"Champagne Fracture": A Superior Fracture-Dislocation of the Proximal Humerus: A Case Report.

A 79-year-old right-handed woman presented with an indirect trauma to her left shoulder after a fall down the stairs. X-rays and computed tomography showed a four-part glenohumeral fracture-dislocation with a subcutaneous ectopic location of the humeral head in the retroclavicular space. A reverse total shoulder arthroplasty was performed using a deltopectoral approach with direct superior extraction of the humeral head. The result at 2 years was a subjective shoulder value of 80%, an absolute Constant score of 59, and a relative Constant score of 92/100. To the best of our knowledge, this is the first description in the literature of such a lesion of superior glenohumeral fracture-dislocation and its treatment.

Long-term survival analysis of 191 MAÏA® prostheses for trapeziometacarpal arthritis.

Surgery for trapeziometacarpal osteoarthritis after failure of medical treatment remains controversial. The aim of this study was to determine the long-term results of the MAÏA® trapeziometacarpal prosthesis (Lépine, Genay, France). This was a retrospective clinical and radiographic study of 191 MAÏA® trapeziometacarpal prostheses implanted between 2001 and 2016 from a single centre. The survival rate of the implants at the final follow-up of 12 years (range 17 days to 140 months) was 88%. Median pain score was 1/10. The median Quick Disabilities of the Arm, Shoulder and Hand (QuickDASH) score was 20. The rate of major complications was 9% (5% dislocations and 4% loosening) with all dislocations needing revision surgery. The risk of prosthetic dislocation was highest during the first 3 years, most often related to malposition of the trapezium implant. The MAÏA trapeziometacarpal prosthesis represents a long-term solution for surgical treatment of thumb rhizarthrosis. Level of evidence: IV.

[Factors predicting falls by patients with vascular hemiplegia at a physical medicine center]. / Facteurs prédictifs de la chute chez l'hémiplégique vasculaire en centre de médecine physique.

OBJECTIVES: To determine factors predicting falls by patients with vascular hemiplegia to establish a program aimed at preventing falls in this population. METHODS: A comparative prospective study performed over 19 months with 44 patients older than 16 years who had had a cerebral vascular accident (CVA, stroke) and were consequently admitted to the Centre Richelie. The exclusion criteria were represented by CVA history, evidence of another form of encephalic lesion, and subsequent admission to hospital after hemiplegia or for follow-up. Assessment consisted of taking note of the mechanism of the fall, possible lesions, and number of falls and analyzing follow-up after the return home. Also included for all patients was information on 20 variables that could be risk factors for fall. RESULTS: The patients' average age was 60.43+/-13.43 years and 20 had had at least one fall (mean 2.2), which allowed us to determine a "falling" group and a control group. Statistical analysis revealed the following factors considered to predict falls: large amount of time prior to hospitalization and lengthy hospitalization, low functional independence measure for entering and leaving, the existence of sensitivity disorders, spatial neglect, failed seated and standing equilibrium, and sedative treatment. In most cases, whatever their nature, falls occurred during transfers (68% of cases). Most often, the post-fall lesions were minor. However, in one case, a femur neck fracture necessitated osteosynthesis. One-third of the patients had a fall at home (as opposed to 5% of the control group). CONCLUSION: Our results confirm those in the literature. The predictive factors for falls in patients with hemiplegia are therefore well established and essentially correlate with the CVA. This consideration must lead to implementation of a prevention program including material-based as well as human measures.

[Botulinum toxin and medical liability: is the patient sufficiently informed?]. / Injections de toxine botulique et responsabilité médicale: le patient est-il suffisamment informé?

INTRODUCTION: The use of botulinum toxin injection therapy is soaring significantly today, with an ever-wider field of applications despite well-known side effects of the treatment. This article aims at analysing the medicolegal practices of practitioners who use this therapy, especially the information given to patients and finding a common practice for providing that information. METHODS: We sent a questionnaire to 340 practitioners who might use the therapy (physiatrists, neurologists, ophthalmologists, ENT specialists, plastic surgeons) working in hospitals and in physical therapy and rehabilitation centres in France. Besides mentioning the possible side effects of the therapy, the questionnaire focused on how such information was transmitted before the injection. RESULTS: Data collection and analysis were performed by use of a spreadsheet software programme. A total of 124 questionnaires were analysed. We did not analyse the items dealing with side effects. Sixty-five percent of the responders said they did not seek statutory authorisation for injections. Only 31% provided written, detailed information and 12% required a signed consent form. Complaints were rare, approximately 12%, were written or verbal, and were always dismissed. DISCUSSION: Side effects after botulinum toxin injection are clearly described in the medical literature. Therefore, it is of utmost importance for this product to be used therapeutically and only by experienced therapists who will carefully respect the product's standard rules of use and inform their patients to the best of their ability. Issuing a detailed letter of information describing all the side effects seems necessary. We suggest a model information letter such as that provided to the patients in our facility. CONCLUSION: Botulinum toxin is a very worthwhile product for numerous abnormalities but has side effects, often brief, at the site of the injection. Therefore it is our duty to inform patients effectively.

[First transplantation of two hands: results after 18 months]. / Première transplantation des deux mains: résultats à 18 mois.

AIM OF THE STUDY: The previous results achieved in single hand transplantations confirmed the feasibility of this procedure and encouraged us to perform the first human double hand transplantation, which was performed in January 2000. In the present study we reported the results obtained eighteen months after transplantation. PATIENT AND METHODS: The recipient was a 33-year old man suffering from a traumatic amputation of both hands in 1996. Surgery included procurement of the upper extremities from a 18-year old multiorgan cadaveric donor, preparation of the graft and recipient's stumps, transplantation of the hands, which included bone fixation, arterial and venous anastomoses, nerve suture, joining of tendons and muscles, and skin closure. Immunosuppressive protocol included tacrolimus, prednisone and mycophenolate mofetil. An intensive rehabilitation program was performed. Follow-up included immunological tests, skin biopsies, arteriography, bone scintigraphy, electromyography and brain functional magnetic resonance imaging. RESULTS: No surgical complications, infectious complications and graft-versus-host-disease occurred. Two episodes of acute skin rejection were demonstrated and they were completely reversed increasing steroid dose. Nerve regeneration and cortical reorganization were shown. Sensorimotor recovery was encouraging and life quality improved. CONCLUSION: This double hand transplantation showed that conventional immunosuppressive protocol is effective and safe as well as that functional results are at least as good as those achieved in replanted upper extremities.

The NH2-terminal region of focal adhesion kinase reconstitutes high affinity IgE receptor-induced secretion in mast cells.

Focal adhesion kinase (FAK) is tyrosine-phosphorylated by adherence of cells and also by FcepsilonRI aggregation in RBL-2H3 mast cells. Using phosphorylation site-specific antibodies, we observed that FcepsilonRI activation in these cells led to an increase in FAK phosphorylation at the same tyrosine residues that are phosphorylated by integrin-induced activation. Previous studies in the 3B6 line, a FAK-deficient variant of the RBL-2H3 cells, suggest that FAK plays a role in FcepsilonRI-induced secretion. Stable cell lines expressing either full-length or truncated forms of FAK were isolated after transfection of the FAK-deficient 3B6 variant cells. The NH(2) domain of FAK, which lacks the enzymatic and the COOH-terminal regions, was sufficient to reconstitute secretion. The different truncated forms of FAK were still tyrosine-phosphorylated after FcepsilonRI aggregation. Therefore, the kinase domain and the COOH-terminal region are not essential for FcepsilonRI-induced tyrosine phosphorylation of FAK or for secretion. Taken together, our data demonstrate that the reconstitution of secretion is dissociated from FAK activation and that the NH(2)-terminal region of FAK is the only critical element that may play a role in FcepsilonRI-induced secretion by acting as an adaptor or linker molecule.

Dioleylphosphatidylglycerol inhibits the expression of type II phospholipase A2 in macrophages.

We have recently shown that modified natural pulmonary surfactant Curosurf inhibits the synthesis of type II phospholipase A2 (sPLA2-II) by cultured guinea-pig alveolar macrophages (AM). The goal of the present study was to identify the surfactant components and the mechanisms involved in this process. We show that protein-free artificial surfactant (AS) mimicked the inhibitory effect of Curosurf, suggesting that phospholipid components of surfactant play a role in the inhibition of sPLA2-II expression. Among surfactant phospholipids, dioleylphosphatidylglycerol (DOPG) was the most effective in inhibiting the synthesis of sPLA2-II. By contrast, the concentrations of platelet-activating factor (PAF)-acetylhydrolase and lysophospholipase activities remained unchanged, indicating that inhibition of sPLA2-II synthesis was caused by a specific effect of surfactant. The effect of DOPG on sPLA2-II synthesis was concentration-dependent and was accompanied by a rapid and time-dependent uptake of DOPG by AM whereas dipalmitoylphosphatidylcholine (DPPC) was only marginally taken up. Curosurf, AS, and DOPG inhibited tumor necrosis factor-alpha (TNF-alpha) secretion, a key step in the induction of sPLA2-II synthesis by AM, in contrast to DPPC which had only a marginal effect. We conclude that phospholipid components, especially DOPG, play a major role in the inhibition of sPLA2-II synthesis by surfactant and that this effect can be explained, at least in part, by an impairment of TNF-alpha secretion.

Ultrafiltration membrane full-scale experience status after 9 years or operation and large scale plant capacity 100.000 m3/day

Se describe la evolucion de la tecnologia de la ultrafiltracion por membranas para el tratamiento del agua en terminos de costos y consideraciones de diseño, incluyendo proyectos a gran escala. Esta tecnologia ha demostrado exceder los requerimientos para el control de la turbiedad, asi como para la remocion de virus y parasitos

Generation of lyso-phospholipids from surfactant in acute lung injury is mediated by type-II phospholipase A2 and inhibited by a direct surfactant protein A-phospholipase A2 protein interaction.

Lyso-phospholipids exert a major injurious effect on lung cell membranes during Acute Respiratory Distress Syndrome (ARDS), but the mechanisms leading to their in vivo generation are still unknown. Intratracheal administration of LPS to guinea pigs induced the secretion of type II secretory phospholipase A2 (sPLA2-II) accompanied by a marked increase in fatty acid and lyso-phosphatidylcholine (lyso-PC) levels in the bronchoalveolar lavage fluid (BALF). Administration of LY311727, a specific sPLA2-II inhibitor, reduced by 60% the mass of free fatty acid and lyso-PC content in BALF. Gas chromatography/mass spectrometry analysis revealed that palmitic acid and palmitoyl-2-lyso-PC were the predominant lipid derivatives released in BALF. A similar pattern was observed after the intratracheal administration of recombinant guinea pig (r-GP) sPLA2-II and was accompanied by a 50-60% loss of surfactant phospholipid content, suggesting that surfactant is a major lung target of sPLA2-II. In confirmation, r-GP sPLA2-II was able to hydrolyze surfactant phospholipids in vitro. This hydrolysis was inhibited by surfactant protein A (SP-A) through a direct and selective protein-protein interaction between SP-A and sPLA2-II. Hence, our study reports an in vivo direct causal relationship between sPLA2-II and early surfactant degradation and a new process of regulation for sPLA2-II activity. Anti-sPLA2-II strategy may represent a novel therapeutic approach in lung injury, such as ARDS.

Down-regulation by prostaglandins of type-II phospholipase A2 expression in guinea-pig alveolar macrophages: a possible involvement of cAMP.

We have demonstrated previously that isolated guinea-pig alveolar macrophages (AM) synthesize type-II phospholipase A2 (PLA2-II) through a tumour necrosis factor-alpha (TNF-alpha)-dependent process. This synthesis is enhanced by lipopolysaccharide (LPS) and accompanied by a release of prostaglandin E2 (PGE2) into the medium. Because agents elevating intracellular cAMP, such as PGE2, have been shown to stimulate PLA2-II expression in various cell types, we investigated the modulation of PLA2-II synthesis by cAMP in AM. Surprisingly, incubation of AM with PGE2, dibutyryl-cAMP, cholera toxin or rolipram (an inhibitor of specific cAMP-phosphodiesterase) inhibited both basal and LPS-stimulated PLA2-II expression. The inhibitory effect of PGE2 was observed at concentrations similar to those released by AM. Moreover, treatment of AM with either aspirin or neutralizing PGE2 monoclonal antibody stimulated PLA2-II synthesis. These effects were closely correlated with the ability of these agents to modulate TNF-alpha release, which was decreased by dibutyryl-cAMP and exogenous PGE2, whereas neutralizing PGE2 antibody markedly increased this release. Hence, in contrast to other cell systems, we report that: (i) agents elevating intracellular cAMP levels down-regulate both basal and LPS-induced PLA2-II synthesis, (ii) prostaglandins exert a negative feedback effect on this synthesis, probably through an elevation of intracellular cAMP levels, and (iii) inhibition of TNF-alpha release may account, at least in part, for the down-regulation of PLA2-II expression by endogenously produced prostaglandins and cAMP-elevating agents.

Inhibition by pulmonary surfactant Curosurf of secretory phospholipase A2 expression in guinea-pig alveolar macrophages.

Replacement therapy with exogenous surfactant has been proven successful in animal models of acute respiratory distress syndrome (ARDS). Here, we investigated the effect of seminatural surfactant Curosurf on the expression of secretory phospholipase A2 (sPLA2) in guinea-pig alveolar macrophages (AM). The latter produced an sPLA2 activity whose level was markedly reduced when culture medium was supplemented with Curosurf. This effect was concentration-dependent and was accompanied by a decrease in sPLA2 mRNA levels. By contrast, when AM were first cultured for 20 hr and then incubated with Curosurf, no significant change was observed in their sPLA2 activity. Finally, f-Met-Leu-Phe (FMLP)-induced thromboxane B2 release from AM was not altered by Curosurf, indicating that the inhibition of sPLA2 expression cannot be attributed to a nonspecific membraneous effect of Curosurf. These findings show that pulmonary surfactant modulates the expression of sPLA2 in AM and suggest that this effect may account for the clinical efficacy of surfactant replacement therapy in ARDS.

Endotoxin induces expression of type II phospholipase A2 in macrophages during acute lung injury in guinea pigs: involvement of TNF-alpha in lipopolysaccharide-induced type II phospholipase A2 synthesis.

Elevated levels of secretory type II phospholipase A2 (sPLA2-II) have been associated with a poor clinical outcome in the acute respiratory distress syndrome. This study identifies the cell source(s) and the mechanisms of sPLA2-II synthesis in the guinea pig model of acute respiratory distress syndrome induced by intratracheal injection of LPS. Administration of LPS led to an increase in lung membrane-associated calcium-dependent sPLA2 activity, which was abrogated by LY311727, a selective inhibitor of sPLA2-II. No sPLA2 activity was detected in the vascular compartment of the lung. LPS administration induced a parallel accumulation of sPLA2-II mRNA in lung tissues. In situ hybridization showed that sPLA2-II transcripts were synthesized in interstitial and alveolar macrophages (AM). Incubation of AM with LPS enhanced the expression of sPLA2-II mRNA, leading to stimulation of sPLA2-II synthesis and secretion. This increase was prevented by the addition of anti-TNF-alpha and anti-p55 TNF receptor Abs. Furthermore, the addition to AM of cellfree bronchoalveolar fluid collected from LPS-treated guinea pigs increased sPLA2-II expression, which was abrogated by anti-TNF-alpha Ab. These findings demonstrate that 1) macrophages are in vivo the major cell source of sPLA2-II in LPS-induced acute lung injury; 2) in contrast to that in other cell systems, regulation of LPS-induced sPLA2-II synthesis in AM is TNF-alpha dependent; and 3) production of TNF-alpha in the air-lung interface is an important step for sPLA2-II synthesis in macrophages.

Expression of the type-II phospholipase A2 in alveolar macrophages. Down-regulation by an inflammatory signal.

We have shown previously that guinea pig alveolar macrophages (AM) synthesize a secretory phospholipase A2 (PLA2) during in vitro incubation. Here, we report the molecular cloning of this enzyme and show that it has structural features closely related to all known mammalian type-II PLA2. The mRNA and PLA2 activity were undetectable in freshly collected AM, but their levels increased dramatically to reach maximal values after 16 h of culture. Thereafter, the PLA2 activity remained constant with a parallel secretion in the medium, in contrast to mRNA level which returned to near basal values after 32 h. Incubation of AM for 16 h with the inflammatory secretagogue peptide f-Met-Leu-Phe (fMLP) markedly reduced the PLA2 activity and mRNA levels. This inhibition was prevented by preexposure of AM to pertussis toxin, an inhibitor of G-protein. In contrast, when AM were first cultured for 16 h and then incubated with fMLP, no significant change was observed in their PLA2 activity. In conditions where the type-II PLA2 was completely abrogated by fMLP, the latter did not alter the lipopolysaccharide-induced accumulation of tumor necrosis factor alpha mRNA or the release of arachidonic acid induced by the subsequent addition of the calcium ionophore A23187. These studies show that the inflammatory peptide fMLP down-regulates the expression of the type-II PLA2 by AM through a process mediated by G-protein. A possible negative control of the type-II PLA2 expression during AM activation is suggested.

Dopamine D2 receptors potentiate arachidonate release via activation of cytosolic, arachidonate-specific phospholipase A2.

Several G(i)-linked neurotransmitter receptors, including dopamine D2 receptors, act synergistically with Ca(2+)-mobilizing stimuli to potentiate release of arachidonic acid (AA) from membrane phospholipids. In brain, AA and its metabolites are thought to act as intracellular second messengers, suggesting that receptor-dependent potentiation of AA release may participate in neuronal transmembrane signaling. To study the molecular mechanisms underlying this modulatory response, we have now used Chinese hamster ovary cells transfected with rat D2-receptor cDNA, CHO(D2). Two antisense oligodeoxynucleotides corresponding to distinct cDNA sequences of cytosolic, AA-specific phospholipase A2 (cPLA2) were synthesized and added to cultures of CHO(D2) cells. Incubation with antisense oligodeoxynucleotides inhibited D2 receptor-dependent release of AA but had no effect on D2-receptor binding or D2 inhibition of cyclic AMP accumulation. In addition, pharmacological experiments showed that D2 receptor-dependent AA release was prevented by nonselective phospholipase inhibitors (such as mepacrine) but not by inhibitors of membrane-bound, non-AA-specific PLA2 (such as p-bromophenacyl bromide). cPLA2 is expressed in brain tissue. The results, showing that cPLA2 participates in receptor-dependent potentiation of AA release in CHO(D2) cells, suggest that this phospholipase may serve a similar signaling function in brain.

[Poor results in 183 threaded acetabular cups at a mean 7 years follow-up]. / Bilan négatif d'une revue de 183 cotyles vissés au recul moyen de 7 ans.

We reviewed 183 threaded rings at a mean 7 years follow-up. Poor résults are frequent: 34 % had been revised and 50 % have radiographic migration, essentially with proximal migration of the cup. Generally, we reoperated with other cememtless implants. The type of threaded cup does not matter (spheric or conic). Only the duration of follow up seems significant. We think that biomecanical strains, rather than physiology, explain these numerous migrations. We have therefore abandoned threaded cups in favour of porous-coated impacted cups.

Selection of alternative G-mediated signaling pathways at the dopamine D2 receptor by protein kinase C.

Evidence indicates that a single membrane receptor subtype may be responsible for the generation of multiple intracellular signals, but mechanisms allowing for the selection of a specific effector pathway have not yet been documented. In neurons and other cells, the stimulation of dopamine D2 receptors produces, via G-protein activation, a spectrum of intracellular responses including inhibition of adenylyl cyclase activity, modulation of K+ currents, and potentiation of Ca(2+)-evoked arachidonic acid (AA) release. In this study, we report that, in Chinese hamster ovary cells, stimulation of protein kinase C (PKC) directs the preferential coupling of transfected D2 receptors from inhibition of adenylyl cyclase to potentiation of AA release, two responses mediated by Gi. The switch between these two signaling systems is accompanied by marked changes in their GTP sensitivities, indicating that it may result from the phosphorylation of component(s) of the receptor-Gi-protein complex. Brain PKC activity is enhanced by neurotransmitters and by neuronal depolarization. Thus, the ability of this protein kinase to remodel signaling pathways at the D2 receptor may regulate these Gi-mediated responses in an activity-dependent manner, and represent a novel form of synaptic plasticity.

[Osteosynthesis of fractures of the trochanteric region using the gamma nail, apropos of 76 reviewed cases]. / Ostéosynthèse des fractures de la région trochantérienne par clou gamma, à propos de 76 cas revus.

The authors present 76 cases of trochanteric fractures, treated by a Gamma nail. The minimal follow-up was 6 months, with clinical and roentgenographical check-ups. The mean age was 74 years, with a female majority as classically; the most common cause was a simple fall. Unstable fractures represented 53% of the cases, with 39% subtrochanteric; nevertheless, full weight bearing was possible in 83% of the cases. The mechanical complications of this new technique have been studied in details and compared with other most common methods of osteosyntheses: the Ender rod and the sliding screw plate. The Gamma nail shows an uncontestable superiority compared to Ender's rods, but it has little advantage to D.H.S.-T.H.S., particularly because of the delay in full-weight bearing and deep infection rate. The Gamma nail moreover seems to be better adapted for the treatment of subtrochanteric fractures.

Algunos determinantes recientes de la lactancia materna en Chile / Some reecent breast-feeding determinants in Chile

Se analizan 4 factores que actualmente explicarían en parte importante las dificultades para producir leche de las madres atendidas por el Ministerio de Salud de Chile. El estado nutricional de la embarazada, medido por antropometría, influye la duración de la lactancia materna y el volumen de leche producido, indicando la necesidad de que la madre tenga un adecuado incremento de peso durante la gestación. El trabajo materno ha sido correlacionado negativamente con la duración de la lactancia materna en diversos estudios. Cuando la madre trabajadora tiene reposo postparto, o cuida directamente al niño en el trabajo, presenta una duración mayor de la lactancia natural. Las madres que fuman durante el embarazo y los seis meses postparto presentan una duración de la lactancia materna menor que las no fumadoras, mientras que los hijos de estas últimas presentan menos desnutrición peso-edad. Los cambios en las prácticas del equipo de salud que interfieren con el proceso de succión pueden influir positivamente en la duración de la lactancia materna según diversos estudios locales, por lo que se recomienda realizar nuevos programas. Se señalan algunos datos disponibles sobre la cantidad de mujeres afectadas por los diferentes factores de riesgo