[Prostatic Urethral Lift under local anesthesia: Single-centre retrospective observational study]. / La pose d'implant UroLift ® sous anesthésie locale : étude observationnelle rétrospective monocentrique.

INTRODUCTION: Urolift implant placement may be preferred to conventional endoscopic surgery for patients who wish to preserve their sexuality or for those who prefer a rapid post-operative recovery. The absence of general anaesthesia is an important element that reinforces the minimally invasive aspect of the procedure and improves the speed of recovery. The aim of this work was to report our preliminary experience of Urolift treatment under local anaesthesia. MATERIALS AND METHODS: A retrospective analysis was conducted including all patients treated with Urolift between 2017 and 2021 in our centre. Local anaesthesia was based on the instillation of 2 Xylocaine gels at 4°C into the urethra 15minutes before the procedure. The primary endpoint was the successful completion of the procedure without interruption due to pain or the need for any other form of anaesthesia or analgesia. RESULTS: Twenty-seven patients were included with a median age of 65 years and a prostate volume of 46mL. The International Prostate Symptom Score (IPSS) was 23. The first 3 patients were operated on under general anaesthesia. Local anaesthesia was introduced from the fourth patient onwards. There was no recourse to other modalities of analgesia or anaesthesia or interruption of the procedure. The operating time was 10minutes and pain was assessed at 1 on a visual analogue scale. At 3 months, the IPSS score was 9 (P=0.001). CONCLUSION: This preliminary experience confirms the feasibility of placing the Urolift implant under local anaesthesia without any failure of the proposed management. The improvement in IPSS score was consistent with previously published clinical trials. LEVEL OF EVIDENCE: 3.

Localization of Mycobacterium avium subspecies paratuberculosis in artificially inoculated milk and colostrum by fractionation.

The purpose of the study was to determine the distribution of Mycobacterium avium ssp. paratuberculosis (MAP) across the main milk and colostrum fractions (cream, curd, and whey). Raw milk and colostrum were inoculated with 1 of 2 MAP strains, ATCC 19698 or S-23, yielding initial concentrations of 10(6) to 10(7) cfu/mL. After fractionation, for milk as well as for colostrum, 80 to 90% of the recovered MAP cells were found in the curd fraction and 10 to 20% in the cream fraction. Total MAP colony counts in milk whey were 4 to 5 log(10) units lower than colony counts of inoculated milk. In colostrum, colony counts were 2 to 3 log(10) units lower in whey than in inoculated colostrum. Because of the slow growth of MAP and to proceed more smoothly with set-up and optimization of the method, luminescent MAP strains were used. The high correlation coefficient (r=0.960) between colony counts and luminescence measurements showed that the use of luminescent MAP strains during method development was plausible.

Inactivation of Escherichia coli and Shigella in acidic fruit and vegetable juices by peroxidase systems.

AIMS: To study the bactericidal properties of the lactoperoxidase (LPER)-thiocyanate and soybean peroxidase (SBP)-thiocyanate systems at low pH, their efficiency for inactivation of Escherichia coli and Shigella in acidic fruit and vegetable juices, their effect on colour stability of the juices and interaction with ascorbic acid. METHODS AND RESULTS: Three-strain cocktails of E. coli and Shigella spp. in selected juices were supplemented with the LPER or SBP system. Within 24 h at 20 degrees C, the LPER system inactivated both cocktails by > or = 5 log10 units in apple, 2-5 log10 units in orange and < or = 1 log10 unit in tomato juices. In the presence of SBP, browning was significant in apple juice and white grape juice, slight in pink grape juice and absent in orange or tomato juice. Ascorbic acid protected E. coli and Shigella against inactivation by the LPER system, and peroxidase systems significantly reduced the ascorbic acid content of juices. CONCLUSIONS: Our results suggest a different specificity of LPER and SBP for SCN-, phenolic substrates of browning and ascorbic acid in acidic juices. The LPER system appeared a more appropriate candidate than the SBP system for biopreservation of juices. SIGNIFICANCE AND IMPACT OF THE STUDY: This work may open perspectives towards the development of LPER or other peroxidases as biopreservatives in acidic foods.

Combinations of pulsed white light and UV-C or mild heat treatment to inactivate conidia of Botrytis cinerea and Monilia fructigena.

The use of pulses of intense white light to inactivate conidia of the fungi Botrytis cinerea and Monilia fructigena, responsible for important economical losses during postharvest storage and transport of strawberries and sweet cherries, was investigated in this study. In the first stage, a light treatment applying pulses of 30 micros at a frequency of 15 Hz was investigated, resulting in a treatment duration varying from 1 to 250 s. The conidia of both fungi showed similar behaviour to pulsed light, with a maximal inactivation of 3 and 4 log units for B. cinerea and M. fructigena, respectively. The inactivation of the conidia increased with increasing treatment intensity, but no complete inactivation was achieved. The sigmoidal inactivation pattern obtained by the pulsed light treatment was described using a modification of the model of Geeraerd et al. [Int. J. Food Microbiol. 59 (2000) 185]. Hereto, the shoulder length was incorporated explicitly and relative values for the microbial populations were used. In the second stage, combinations of light pulses and ultraviolet-C or heat were applied. The UV light used in the experiments is the short-wave band or UV-C, running from 180 to 280 nm with a peak at 254 nm (UV-B runs from 280 to 320 nm and UV-A from 320 to 380 nm). The UV-C doses were 0.025, 0.05 and 0.10 J/cm(2), and the temperatures for the thermal treatment ranged from 35 to 45 degrees C during 3-15 min. When combining UV-C and light pulses, there was an increase in inactivation for both B. cinerea and M. fructigena, and synergism was observed. There was no effect of the order of the treatments. For the heat-light pulses combination, there was a difference between both fungi. The order of the treatments was highly significant for B. cinerea, but not for M. fructigena. Combining heat and light treatments improved the inactivation, and synergism between both methods was again observed. Complete inactivation of M. fructigena conidia was obtained after, e.g., a 40-s pulsed light treatment and 15 min at 41 degrees C, or after an 80-s light treatment and 10 min at 41 degrees C.

Using survival analysis to investigate the effect of UV-C and heat treatment on storage rot of strawberry and sweet cherry.

Ultraviolet light and heat treatment are proposed as alternative techniques for the use of chemicals to reduce the development of the spoilage fungi Botrytis cinerea and Monilinia fructigena on strawberry and sweet cherry, respectively, during storage. In order to investigate the effect of both physical techniques on microbial inactivation and on fruit quality, inoculated berries were subjected to different temperatures (40-48 degrees C) and UV-C doses (0.05-1.50 J/cm2). For each condition, 20 berries were used. After the treatment, fungal growth, visual damage (holes, stains) and fruit firmness were evaluated during a period of 10 days. The experimental data were analysed statistically using survival analysis techniques. Fungal growth on strawberries was significantly retarded using UV-C doses of 0.05 J/cm2 and higher. The same treatment had no significant effect when applied to cherries. The highest doses (1.00 and 1.50 J/cm2) had a negative effect on the calyx of the strawberry, causing browning and drying of the leaves. No beneficial effect of a low temperature treatment (40-48 degrees C) on the shelf life of strawberries was observed, but fungal development on cherries was retarded at temperatures of 45 and 48 degrees C. These temperatures caused severe damage on strawberries (soft stains, holes, decreased firmness), but had no influence on the quality of sweet cherries.

Inactivation of conidia of Botrytis cinerea and Monilinia fructigena using UV-C and heat treatment.

The effect of UV-C (lambda = 254 nm) and heat treatment was investigated on the inactivation of conidia of Botrytis cinerea and Monilinia fructigena, two major postharvest spoilage fungi of strawberries and cherries, respectively. Both fungi were grown at 21 degrees C in the dark and conidia were isolated after 1 week by washing the mycelium with a mild detergent solution. After filtration and resuspension in phosphate buffer to a titer of 10(5) to 10(6) cfu/ml, the conidia were subjected to different treatments. The applied UV-C doses varied from 0.01 to 1.50 J/cm2, and the conditions for the thermal treatment were 3, 5, 10, 15 and 20 min at temperatures ranging from 35 to 48 degrees C. Both techniques were applied individually and in combination. Spore inactivation increased with increasing intensity of single treatments. No surviving spores of B. cinerea were observed after 15 min at 45 degrees C or an UV-C treatment of 1.00 J/cm2. M. fructigena was more sensitive and a thermal treatment of 3 min at 45 degrees C or an UV-C treatment of 0.50 J/cm2 resulted in complete spore inactivation. Combination of both techniques reduced the required intensity of the treatment for inactivation of both fungi. The order of the applications had a significant effect on the degree of inactivation. The inactivation of B. cinerea conidia was greater when the heat treatment came first, and for M. fructigena, most inactivation was achieved when the heat treatment was preceded with an UV-C irradiation.

Role of the endothelium and blood stasis in the development of varicose veins.

Today, chronic venous insufficiency affects millions of people but the investigation of veins and of venous diseases is still very poor. Additionally, the mechanism of the occurrence of varicose veins is not understood. Blood stasis is often associated with these pathological situations and we propose that resulting ischemic conditions can trigger the endothelium to release inflammatory mediators and growth factors. On one hand, the inflammatory mediators will recruit and activate neutrophils, which then infiltrate the venous wall and damage components of the extracellular matrix. On the other hand, growth factors induce smooth muscle cell migration, proliferation and de-differentiation into the synthetic phenotype, all together leading to the formation of neointima. These processes, being repeated over time, would eventually lead to alterations of the venous wall as observed in varicose veins. Venotropic drugs are used to treat chronic venous insufficiency. They are able to increase venous tone and to decrease vein and capillary permeability but they are also able to protect the endothelial cells against ischemia. Indeed, they target complexes of the mitochondrial respiratory chain and maintain ATP production during hypoxia. Hence, the cells are resistant to ischemia and do not release inflammatory mediators and growth factors. These drugs should thus be able to prevent the alterations of the venous wall induced by blood stasis.

Effect of venotropic drugs on the respiratory activity of isolated mitochondria and in endothelial cells.

Several drugs used in the treatment of chronic peripheral ischaemic and venous diseases, i.e. aescine, Cyclo 3, Ginkor Fort, hydroxyethylrutosides, naftidrofuryl, naphthoquinone and procyanidolic oligomers, were tested on the mitochondrial respiratory activity. The results show that all these drugs protected human endothelial cells against the hypoxia-induced decrease in ATP content. In addition, they all induced a concentration-dependent increase in respiratory control ratio (RCR) of liver mitochondria pre-incubated with the drugs for 60 min. The drugs were divided into two groups according to their effects. The first group (A), comprising aescine, Ginkor Fort, naftidrofuryl and naphthoquinone, increased RCR by decreasing state 4 respiration rate. The second group of drugs (B), comprising hydroxyethylrutosides, procyanidolic oligomers and Cyclo 3, increased RCR by increasing state 3 respiration rate. The drugs of group A were able to prevent the inhibition of complexes I and III respectively by amytal and antimycin A while the first two drugs of group B increased adenine nucleotide translocase activity. Cyclo 3 inhibited the carbonylcyanide m-chlorophenyl hydrazone (mCCP)-induced uncoupling of mitochondrial respiration. None of these seven drugs could protect complexes IV and V, respectively, from inhibition by cyanide and oligomycin. When tested on endothelial cells the drugs of group A, in contrast to group B, prevented the decrease in ATP content induced by amytal or antimycin A. The present results suggest that the protective effects on mitochondrial respiration activity by these venotropic drugs may explain their protective effect on the cellular ATP content in ischaemic conditions and some of their beneficial therapeutic effect in chronic vascular diseases.

Increase in circulating endothelial cells in patients with primary chronic venous insufficiency: protective effect of Ginkor Fort in a randomized double-blind, placebo-controlled clinical trial.

One possible mechanism that accounts for the alterations observed in varicose veins is the activation of endothelial cells by ischemia occurring in the leg veins during blood stasis and the cascade of reactions that follows. Because in vitro data suggest that endothelium alteration is a key event in the development of the pathology, it was important to confirm this hypothesis in patients. We used the number of circulating endothelial cells detached from the vascular wall as a criterion of the endothelium injury. We first compared the number of circulating endothelial cells (CECs) in patients with chronic venous insufficiency (CVI) with those of a control population. A twofold increase in the CEC count (1,001+/-127 CEC/ml of plasma compared with 514+/-82 CECs/ml) was observed in CVI patients, which indeed suggests an alteration of the endothelium in this disease. Second, the protective effect of a venotropic drug, Ginkgo biloba extract, troxerutine, and heptaminol (Ginkor Fort), was tested by a randomized double-blind, placebo-controlled clinical trial. In the active-treatment group, the mean values of the CEC count decreased by 14.5% after a 4-week treatment, whereas in the placebo group, the decrease was less (8.4%). The decrease from week 0 to the end of treatment was significantly higher in the active-treatment group than in the placebo group. These results confirm the important role of the endothelium alterations in the development of varicose veins and suggest a potential beneficial action of a venotropic drug on the venous wall.

Effect of Ruscus extract and hesperidin methylchalcone on hypoxia-induced activation of endothelial cells.

BACKGROUND: Ruscus aculeatus extract and the flavonoid hesperidin methylchalcone (HMC) are drugs used in the treatment of chronic venous insufficiency. METHODS: In the present study, we investigated their effects on the activation of endothelial cells by hypoxia, a condition which mimics venous blood stasis. RESULTS: We observed that Ruscus extract was able to inhibit the activation of endothelial cells by hypoxia: the decrease in ATP content, the activation of phospholipase A2 as well as the subsequent increase in neutrophil adherence with a maximal protection obtained at 50 microg/ml. HMC was also able to inhibit the hypoxia-induced decrease in ATP content. Furthermore, the effects of Ruscus extract and of HMC on this decrease seem to be additive. CONCLUSIONS: The biochemical mechanism evidenced in this work might explain some of the beneficial therapeutic effects of these products in the treatment of chronic venous insufficiency patients.

Effect of Ginkor Fort on hypoxia-induced neutrophil adherence to human saphenous vein endothelium.

This study was performed to evaluate the effects of Ginkor Fort, a venotropic drug composed of Ginkgo biloba extract, troxerutine, and heptaminol, on neutrophil adherence to the endothelium of saphenous veins. When saphenous veins were incubated 2 h in hypoxic conditions, they showed a five- to sixfold increase in neutrophil adherence to the endothelium. Ginkor Fort at 0.3 mg/ml was able to inhibit this increase by 69%. These results were confirmed by observations in scanning electron microscopy. Ginkor Fort also inhibited the subsequent activation of these neutrophils, as evidenced by the inhibition of superoxide anion release. The biochemical mechanism of this inhibition of neutrophil adherence was studied on endothelial cells in culture. We observed that Ginkor Fort was able to inhibit the different steps of the activation of endothelial cells by hypoxia: the activation of phospholipase A2 and the decrease in adenosine triphosphate (ATP) content. By preventing the first step of the activation cascade, the decrease in ATP content, Ginkor Fort blocks the subsequent increase in neutrophil adherence as well as neutrophil activation. The biochemical mechanism evidenced in this work might explain the beneficial effect of this drug in the treatment of patients with chronic venous insufficiency.

Protection of hypoxia-induced ATP decrease in endothelial cells by ginkgo biloba extract and bilobalide.

Due to their localization at the interface between blood and tissue, endothelial cells are the first target of any change occurring within the blood, and alterations of their functions can seriously impair organs. During hypoxia, which mimics in vivo ischemia, a cascade of events occurs in the endothelial cells, starting with a decrease in ATP content and leading to their activation and release of inflammatory mediators. EGb 761 and one of its constituents, bilobalide, were shown to inhibit the hypoxia-induced decrease in ATP content in endothelial cells in vitro. Under these conditions, glycolysis was activated, as evidenced by increased glucose transport, as well as increased lactate production. Bilobalide was found to increase glucose transport under normoxic but not hypoxic conditions. In addition, EGb and bilobalide prevented the increase in total lactate production observed after 60 min of hypoxia. However, after 120 min of hypoxia, the total lactate production was similar under normoxic and hypoxic conditions, and both compounds increased this production. These results indicate that glycolysis slowed down between the 60th and 120th minute of hypoxia, while EGb and bilobalide delayed the onset of glycolysis activation. In another experimental model, both compounds were shown to increase the respiratory control ratio of mitochondria isolated from liver of rats treated orally. Since ischemia is known to uncouple mitochondria, the protection of ATP content and the delay in glycolysis activation observed during hypoxia in the presence of EGb 761 or bilobalide is best explained by a protection of mitochondrial respiratory activity, at least during the first 60 min of hypoxia incubation. Both products retain the ability to form ATP, thereby reducing the cell's need to induce glycolysis, probably by preserving ATP regeneration by mitochondria as long as oxygen is available.

Importance of Se-glutathione peroxidase, catalase, and Cu/Zn-SOD for cell survival against oxidative stress.

Eukaryotic cells have to constantly cope with highly reactive oxygen-derived free radicals. Their defense against these free radicals is achieved by natural antioxidant molecules but also by antioxidant enzymes. In this paper, we review some of the data comparing the efficiency of three different antioxidant enzymes: Cu/Zn-superoxide dismutase (Cu/Zn-SOD), catalase, and selenium-glutathione peroxidase. We perform our comparison on one experimental model (human fibroblasts) where the activities of these three antioxidant enzymes have been modulated inside the cells, and the repercussion of these changes was investigated in different conditions. We also focus our attention on the protecting role of selenium-glutathione peroxidase, because this enzyme is very rarely studied due to the difficulties linked to its biochemical properties. These studies evidenced that all three antioxidant enzymes give protection for the cells. They show a high efficiency for selenium-glutathione peroxidase and emphasize the fact that each enzyme has a specific as well as an irreplaceable function. They are all necessary for the survival of the cell even in normal conditions. In addition, these three enzymes act in a cooperative or synergistic way to ensure a global cell protection. However, optimal protection is achieved only when an appropriate balance between the activities of these enzymes is maintained. Interpretation of the deleterious effects of free radicals has to be analyzed not only as a function of the amount of free radicals produced but also relative to the efficiency and to the activities of these enzymatic and chemical antioxidant systems. The threshold of protection can indeed vary dramatically as a function of the level of activity of these enzymes.

[A comparative study of the protective effect of different phlebotonic agents on endothelial cells in hypoxia]. / Etude comparative de l'effet protecteur des différents phlébotoniques sur les cellules endothéliales en hypoxie.

Numerous reported findings indicate that the etiology of venous diseases is multifactorial. One of the chief factors is certainly stasis of blood in the veins of the lower limbs during long periods spent standing up. This stasis causes tissue hypoxia which first affects the venous wall. Because of their location at the interface between blood and vein wall and because of their fragility, endothelial cells are the first to suffer from the lack of oxygen. With the aim of understanding these events, the authors have developed a model of endothelial cells in culture subjected to hypoxia in vitro which mimics the conditions encountered clinically. This model has enabled us to test various drugs commonly used in venous disease. These included GbE, the active ingredient of GINKOR FORT, diosmin and procyanidol oligomers. It was thus shown that only GbE was not toxic to endothelial cells. GbE was also found to be capable of effectively protecting cells exposed to hypoxia. Protection under the influence of diosmin was obtained only at concentrations very close to toxic doses. In contrast, procyanidol oligomers offered no protection. The protective effect of GbE is believed to be due to the action of terpenes on the energy metabolism of the cell.

[A comparative study of the protective effect of various phlebotonic agents on hypoxic endothelial cells]. / Etude comparative de l'effet protecteur des différents phlébotoniques sur les cellules endothéliales en hypoxie.

Many findings indicate that the etiology of venous disease is multifactorial. One of the chief factors is certainly the stasis of blood in the lower limbs during long periods of standing. This stasis causes tissue hypoxia which first affects the venous wall. Because of their site at the blood/vein wall interface as well as their fragility, endothelial cells are the first to suffer from lack of oxygen. In order to understand these events, the authors have developed a model of endothelial cells in culture subjected to hypoxia in vitro which imitates conditions encountered clinically. This model was used to test different drugs commonly used in venous pathology. These included GbE, the active ingredient of GINKOR FORT, diosmine and procyanidolic oligomers. It was thus shown that only GbE was not toxic to endothelial cells. Furthermore, GbE was capable of effectively protecting cells subjected to hypoxia. Protection with diosmine was obtained only at concentrations very close to toxic doses. In contrast, procyanidolic oligomers afforded no protection. The protective effect of GbE is believed to be due to the action of terpenes on cellular energy metabolism.

Importance of a threshold for error accumulation in cell degenerative processes. I. Modulation of the threshold in a model of free radical-induced cell degeneration.

Antioxidant enzymes (catalase, superoxide dismutase and glutathione peroxidase) have been injected into human fibroblasts exposed to 2 atm O2 in order to test if the threshold of oxidative damage versus antioxidant defenses could be modulated and if the damage remains reversible beyond the threshold. Cell damage was estimated by thymidine incorporation and cell survival curves. The proportion of dividing cells, measured by thymidine incorporation, rapidly decreased after O2 incubation: no cells could divide after 15 h of hyperoxia. However, cells incubated for a short time and injected with a high concentration of any of the three enzymes divided like non-oxygen-incubated cells: the enzymes could protect the cells against their loss of division potential. However, when cells were incubated for a longer period and/or when the injected enzyme concentration was lower, cells were either less or not protected and could no longer divide. These results suggest the presence of a threshold for the oxidative damage which cannot be totally repaired and which impairs the cell division; this threshold can, however, be modulated by supplementation of antioxidant enzymes, glutathione peroxidase being the most efficient.