages in the promptness of recovery, we do not recommend PET by either technique at this time. Future modifications may make this approach more tenable.     

Extracranial stereotactic radiosurgery: applications for the spine and beyond

The role stereotactic radiosurgery has in the management of malformations of the spine is examined in this article. Specific problems in the application of stereotactic radiosurgery to the spine are discussed and the three techniques for spinal stereotaxis, bone screw fixation, contour mold fixation, and frameless stereotaxis, are reviewed.     

Immunogenicity of peptides derived from a fibronectin-binding protein of S. aureus expressed on two different plant viruses

The D2 peptide derived from an S. aureus fibronectin-binding protein (FnBP) was expressed on the surface of the icosahedral cowpea mosaic virus (amino acids 1-30 of D2) or on the rod-shaped potato virus X (amino acids 1-38 of D2), termed CPMV-MAST1 and PVX-MAST8, respectively. Mice and rats were immunized subcutaneously with CPMV-MAST1 and mice with PVX-MAST8 in adjuvant and high titres of FnBP-specific antibody were obtained. The mouse IgG was predominantly of the IgG2a and IgG2b isotypes, which strongly bound complement component C1q, suggesting a TH1-bias in the peptide-specific responses. Sera from mice and rats immunized with CPMV-MAST1 and from mice immunized with PVX-MAST8 were shown to completely inhibit the binding of fibronectin to immobilised recombinant FnBP and rat sera against CPMV-MAST1 were able to block adherence of S. aureus to fibronectin. These studies demonstrate that the D2 peptide is highly immunogenic when expressed on 2 different plant viruses and highlight the potential of plant virus-based vaccines to protect against S. aureus infections.     

In vitro antitumor activity of MIC2 protein-doxorubicin conjugates

The pseudoautosomal encoded MIC2 glycoprotein is a tumor-associated antigen of Ewing's sarcoma (ES) and closely related tumors of unknown function. To investigate the use of this protein as selective drug carrier recombinant MIC2 was coupled to doxorubicin by a two step glutaraldehyde method (molar ratio DOX/MIC2 of 32 and 16). The conjugates showed dose-dependent cytostatic activity against the ES cell line SK-ES1, the peripheral neuroectodermal line KAL and the prostate cancer cell line PC-3 concurrent with reduced toxicity against normal lymphoblasts. In comparison to free doxorubicin the MIC2-doxorubicin conjugates exhibited highest activity against the PC-3 cell line. Confocal microscopy showed intracellular accumulation of MIC2 conjugates.     

Chemotherapy for desmoid tumours in association with familial adenomatous polyposis: a report of three cases

Objective

To determine the efficacy of chemotherapy for inoperable desmoid tumours associated with familial adenomatous polyposis.

Design

A review of three cases of unresectable desmoid tumours and of the literature on the subject.

Setting

The Steven Atanas Stavro Polyposis Registry at Mount Sinai Hospital in Toronto.

Patients

Three patients with symptomatic, unresectable desmoid tumours associated with familial adenomatous polyposis and unresponsive to conventional hormone therapy.

Intervention

A chemotherapy regimen of seven cycles of doxorubicin (dose ranging from 60 to 90 mg/m²) and dacarbazine (1000 mg/m²), followed by carboplatin (400 mg/m²) and dacarbazine.

Outcome Measures

Clinical improvement and tumour regression demonstrated by computed tomography.

Results

In each of the three cases significant tumour regression was seen clinically and radiologically.

Conclusions

Cytotoxic chemotherapy is an effective treatment for desmoid tumours associated with familial adenomatous polyposis. The chemotherapy should be started early in cases of symptomatic desmoid tumour unresponsive to conventional medical therapy.     

Inherent Abnormalities of Fat Cells from Massively Obese Individuals

In vitro investigations into adipose cell dynamics have revealed intrinsic characteristics of massively obese individuals' cells that could contribute to a relatively intractable expanded fat mass. Morbidly corpulent peoples' preadipocytes replicate to a greater degree than those from lean individuals. Coupled with exaggerated differentiation this enhanced growth would result in a greater number of fat cells which would increase adipose tissue mass. The relative resistance to de-differentiation that adipocytes from the massively obese demonstrate would contribute to stability of an increased number of adipocytes further exacerbating the problem. The increased message of an energy sensing protein, the obese gene product, suggests that the morbidly obese are insensitive to its action. Together these attributes provide a strong argument for a significant genetic role in the pathogenesis of obesity.