Video self-confrontation as a therapeutic tool in schizophrenia: A randomized parallel-arm single-blind trial.

BACKGROUND: Lack of insight is a barrier to treating psychosis. Preliminary studies have suggested that showing people videos of their psychotic behaviour may improve personal insight. This clinical trial aimed to assess the effect of video self-confrontation. METHODS: Inpatients between 18 and 65 years old with schizophrenia or schizoaffective disorder were filmed upon admission to two psychiatric hospitals while experiencing acute psychosis. After stabilization, individuals were randomized 1:1 to the "self-video" group where they watched their own video or to the "no video" control group. The primary outcome was the Scale to assess Unawareness of Mental Disorder (SUMD) at 48 h by a blinded assessor. Secondary objectives included psychotic and depressive symptoms, medication adherence and functioning using the Functional Remission of General Schizophrenia. Patients were followed up for four months. RESULTS: 60 participants were randomized and the level of insight did not differ between groups at 48 h (p = 0.98). There was no impact on SUMD subscores or the other insight questionnaires at any timepoint, nor on psychopathology or medication adherence. At one month, the level of functioning of those in the "self-video" group (n = 23) was higher (61.8 vs 53.5, p = 0.02), especially concerning "Treatment" and "Daily life". No adverse effects were reported. After video self-confrontation, people expressed more positive than negative emotions and were less lost to follow-up. CONCLUSION: Video self-confrontation did not change levels of insight, but may have a therapeutic impact nonetheless, by improving levels of self-care and adherence to care, indicating that this innovative therapeutic tool requires further study. TRIAL REGISTRATION NUMBER: NCT02664129.

[Long-term review of homogeneous and consecutive series of 100 "Charnley"-type total hip prostheses]. / Révision á long terme d'une série homogéne et consécutive de 100 prothéses totales de hanche type "Charnley".

PURPOSE OF THE STUDY: Long-term studies of total hip replacements often give diverse results because the series studied are not homogeneous. We report the long-term result in a homogeneous, consecutive series of 100 Charnley total hip replacements for idiopathic hip osteoarthritis in patient without previous surgery, by the same operator. MATERIALS: Of 200 patients with 223 Charnley or Charnley-Kerboull total hip prostheses, implanted more than 13 years earlier, 94 patients with 104 implants were alive at the time of the study. Ninety of them (95.7 per cent) with 100 implants were clinically and radiographically examined. Mean follow-up was 14 yr 8 mo and minimum follow-up was over 13 yr 6 mo. METHODS: Hip function was clinically assessed according to Merle d'Aubigné's criteria. Immediate postoperative x-rays and x-rays at 1, 5 and 10 years and at maximum follow-up were examined. For the acetabulum, alignment, radiolucent line, loosening and wear of the socket were analysed. For the femur, the position of the implant, radiolucent line and loosening, changes in the calcar and cortical bone were analysed. RESULTS: Two femoral implants had to be replaced because of implant fracture. The acetabulum became loose in 3 cases and the femur in 2, but did not require revision at the time of examination. Mean acetabular wear was 0.93 mm (0-5 mm). Wear was greater if the subjects were active (p < 0.05) overweight (p < 0.05) and if the acetabulum was vertical (p < 0.05). Changes in calcar, generally lysis, were more frequent when wear was marked (p < 0.001). Thinning of cortical bone was more frequent in women (p < 0.05), sedentary subjects (p < 0.001) and those in poor general condition (p < 0.05) and was less frequently associated with acetabular wear (p < 0.01). DISCUSSION: This study is characterised by its homogeneity: same etiology, same operator, same implants. Functional outcome at a mean of 14 yr 8 mo after surgery was good, as in most series of Charnley's total hip prostheses. Acetabular wear gave most cause for concern. It was linked with the weight and activity of the patients and with socket alignment. This wear led to deterioration of the calcar, due to granulomas and not to stress shielding. In spite of the homogeneity of the series, no factor was found to account for cortical thickening, whereas cortical thinning occurred in light-weight, osteoporotic patients whose prosthesis did not entirely fill the medullary canal. CONCLUSION: Charnley's total hip prostheses are a good method for treatment of idiopathic hip osteoarthritis. Cement does not appear to be a major deterioration factor over time, unlike polyethylene sockets in which wear and its consequences are a matter for concern.

Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction.

The intervention of the L-arginine-NO pathway in renal vasodilation and renin secretion was studied in an isolated perfused rat kidney model. NG-nitro-L-arginine methyl ester (L-NAME, 1-25 microM), an inhibitor of nitric oxide (NO) synthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin was inhibited independently of the rise in PP, since the effect of L-NAME on renin release was the same when PP was maintained constant. Exposure of rats to low [salt depleted (SD)] or high [salt repleted (SR)] salt intake for 1 mo influenced the renal vascular response to L-NAME (3 microM). Isolated SR rat kidney vasculature vasoconstricted to a greater extent after inhibition of NO synthase than did that of SD kidneys. A similar fall in renin release was observed after L-NAME in both groups, despite a higher renin secretion rate in SD than in SR rats. These results suggest that NO-dependent vasodilation counteracts the renal vasoconstrictor effect of sodium loading.

[Control of vascular tone by the endothelium: the coupling active vasodilation in the kidney to renin secretion]. / Le contrôle de la vasomotricité par l'endothélium: le couplage de la vasodilatation active rénale à la sécrétion de rénine.

The vascular endothelium plays an essential role in regulating the contractility of the adjacent smooth muscle cell through its secretory and metabolic properties. One of these well known properties is the conversion of angiotensin I into angiotensin II. But the endothelium also secretes at least three compounds able to diffuse to the smooth muscle cell and exerting a paracrine action: these are the prostacyclin (PGI2), the endothelium derived relaxing factor (EDRF) and the endothelin 1. The secretion of these different vasoactive compounds by endothelial cells is triggered by mechanical events, such as the shear stress, or by the effect of several humoral factors locally released, for example from platelets. The compound NO (nitric oxide) is produced by the endothelial enzyme NO synthase from its precursor L-arginine, and is responsible for the vasodilatory and antiplatelets properties of EDRF. NO, by activating the soluble guanylate cyclase in the smooth muscle cell, is responsible for the endothelium dependent vasodilatation. We observed in an isolated perfused rat kidney that the compound L-NAME (NG-monomethyl-L-arginine methyl ester), a competitive inhibitor of NO synthase blocking the production of NO, induces renal vasoconstriction and inhibits renin release. This suggests that not only the renal vasoconstriction but also the renal vasodilatation are active processes, permanently regulated by vasoactive compounds such as EDRF. It seems also that EDRF plays an important role in maintaining the secretion of renin. It can be hypothetized that an abnormality in the release or fate of EDRF might perhaps contribute to high blood pressure, by both a direct effect on the vascular tone and an indirect effect on the release of renin, which in turn regulates also the renal and systemic hemodynamics.

Decreased renin release and constant kallikrein secretion after injection of L-NAME in isolated perfused rat kidney.

A possible role of the endothelial L-arginine/NO pathway in the control of renal hemodynamics, renin release and kallikrein secretion was studied in an isolated rat kidney model perfused in a closed-circuit. NG-nitro-L-arginine methyl ester (L-NAME, 1-50 microM), an inhibitor of nitric oxide biosynthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin release was inhibited independently of a rise in PP. L-NAME did not change the urinary kallikrein secretion. These results confirm the intervention of the L-arginine/NO pathway in the vasodilation of this isolated perfused kidney model and demonstrate the inhibitory effect of L-NAME on renin release. They suggest that nitric oxide synthesis plays a role in stimulating renin release and is not involved in the regulation of urinary kallikrein secretion.

[Irreducible palmar dislocation of the metacarpophalangeal thumb joint by a skiing accident]. / Luxation palmaire irréductible de la métacarpo-phalangienne du pouce par accident de ski.

Amongst the large number of severe sprains of the lateral ulnar ligament of the metacarpophalangeal joint of the thumb by skiing accidents which we treat each year as a result of our geographical situation, we have encountered an original lesion on two occasions. The patients were referred with unstable palmar dislocation of the metacarpophalangeal joint of the thumb despite an attempt of reduction under local anaesthesia performed at the ski resort by practitioners particularly well trained in this form of traumatology. On examination, the thumb was globally painful and presented a defect of active extension of the MP joint suggestive of a complex lesion of the extensor apparatus. X-rays showed palmar dislocation of the MP joint of the thumb. Surgical exploration in both cases revealed identical lesions: complete rupture of the two bundles of the lateral ulnar ligament of the MP joint of the thumb, whose distal extremities could be seen as soon as the skin was opened with incarceration of the extensor apparatus between the palmar surface of the neck of the first metacarpal and the dorsal surface of the first phalanx. Perfectly classical treatment consisted of a dorso-lateral incision to reduce the extensor apparatus and to suture the two bundles of the lateral ulnar ligament; immediately restoring the stability which is usually observed in "classical" severe sprains. The current result is good, entirely comparable to that of severe sprains of the MP joint of the thumb.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of bradykinin and kininogens in isolated rat kidney vasoconstricted by angiotensin II.

The hemodynamic and endocrine effects of bradykinin and kininogens were investigated using a closed-circuit isolated rat kidney perfused with angiotensin II (ANG II). ANG II induced vasoconstriction, stimulation of urinary kallikrein release, and inhibition of renin secretion. Bradykinin markedly increased renal perfusate flow (RPF) and produced a slight but significant diuresis and natriuresis. The inhibitory effect of ANG II on renin secretion was delayed. Urinary kallikrein secretion was unchanged. The effect of bradykinin was suppressed by the competitive kinin antagonist [DArg,Hyp3,Thi5,8,DPhe7]bradykinin. Kallikrein-sensitive rat high-molecular-weight kininogen produced a progressive rise in renal perfusate flow. Exocrine function and renin and kallikrein secretions were unchanged. Immunoreactive kinins, identified as bradykinin by high-pressure liquid chromatography, were liberated into the perfusate. Perfusate immunoreactive high-molecular-weight kininogen decreased in parallel as a result of consumption. The kalikrein-resistant T-kininogen was not hydrolyzed to release a kinin, had no effect on renal function, and its concentration in the perfusate remained constant. These results suggest that kinin can be produced in the renal circulation from kallikrein-sensitive circulating kininogens and can antagonize the vasoconstrictor effect of ANG II and alter renal hemodynamics. They provide evidence that the kallikrein-kinin system can participate with the renin-angiotensin system in the control of renal blood flow.

Angiotensinogen's role in ANG formation, renin release, and renal hemodynamics in isolated perfused kidney.

Isolated perfused rat kidneys were used to investigate the effects of the addition of pure angiotensinogen or renin-free plasma to the perfusate on angiotensin I (ANG I) and angiotensin II (ANG II) generation, renal hemodynamics, and renin release. When no angiotensinogen or plasma is added, a very small amount of angiotensinogen is initially detected in the perfusate. Whereas renin secreted by the kidney accumulates in the perfusate, angiotensinogen disappears during the perfusion and immunoreactive ANG II cannot be detected. The addition of angiotensinogen reactivates the renin-angiotensin system. ANG I, [des-Asp1] ANG I, ANG II, and [des-Asp1] ANG II are progressively generated in the perfusate. At a constant perfusion pressure, as well as at a variable perfusion pressure, a progressive fall in renal perfusate flow is observed that is significantly correlated to the level of immunoreactive ANG II. ANG II significantly blunts the rise in renin, and renin release in the perfusate is negatively correlated to immunoreactive ANG II levels. Comparison of the ANG I and ANG II levels in in vitro incubated perfusates and circulated perfusates shows that in plasma-injected perfusates the level of immunoreactive ANG II is dependent on both the production of ANG I and its conversion to ANG II by renal and perfusate converting-enzyme activity, and on ANG I and ANG II degradation by the kidney and the perfusate.

[Immunologic approach of the blockage of the renin angiotensin system in vivo]. / Approche immunologique du blocage du système rénine angiotensine in vivo.

To block the renin-angiotensin system by antibodies directed against renin or angiotensins is an old and recent goal. This goal can be attained by passive transfer of antibodies or by active immunization against the different molecules of the system. Only passive transfer of polyclonal antibodies directed against the native substrate (angiotensinogen) has been performed in rats. This acute blockade of angiotensinogen substrate availability decrease blood pressure about 30 mmHg in salt depleted rats. Passive transfer of anti-converting enzyme immunoglobulins has been already performed in rabbit and rat. It induced an immunoallergic reaction in the pulmonary capillary bed. Immunization against angiotensin II has been a powerful tool in the exploration of the role of the renin angiotensin system in hypertension. Passive and active immunization have been performed in different species: rabbit, rat. The majority of the results concerning the decrease in blood pressure was negative. However, some works reported positive results which could be related to the high affinity of antibodies for angiotensins. Passive and active immunizations against renin were also performed in different species: dog, pig, rat, rabbit, primates. The majority of the results concerning the decrease of blood pressure were positive, if species specificity of renin was taken into account. Recently passive transfer of polyclonal and monoclonal antibodies, directed against human renin have been performed in normotensive and hypertensive primates, demonstrating an acute fall in blood pressure comparable to that observed with converting enzyme inhibitors. Active immunization against human renin has also been performed in primates; and the chronic blockade of the renin-substrate reaction obtained in this way was associated with a significant decrease in blood pressure, aldosterone secretion and a disappearance of plasma renin activity. Unfortunately, such an active immunization was associated with an organ specific autoimmune disease within the kidney. In conclusion, passive and active immunization against the different proteins and peptides of the system offers specific models of blockade which can be compared with synthetic inhibitors of renin, converting enzyme and angiotensins. Therapeutic application of this immunological approach necessitates the verification of the total absence of autoimmune disease.

[Kallikrein-kinin system, the kidney and arterial pressure]. / Système kallicréine-kinine, rein et pression artérielle.

Renal kallikrein is synthetized in the distal nephron and secreted in urine. Studies on the microdissected nephron and on the whole kidney using immunohistochemistry indicate that kallikrein is produced at the level of the distal part of the distal tubule and in some species in the cells of the initial part of the collecting duct. Urinary kinins are formed at these same sites. The renal tubule contains high levels of kininases, able to inactivate kinins, but the kininases are located mainly up-stream the sites of kinin production, i.e. in the glomerulus and in the proximal tubule. A kininase activity is however also found in the medullary collecting duct. This collecting duct kininase activity might contribute to the control of kinin levels in kidney and urine. The physiological role of the renal kallikrein kinin system is not completely understood. There is some evidence for a role of urinary kinins in water and solute transferrence in the distal nephron. Also kinin production in the renal interstitium and/or circulation may contribute to the control of renal blood flow. In the isolated perfused rat kidney vasoconstricted by angiotensin II for example, the high molecular weight kininogen is hydrolyzed to release kinins and induces a vasodilatation. The kallikrein-kinin system therefore might play a role in kidney function by antagonizing the vascular effect of angiotensin II in the renal circulation and the maintenance renal blood flow.

Influence of converting enzyme inhibition on the hormonal and renal adaptation to hyper- and hyponatraemic dehydration.

The present study was designed to investigate in rats the influence of converting enzyme inhibition with captopril on blood pressure, plasma urea, plasma renin concentration (PRC), plasma aldosterone and plasma vasopressin, and to define the interrelationships between PRC and these variables during equal degrees of either hyponatraemic (furosemide, 40 mg/kg for 2 days) or hypernatraemic (48-h water deprivation) dehydration. Chronic treatment with captopril (40 mg/kg daily) decreased blood pressure by 19% in normally hydrated treated rats, by 27% in water-deprived treated rats and by 40% in furosemide-treated rats. Plasma renin concentration, plasma aldosterone and plasma vasopressin were increased during both hypo- and hypernatraemic dehydration. Captopril decreased plasma aldosterone in water-deprived and furosemide-treated rats, whereas plasma vasopressin was unchanged. The significant correlation observed between plasma aldosterone and PRC in non-treated rats persisted in treated rats, the same level of plasma aldosterone being observed at values of PRC 10 times higher. On the other hand, the correlation between plasma vasopressin and PRC did not persist in captopril-treated rats. An increase in plasma urea was observed in both water-deprived treated rats and furosemide-treated rats. These data indicate that during hypo- and hypernatraemic dehydration, the renin-angiotensin system plays a role in regulating blood pressure, urea elimination and plasma aldosterone, but vasopressin regulation is not modified by its inhibition.

[Kallikrein secretion by the isolated perfused rat kidney. Role of perfusion pressure and the renin-angiotensin system]. / Sécrétion de kallicréine par le rein de rat isolé perfusé. Rôle de la pression de perfusion et du système rénine-angiotensine.

The isolated perfused rat kidney (IPRK) releases kallikrein in urine and renin in perfusate. We have previously shown (Kidney Int 24: 58-65, 1983) and confirm here that kallikrein, as well as renin releases are influenced by changes in renal hemodynamics in this model: a rise in perfusion pressure (PP) from 80 to 98 mmHg increases renal perfusate flow (RPF) by 48 +/- 3 p. 100, inhibits renin release and stimulates kallikrein secretion to 234 +/- 84 p. 100 of control values (n = 8). Since the perfusate lacks angiotensinogen, we decided to study the effect on kallikrein of the reconstitution of the renin-angiotensin system in the IPRK by adding angiotensinogen + angiotensin converting enzyme (AG + ACE) to the perfusion medium. After AG + ACE, PP rose to 107 +/- 4 mmHg, RPF decreased by 82 +/- 3 p. 100 as a consequence of the vasoconstrictor effect of angiotensin II, and renin release was suppressed. Again kallikrein secretion was stimulated and increased to 333 +/- 153 p. 100 of control values (n = 4). It is concluded 1) that kallikrein release is influenced by changes in PP but not in RPF on the IPRK. 2) that reconstitution of the renin-angiotensin system by addition of AG + ACE to the perfusate leads to vasoconstriction, suppression of renin release and a marked increase in kallikrein secretion.

The role of the renin-angiotensin system in blood pressure regulation in normotensive animals and man.

The role of the renin-angiotensin system in the control of blood pressure in normal rodents, primates and man has been evaluated using inhibitors which block the system at various stages. Renin plays a major role in the maintenance of blood pressure under volume depletion. In subjects with a normal salt intake, the contribution of the renin-angiotensin system in maintaining blood pressure levels can be evaluated using angiotensin converting enzyme (ACE) inhibitors. The contribution of the renin-angiotensin system can now be evaluated more closely following the development of new substances which block the renin-angiotensinogen reaction. Available data strongly suggest that renin contributes to the maintenance of blood pressure levels in subjects with a normal salt intake, although to a lesser degree than in subjects on a low sodium intake. The renin-angiotensin system plays a role in the regulation of blood pressure levels in normal experimental animals and man--its importance depending on the state of sodium balance.

[Clinical trial of loxapine succinate in the treatment of 30 cases of psychotic states]. / Essai clinique du succinate de loxapine appliqué au traitement de 30 cas d'états psychotiques.

An open clinical study of loxapine succinate was developed on 30 hospitalized psychiatric patients in order to confirm its antipsychotic properties and its originality opposite the other major neuroleptics. Dosages ranged from 100 to 200 mg per day in 12 cases (40%), and more than 200 mg in serious psychosis or unamenable to therapeutic for which inferior dosages were inefficacious (11 cases). 56,7% of favourable results have been obtained, with a fair improvement of whole symptoms, paranoïd schizophrenic attack and acute delusions. Tolerance was remarkable: no neuro-vegetative manifestation was reported. The considerable sedative effect of loxapine had involved moderate and no invalidating drowsiness in 23% of cases. The extra-pyramidal occurring symptoms disappeared within 2 or 3 days. So loxapine succinate in proving to be a major first intention neuroleptic, suiting a considerable antipsychotic efficacy to a good tolerance, allowing new perspectives in the therapeutic and the approach of psychotic patients.