Anti-Donor HLA Antibody Response After Pancreatic Islet Grafting: Characteristics, Risk Factors, and Impact on Graft Function.

Pancreatic islet grafting restores endogenous insulin production in type 1 diabetic patients, but long-term outcomes remain disappointing as a result of immunological destruction of allogeneic islets. In solid organ transplantation, donor-specific anti-HLA antibodies (DSA) are the first cause of organ failure. This retrospective multicentric study aimed at providing in-depth characterization of DSA response after pancreatic islet grafting, identifying the risk factor for DSA generation and determining the impact of DSA on graft function. Forty-two pancreatic islet graft recipients from the Groupe Rhin-Rhône-Alpes-Genève pour la Greffe d'Ilots de Langerhans consortium were enrolled. Pre- and postgrafting sera were screened for the presence of DSA and their ability to activate complement. Prevalence of DSA was 25% at 3 years postgrafting. The risk of sensitization increased steeply after immunosuppressive drug withdrawal. DSA repertoire diversity correlated with the number of HLA and eplet mismatches. DSA titer was significantly lower from that observed in solid organ transplantation. No detected DSA bound the complement fraction C3d. Finally, in contrast with solid organ transplantation, DSA did not seem to negatively affect pancreatic islet graft survival. This might be due to the low DSA titers, specific features of IgG limiting their ability to activate the complement and/or the lack of allogenic endothelial targets in pancreatic islet grafts.

Penetration of acoustic waves into rippled sandy seafloors

The Helmholtz-Kirchhoff integral and the Kirchhoff approximation are applied to model the penetration of sound waves into rough sandy seafloors at grazing angles above and below the critical angle. As the seafloor of interest is anisotropic, emphasis is placed on simulating the response from a two-dimensional interface. The analytical development of the method is first presented, followed by numerical examples. Simulations and data acquired at sea are in very good agreement in the 2-15 kHz band [Maguer et al., J. Acoust. Soc. Am. 107, 1215-1225 (2000)]. The model predicts, in agreement with the 2-15 kHz acoustic data, the contributions due to roughness effects that dominate the evanescent wave component over most of this frequency band. Secondary effects such as coherent (Bragg) influence patterns and the loss of signal coherence with grazing angle or depth are correctly predicted. The model simulations strongly suggest that roughness of the sediment interface is most likely the cause of anomalous sound penetration into the seabed.

Mechanisms for subcritical penetration into a sandy bottom: experimental and modeling results

This paper presents preliminary results of a recent study whose overall objectives are to determine the mechanisms contributing significantly to subcritical acoustic penetration into ocean sediments, and to quantify the results for use in sonar performance prediction for the detection of buried objects. In situ acoustic measurements were performed on a sandy bottom whose geoacoustical and geomorphological properties were also measured. A parametric array mounted on a tower moving on a rail was used to insonify hydrophones located above and below the sediment interface. Data covering grazing angles both above and below the nominal critical angle and in the frequency range 2-15 kHz were acquired and processed. The results are compared to two models that account for scattering of sound at the rough water-sediment interface into the sediment. Although all possible mechanisms for subcritical penetration are not modeled, the levels predicted by both models are consistent with the levels observed in the experimental data. For the specific seafloor and experimental conditions examined, the analysis suggests that for frequencies below 5-7 kHz sound penetration into the sediment at subcritical insonification is dominated by the evanescent field, while scattering due to surface roughness is the dominant mechanism at higher frequencies.

[Postpneumonectomy syndrome in adults: description and therapeutic propositions apropos of 8 cases]. / Syndrome postpneumonectomie de l'adulte. Description et propositions thérapeutiques à propos de 8 observations.

BACKGROUND: Adult post-pneumonectomy syndrome can be defined as an extrinsic compression of the main bronchus or a lobe bronchus on the aorta resulting from excessive mediastinal deviation after pneumonectomy. PATIENTS: Eight cases in adults are reported. The delay to symptom onset was a mean 34 months. Three patients complained of increased dyspnea and 5 patients experienced a must more rapid course with adult respiratory distress syndrome in 1. Fibroscopy and chest CT confirmed the diagnosis of extrinsic compression of the main bronchus or a lobe bronchus. RESULTS: In the first 2 patients, endoscopic treatment with an endobronchial prosthesis was unsuccessful. The mediastinum was recentered in the following patients using an inflatable prosthesis positioned in the pneumonectomy cavity. Clinical improvement was achieved in all patients. Fibroscopy and chest CT confirmed the reduction in bronchial compression. DISCUSSION: Early diagnosis and mediastinal recentering are required for good outcome. Surveillance after pneumonectomy should include a search for mediastinal deviation and its consequences, particularly concerning the permeability of the remaining bronchi.

[Traumatic intestinal infarction (author's transl)]. / L'infarctus intestinal traumatique.

A study of 25 cases of traumatic intestinal infarction, often old cases, did not show any characteristic clinical picture or course but showed the following points: --abdominal contusion, even mild, may induce intestinal infarction, without any other intra- or retroperitoneal lesion. The frequency of infarction is low, but the notion of trauma is often neglected; --the ileum and ascending colon are most commonly involved, and infarction usually follows a thrombosis of the mesenteric veins. When there is an arterial infarction, this is usually due to mobilisation of an atheromatous plaque; --the clinical course usually includes an interval between the trauma and the infarction, due to a prodromic phase corresponding to the constitution then the extension of the thrombosis. These characteristics suggest a relationship between infarction and venous infarction in general, especially postoperative infarction, where there is local trauma and slowing of the circulation and hypercoagulability and raised platelet count. The treatment is nevertheless the same, associating intestinal resection and exploration with endarterectomy of the vascular pedicles and prolonged postoperative anticoagulant treatment.