Conversions and complications in 185 laparoscopic adjustable silicone gastric banding cases

Background: Kuzmak's gastric silicone banding technique is the least invasive operation for morbid obesity. The purpose of this study was to analyze the complications of this approach. Methods: Between September 1992 and March 1996, 185 patients underwent laparoscopic gastroplasty by the adjustable silicone band technique. A minimally invasive procedure using five trocars was performed. Results: In 11 patients exposure of the hiatus was impeded because of hypertrophy of the left liver lobe which led to conversion in eight patients and abortion of the procedure in three other patients. Anatomical complications: We observed two gastric perforations and one band slippage at the early stage, one infection and three rotations of the access port. Functional complications: There were eight (4%) cases of irreversible total food intolerance resulting in pouch dilation and eight cases (4%) of esophagitis. One fatality on the 45th day in a patient with a Prader-Willi syndrome. Conclusion: The most disturbing complications of gastric banding technique are gastric perforation and pouch dilation. Their incidence may be reduced by improving the technique and by considering pitfalls of the procedure. Received: 28 May 1996/Accepted: 25 July 1996     

Laparoscopic surgery and the third world

Surgical Endoscopy -     

Possible occurrence and meaning of lymphocytes bearing autoanti-idiotypic receptors during the immune response.

During an immune response, the increase in binding affinity of antibodies is followed by a fall. Lymphocytes bearing autoanti-idiotypic receptors were detected during a normal immune response. The kinetics of appearance and disappearance of such lymphocytes led us to propose a network model to explain the changes occurring in antibody properties during an immune response.     

Persistence of anti-donor allohelper T cells after neonatal induction of allotolerance in mice

BALB/c mice rendered tolerant to A/J alloantigens by neonatal injection of 10(8) (A/J X BALB/c)F1 spleen cells develop an autoimmune disease associated with a polyclonal activation of donor B cells. To study the mechanisms leading to donor B cell activation in tolerant mice, we prepared mixed lymphocyte cultures (MLC) between splenic T cells from neonatally injected mice and donor-type (A/J X BALB/c)F1 or third-party (C57BL/6 X BALB/c)F1 B cells. T cells from tolerized mice were unable to generate cytotoxic T lymphocytes, to proliferate or to secrete interleukin (IL)2 after stimulation with donor alloantigens in MLC. These T cell responses were present after MLC with third-party antigens, but were of lower intensity than those generated by control BALB/c T cells. In contrast, T cells from tolerized mice stimulated immunoglobulin production by donor-type (A/J X BALB/c)F1 B cells much more powerfully than T cells from control BALB/c mice. The stimulation of donor-type (A/J X BALB/c)F1 B cells was polyclonal, as attested by the levels of anti-hapten and anti-DNA antibodies in the MLC supernatants. IgM was the dominant isotype secreted in vitro, but IgG1 and IgG3 were also produced in significant amounts. Lysis experiments indicated that the T cells responsible for F1 B cell stimulation in MLC were CD4+ host T cells. These T helper cells were alloreactive since they did not stimulate syngeneic BALB/c B cells, and their effect on donor B cells was specifically blocked by anti-donor Ia monoclonal antibodies. Addition of anti-IL 4 monoclonal antibody to MLC between T cells from tolerant mice and (A/J X BALB/c)F1 B cells almost completely abolished the production of IgG1, but not that of IgM or IgG3. Taken together, these findings indicate that neonatal injection of alloantigens in BALB/c mice induces a state of dissociated tolerance, with unresponsiveness of anti-donor T cells secreting IL 2 on the one hand, and persistence of T cells responsible for B cell help and IL 4 secretion on the other hand.     

Single-access laparoscopic primary and incisional prosthetic hernia repair: first 50 patients

Background

Primary and incisional hernia can be repaired by multitrocar laparoscopy. Single-access laparoscopy (SAL) recently gained interest to decrease the invasiveness and to reduce the abdominal trauma, besides improved cosmetic results. The authors report first 50 patients who consulted for primary and incisional hernia and treated by SAL prosthetic repair.

Patients and methods

Between December 2009 and March 2012, 50 patients (24 females, 26 males) were submitted to SAL for primary (23) and incisional hernia (27). Mean age was 49.1 ± 15.1 years (17–75), and mean body mass index 29.7 ± 5.7 kg/m² (19–44.1). A total of 26 primary and 30 incisional hernias were treated. The technique consisted in implied the use of an 11-mm trocar for 10-mm scope, curved reusable instruments without trocars, and dualface prosthesis fixed by tacks without transfascial closures.

Results

No conversion to open surgery nor addition of one or more trocars was necessary. Mean perioperative hernia sizes were 7.0 ± 5.0 cm (2–24) in length and 6.0 ± 3.4 cm (1–16) in width, for a surface of 55.0 ± 64.6 cm² (2.8–268.2). Mean prosthesis size used was 188.1 ± 113.4 cm² (56.2–505.6). Mean laparoscopic time was 60.2 ± 32.8 min (26–153), and mean final scar length was 21.2 ± 4.5 mm (13–35). Mean hospital stay was 2.2 ± 1.2 days (1–8). Perioperative complications were registered in 4 patients and minor early complications in 13 patients of each group. After a mean follow-up of 16.1 ± 8.8 months (4–34), 2 late complications were observed in one patient of each group.

Conclusion

Primary and incisional hernia can safely be treated by SAL prosthetic repair, but a learning curve is unavoidable. Thanks to this approach, in patients with primary hernia, only a small scar is finally visible, and in patients who proved to be prone to develop incisional hernia, the number of fascial incisions can be reduced.     

IL-10 in vivo gene expression in a cell-induced animal model of proliferative vitreoretinopathy

Due to inhibitory activities on cell-mediated immune responses, interleukin-10 (IL-10) has been proposed as a good candidate to treat inflammatory eye disease and proliferative vitreoretinopathy (PVR). In this study we evaluate the effect of human IL-10 (hIL-10) expression in a cell-induced animal model of PVR. Rabbit dermal fibroblasts were genetically modified by infection with retroviral particles carrying the neomycin resistance gene (neoR) alone or in combination with the hIL-10 gene. PVR was induced in rabbits by intravitreal injections of RDF hIL-10 or RDF neo. Some rabbits received instead injections of soluble recombinant hIL-10 (rhIL-10). PVR was graded by fundoscopy. Eyes were enucleated for histology at day 28. ELISA was performed to measure hIL-10 production in RDF supernatants and in vitreous samples, 24 h after injection. Results showed that in vitro hIL-10 production by RDF was 24,500 pg/10(6) cells/ml/24 h. In vivo IL-10 secretion was detected in all rabbits injected with RDF hIL-10 but was undetectable in control rabbits. Similar clinical grades of PVR were found in rabbits injected with RDF hIL-10 or RDF neo. Histology showed that all eyes injected with RDF hIL-10 had significant inflammatory infiltration whereas only one control eye was clearly inflamed. Rabbits injected with soluble rhIL-10 had normal fundoscopy and normal histology. In conclusion, our results show that in vivo, in a cell-induced model of PVR, hIL-10 has no effect in the clinical progression of PVR. Histology, however, shows that pro-inflammatory effects seem to overcome its suppressive properties.     

CXCR4 expression in vitreoretinal membranes

BACKGROUND/AIM: Proliferative vitreoretinopathy (PVR) and macular pucker (MP) vitreoretinal membranes are caused by abnormal cell migration. By their role in chemotactism, chemokine receptors represent good candidates to sustain this process. The authors thus investigated the expression of one of them, CXCR4, in these pathologies. METHODS: Three PVR and four MP membranes were surgically removed and processed for immunochemical studies with antibodies for CXCR4, cytokeratins or smooth muscle actin. RESULTS: CXCR4 expression was found in all membranes. There was no relation between severity of PVR or MP and presence of CXCR4. In addition, there was no difference in CXCR4 expression between MP and PVR. CONCLUSION: CXCR4 is expressed in PVR and MP. Further experiments are needed to test if CXCR4 and other chemokine receptors are implicated in vitreoretinal membrane formation.     

The transmembrane adaptor protein TRIM regulates T cell receptor (TCR) expression and TCR-mediated signaling via an association with the TCR zeta chain

T cell receptor (TCR)-interacting molecule (TRIM) is a recently identified transmembrane adaptor protein, which is exclusively expressed in T cells. Here we demonstrate that in mature T cells, TRIM preferentially interacts with the TCR via the TCR-zeta chains and to a lesser extent via the CD3-straightepsilon/gamma heterodimer. Transient or stable overexpression of TRIM in Jurkat T cells results in enhancement of TCR expression on the cell surface and elevated induction of Ca(2+) mobilization after T cell activation. TRIM-mediated upregulation of TCR expression results from inhibition of spontaneous TCR internalization and stabilization of TCR complexes on the cell surface. Collectively, our data identify TRIM as a novel integral component of the TCR complex and suggest that one function of TRIM might be to modulate the strength of signals transduced through the TCR through regulation of TCR expression on the cell surface.