A further search was performed for studies analysing re-infection or late relapse rates in cohorts achieving SVR24. Results: There were results available from 15,067 patients with mono-HCV infection, 4987 patients with HCV and cirrhosis at baseline, 1170 patients who had already been transplanted, and 2085 with HIV-HCV co-infection.

Table 1 shows the relative risk of HCC and death for patients achieving SVR versus not achieving SVR after treatment (predominantly with pegylated interferon plus ribavirin). During follow up after treatment, the annual absolute risk of death (all cause) was 0.71% for HCV mono-infected patients Y-27632 ic50 achieving SVR versus 1.68% for those not achieving SVR. Overall, the 10-year mortality rate was 6.88% in patients achieving SVR and 15.59% in those not achieving SVR; 10-year mortality rates by subgroup are shown in Table 1. In five studies of 3123 patients, the risk of liver transplantation was reduced by 90% (RR 0.10, 95% CI 0.04-0.23) for patients with SVR versus non-SVR, however the absolute annual risk of transplantation was low in both groups (0.03%

vs 1.15% in SVR and non-SVR groups respectively). After SVR24, the annual risk of re-infection or late relapse was 1.4% in mono-infected patients and 8.2% in HIV-HCV co-infected patients. Conclusions: Achieving SVR after treatment for Hepatitis C was associated with 68-79% reductions in click here the risk of HCC, 60-84% reductions in the risk of death and a 90% reduction in the risk of liver transplantation, compared with patients who did not achieve SVR. However annual absolute risk reductions

selleck inhibitor in mortality were small (1%) in mono-infected patients and there was a significant risk of subsequent re-infection after SVR in some studies. Disclosures: Andrew M. Hill – Consulting: Janssen The following people have nothing to disclose: Jawaad Saleem, Katherine A. Heath, Bryony Simmons The approval of direct-acting antivirals (DAA), such as sofosbu-vir (SOF) and simeprevir (SIM), in late 2013 created a major paradigm shift in the treatment of chronic hepatitis C. The aim of the present study was to evaluate the safety and efficacy of DAAs utilized in clinical practice. METHODS: HCV-TARGET (HCVT) is a longitudinal observational study of patients treated with DAAs at academic (n=43) and community medical centers (n=13) in North America (n=51) and Europe (n=5). HCVT utilizes a unique centralized data abstraction core along with independent data monitors who systematically review data entries for completeness and accuracy. Demographic, clinical, adverse events, and virological data are collected throughout treatment and post-treatment follow-up from enrolled patients. RESULTS: Since January 2014, 1,950 patients have been consented and 1,107 patients have started treatment and are included in the current analysis (excluding n=6 pts receiving PEG/RBV alone or with telaprevir or boceprevir) .

Moreover, the Expression

of key co-stimulatory and co-regulatory molecules on DC and Treg were examined by flow cytomeric analysis. Results: our findings show that everolimus-treated liver transplant patients maintain a stable DC subset distribution and phenotype. Thus, expression of co-stimulatory and co-regulatory molecule (CD86, CD83, PD-L1 and ICOS-L) did not differ between the 2 groups. Moreover, expression on DC subsets of HLA-DR and human leukocyte antigen (HLA)-G, a non-classical HLA class I molecule, and of its receptor, the immunoglobulin (Ig)-like transcript (ILT)-4 did not Roxadustat clinical trial differ between the mTOR and CNI groups. Notably, however, expression of the ectonucleoti-dase CD39 was significantly higher

on myeloid DC in patients taking everolimus compared with the CNI. Notably, selleck chemical in the ever-olimus group the incidence of Treg was significantly higher and the expression of Programmed death-1 (PD-1) on Treg was significantly lower as compared with CNI group. Conclusions: this preliminary study provides new information about how mTOR inhibitor-based immnosuppression may influence peripheral innate and adaptive immune cells in liver transplant patients. Our findings also point out possible new biomarkers of liver graft acceptance which could be monitored after transplantation. Disclosures: The following people have nothing to disclose: Antonino Castellaneta, Antonio Massaro, María Rendina, Francesca D’Errico, Sonia Carparelli, Angus W. Thomson, Alfredo Di Leo Background Progression of fibrosis after liver transplantation (LT) is associated with a worse outcome. One study suggested that abusive drinking after LT for pure alcoholic cirrhosis was associated selleck chemicals llc with liver fibrosis progression. Aims (1) to evaluate alcohol consumption in France after LT for alcoholic cirrhosis using

carbohydrate deficient transferrin (CDT); (2) To assess fibrosis progression using 2 non-invasive methods. Methods Liver fibrosis progression was assessed using FibroTest (FT, Biopredictive, France) and FibroScan (FS, Echosens, France) in all patients who underwent LT for pure alcoholic cirrhosis in our center, on the same day, once a year. Discordances between the 2 methods were resolved by consensus, after repeating the tests and analysing the files of each patients (clinical examination, biology, ultrasound exam). Excessive drinking was defined by a CDT>1.8%. Parameters of metabolic syndrome were assessed each year. Results Overall, 93 patients were transplanted in La Pitie-Salpetriere (Paris, France) for pure alcoholic cirrhosis, all other causes of hepatopathy being ruled out, between February 2000 and June 2012. Among them, 9 died within the first year after LT, and 9 were not evalu ated (lost of follow-up or residing in a foreign country).

Moreover, the Expression

of key co-stimulatory and co-regulatory molecules on DC and Treg were examined by flow cytomeric analysis. Results: our findings show that everolimus-treated liver transplant patients maintain a stable DC subset distribution and phenotype. Thus, expression of co-stimulatory and co-regulatory molecule (CD86, CD83, PD-L1 and ICOS-L) did not differ between the 2 groups. Moreover, expression on DC subsets of HLA-DR and human leukocyte antigen (HLA)-G, a non-classical HLA class I molecule, and of its receptor, the immunoglobulin (Ig)-like transcript (ILT)-4 did not Hedgehog inhibitor differ between the mTOR and CNI groups. Notably, however, expression of the ectonucleoti-dase CD39 was significantly higher

on myeloid DC in patients taking everolimus compared with the CNI. Notably, Selleckchem GPCR Compound Library in the ever-olimus group the incidence of Treg was significantly higher and the expression of Programmed death-1 (PD-1) on Treg was significantly lower as compared with CNI group. Conclusions: this preliminary study provides new information about how mTOR inhibitor-based immnosuppression may influence peripheral innate and adaptive immune cells in liver transplant patients. Our findings also point out possible new biomarkers of liver graft acceptance which could be monitored after transplantation. Disclosures: The following people have nothing to disclose: Antonino Castellaneta, Antonio Massaro, María Rendina, Francesca D’Errico, Sonia Carparelli, Angus W. Thomson, Alfredo Di Leo Background Progression of fibrosis after liver transplantation (LT) is associated with a worse outcome. One study suggested that abusive drinking after LT for pure alcoholic cirrhosis was associated selleck screening library with liver fibrosis progression. Aims (1) to evaluate alcohol consumption in France after LT for alcoholic cirrhosis using

carbohydrate deficient transferrin (CDT); (2) To assess fibrosis progression using 2 non-invasive methods. Methods Liver fibrosis progression was assessed using FibroTest (FT, Biopredictive, France) and FibroScan (FS, Echosens, France) in all patients who underwent LT for pure alcoholic cirrhosis in our center, on the same day, once a year. Discordances between the 2 methods were resolved by consensus, after repeating the tests and analysing the files of each patients (clinical examination, biology, ultrasound exam). Excessive drinking was defined by a CDT>1.8%. Parameters of metabolic syndrome were assessed each year. Results Overall, 93 patients were transplanted in La Pitie-Salpetriere (Paris, France) for pure alcoholic cirrhosis, all other causes of hepatopathy being ruled out, between February 2000 and June 2012. Among them, 9 died within the first year after LT, and 9 were not evalu ated (lost of follow-up or residing in a foreign country).

This hypothesis is strengthened by the fact that the two selected substitutions, sS143T and sM197T, are located at the external side of HBsAg, within known immunodominant epitopes. However, this was noted in only 1 patient in this study. Adefovir dipivoxil is still widely used worldwide, alone or in combination with lamivudine. As shown in this study, variants with amino acid substitutions histone deacetylase activity known to confer resistance to various nucleoside/nucleotide analogs, including adefovir, can be detected in a substantial proportion of treatment-naïve patients with CHB. Larger scale studies are now required to determine

whether baseline testing with UDPS will be useful to orientate HBV treatment strategies. BAY 73-4506 datasheet In addition, next-generation sequencing methods, such as UDPS, could be of considerable interest for early diagnosis of viral resistance during antiviral therapy. Indeed, with our approach, resistance could be diagnosed at approximately the same time as with cloning and sequencing (thus considerably earlier than with population sequencing), in a user-friendly and rapid way, compatible

with clinical practice (data not shown). This will be facilitated in the future when the costs are reduced and the technology becomes easily available through specialized platforms. In conclusion, using an original software package for analyzing viral sequences generated by UDPS and other next-generation sequencing methods in the context of antiviral resistance, (1) we showed that substitutions conferring HBV

resistance to nucleoside/nucleotide analogs preexist in patients who have never been exposed to these drugs, (2) we characterized the complex and heterogeneous dynamics of adefovir-resistant viral populations in a group of HBV-infected patients in whom resistance emerged during long-term adefovir therapy, and (3) we identified thus far unknown amino acid substitutions that appeared to play an important role in HBV resistance to adefovir. These findings will also be helpful for understanding resistance to tenofovir, which shows cross-resistance click here with adefovir in vitro. Our findings imply that next-generation sequencing data analysis will have a number of applications in viral resistance assessment, as we recently reported with hepatitis C virus and human immunodeficiency virus.[29, 30] The authors thank Thierry Ravard for his help with mathematical modeling and Françoise Roudot-Thoraval for her help with statistical tests, as well as Katyna Borroto-Esoda and Manh-Tong Dao. Additional Supporting Information may be found in the online version of this article. “
“Invasive fungal infection (IFI) related to surgery in elderly patients is often associated with high morbidity and mortality.

Recent works demonstrating buy Ivacaftor a strong protective effect of the bile acids receptor FXR and TGR5 in a mice models of atheroma1, 2 could change this old rule in the not so distant future, but so far no evidences exists in humans. The level of activation of these receptors depends on the type of bile acids that activate them.3 We designed a pilot

prospective and observational study conducted between June 2010 and September 2010 to search for variations in the bile acid pool composition between 2 populations: patients with or without coronary atheroma. We determined the serum concentrations of cholic, chenodeoxycholic, deoxycholic, and lithocholic acids in a fasting blood sample in all consecutive patients undergoing coronary angiograms in the cathlab unit of Cochin Hospital. Applying very restrictive exclusions criteria to avoid artificial variations of the bile acid pool (post-cardiac arrest; nonfasting states; hepatic disease; treatment with antimicrobials, corticosteroids, statins, or fibrates) of 393 screened patients, 44 met the criteria and were divided between 27 with (group A) and 17 without (group B) angiographically visible coronary atheromas. Except for more males in group A, the groups were comparable. The serum lithocholic acid (LCA) concentration was

significantly Vismodegib research buy lower in group A (median 0.03 μmol/L; interquartile range 0.02–0.05) than in group B (0.08 μmol/L; interquartile range 0.05–0.11; P = 0.015) (Fig. 1). In the multivariate analysis, LCA was the only predictor of coronary atheroma independently of patient gender (odds ratio 2.41 per 0.05 decrease; 95% confidence interval 1.11-5.25; P = 0.027). Although the populations were small, we believe this observation connecting LCA and coronary atheroma is a field worth investigating further, as LCA is the most powerful activator of TGR5.3 A study targeting the proinflammatory mechanism acting in atheroma plaque evidenced that the activation

of the TGR5 receptor significantly limits the formation of plaques check details in LDL−/− mice by decreasing the inflammation inside the plaque and the proinflammatory cytokines secretion by macrophages. This raises the hypothesis that lowering the most prominent activator of TGR5 is likely to lower the protection against plaque development in humans. Further studies are needed to confirm this observation, to better understand the origin and the extent to which a decrease in LCA is implicated in the development of coronary atheromatous plaques, and to maybe put us hepatologists and cardiologists more often around the same table. Henri Duboc M.D.† ‡, Hélène Aelion M.D.*, Dominique Rainteau Ph.D.‡, Sylvie Rajca M.D.‡, Harry Sokol M.D., Ph.D.‡, Lydie Humbert‡, Dominique Farabos‡, Benoit Coffin M.D., Ph.D.†, Simon Weber M.D.

Recent works demonstrating Roscovitine ic50 a strong protective effect of the bile acids receptor FXR and TGR5 in a mice models of atheroma1, 2 could change this old rule in the not so distant future, but so far no evidences exists in humans. The level of activation of these receptors depends on the type of bile acids that activate them.3 We designed a pilot

prospective and observational study conducted between June 2010 and September 2010 to search for variations in the bile acid pool composition between 2 populations: patients with or without coronary atheroma. We determined the serum concentrations of cholic, chenodeoxycholic, deoxycholic, and lithocholic acids in a fasting blood sample in all consecutive patients undergoing coronary angiograms in the cathlab unit of Cochin Hospital. Applying very restrictive exclusions criteria to avoid artificial variations of the bile acid pool (post-cardiac arrest; nonfasting states; hepatic disease; treatment with antimicrobials, corticosteroids, statins, or fibrates) of 393 screened patients, 44 met the criteria and were divided between 27 with (group A) and 17 without (group B) angiographically visible coronary atheromas. Except for more males in group A, the groups were comparable. The serum lithocholic acid (LCA) concentration was

significantly MG-132 supplier lower in group A (median 0.03 μmol/L; interquartile range 0.02–0.05) than in group B (0.08 μmol/L; interquartile range 0.05–0.11; P = 0.015) (Fig. 1). In the multivariate analysis, LCA was the only predictor of coronary atheroma independently of patient gender (odds ratio 2.41 per 0.05 decrease; 95% confidence interval 1.11-5.25; P = 0.027). Although the populations were small, we believe this observation connecting LCA and coronary atheroma is a field worth investigating further, as LCA is the most powerful activator of TGR5.3 A study targeting the proinflammatory mechanism acting in atheroma plaque evidenced that the activation

of the TGR5 receptor significantly limits the formation of plaques selleckchem in LDL−/− mice by decreasing the inflammation inside the plaque and the proinflammatory cytokines secretion by macrophages. This raises the hypothesis that lowering the most prominent activator of TGR5 is likely to lower the protection against plaque development in humans. Further studies are needed to confirm this observation, to better understand the origin and the extent to which a decrease in LCA is implicated in the development of coronary atheromatous plaques, and to maybe put us hepatologists and cardiologists more often around the same table. Henri Duboc M.D.† ‡, Hélène Aelion M.D.*, Dominique Rainteau Ph.D.‡, Sylvie Rajca M.D.‡, Harry Sokol M.D., Ph.D.‡, Lydie Humbert‡, Dominique Farabos‡, Benoit Coffin M.D., Ph.D.†, Simon Weber M.D.

(LE 5, GR C1) Rifampicin is effective against dermal pruritus in PBC patients. (LE 1a, GR B) Osteoporosis is frequently observed in patients with PBC because intestinal absorption of fat-soluble vitamins is disturbed due to reduced secretion of bile acids, and PBC is common in middle-aged and postmenopausal women. For prevention of osteoporosis, abundant oral intake of calcium (1 to 1.2 g/day) and vitamin D (plentiful in fish and mushrooms) and weight-bearing exercise are recommended, and medical treatment should be given if necessary. Bisphosphonates, bioactive

vitamin D3 agents, and vitamin K2 are prescribed. Among bisphosphonates, alendronate improves bone density more than etidronate. Nevertheless, there is no evidence selleck that alendronate suppresses bone fracture. Administration once weekly is preferable to daily administration. Alendronate is contraindicated for cases with esophageal stenosis due to sclerotherapy for esophageal varices. selleck chemical Vitamin D3 and vitamin K2 formulations have frequently been prescribed for PBC in Japan. Both drugs have been proven to be effective for osteoporosis itself, and are regarded as Grade B in guidelines for the prevention and treatment of osteoporosis.

Recommendations: It is desirable to start treatment for the prevention of fractures in cases with a T score below −1.5. (LE 4, GR C1) Alendronate improves bone density in PBC patients. (LE 1b, GR A) Although there is scarce evidence in PBC patients, vitamin D3 and vitamin K2 formulations can be effective for osteoporosis. (LE 1b, GR C1) Hypercholesterolemia is likely to develop in PBC due to cholestasis. Xanthoma is seen around the eyelids. No specific treatment for hypercholesterolemia in PBC is required in most cases,

while bezafibrate is expected to be effective for both PBC and hypercholesterolemia. Sicca syndrome, a major symptom of Sjögren’s syndrome, is frequently complicated with PBC. The diagnosis of Sjögren’s syndrome should be made by detection of serum anti-SS-A/SS-B antibodies, presence of corneal erosion, and lip biopsy if necessary. Artificial lachrymal fluids are indicated for eye symptoms. If the response is not favorable, pilocarpine hydrochloride and cevimeline hydrochloride hydrate are used under the guidance of ophthalmologists. As for oral symptoms, artificial saliva check details should be used first, and pilocarpine hydrochloride and cevimeline hydrochloride hydrate can also be prescribed. Recommendations: Cevimeline hydrochloride and pilocarpine hydrochloride may be effective for xerostomia in PBC, although there are no studies evaluating their potential to alleviate the symptoms occurring in PBC patients with concurrent Sjögren’s syndrome. (LE 6, GR B) Patients with PBC frequently experience cholestasis, comorbid autoimmune diseases, and symptoms associated with liver injury and cirrhosis. Prevention and management of these symptoms are required.

(LE 5, GR C1) Rifampicin is effective against dermal pruritus in PBC patients. (LE 1a, GR B) Osteoporosis is frequently observed in patients with PBC because intestinal absorption of fat-soluble vitamins is disturbed due to reduced secretion of bile acids, and PBC is common in middle-aged and postmenopausal women. For prevention of osteoporosis, abundant oral intake of calcium (1 to 1.2 g/day) and vitamin D (plentiful in fish and mushrooms) and weight-bearing exercise are recommended, and medical treatment should be given if necessary. Bisphosphonates, bioactive

vitamin D3 agents, and vitamin K2 are prescribed. Among bisphosphonates, alendronate improves bone density more than etidronate. Nevertheless, there is no evidence ICG-001 molecular weight that alendronate suppresses bone fracture. Administration once weekly is preferable to daily administration. Alendronate is contraindicated for cases with esophageal stenosis due to sclerotherapy for esophageal varices. Alpelisib Vitamin D3 and vitamin K2 formulations have frequently been prescribed for PBC in Japan. Both drugs have been proven to be effective for osteoporosis itself, and are regarded as Grade B in guidelines for the prevention and treatment of osteoporosis.

Recommendations: It is desirable to start treatment for the prevention of fractures in cases with a T score below −1.5. (LE 4, GR C1) Alendronate improves bone density in PBC patients. (LE 1b, GR A) Although there is scarce evidence in PBC patients, vitamin D3 and vitamin K2 formulations can be effective for osteoporosis. (LE 1b, GR C1) Hypercholesterolemia is likely to develop in PBC due to cholestasis. Xanthoma is seen around the eyelids. No specific treatment for hypercholesterolemia in PBC is required in most cases,

while bezafibrate is expected to be effective for both PBC and hypercholesterolemia. Sicca syndrome, a major symptom of Sjögren’s syndrome, is frequently complicated with PBC. The diagnosis of Sjögren’s syndrome should be made by detection of serum anti-SS-A/SS-B antibodies, presence of corneal erosion, and lip biopsy if necessary. Artificial lachrymal fluids are indicated for eye symptoms. If the response is not favorable, pilocarpine hydrochloride and cevimeline hydrochloride hydrate are used under the guidance of ophthalmologists. As for oral symptoms, artificial saliva selleck should be used first, and pilocarpine hydrochloride and cevimeline hydrochloride hydrate can also be prescribed. Recommendations: Cevimeline hydrochloride and pilocarpine hydrochloride may be effective for xerostomia in PBC, although there are no studies evaluating their potential to alleviate the symptoms occurring in PBC patients with concurrent Sjögren’s syndrome. (LE 6, GR B) Patients with PBC frequently experience cholestasis, comorbid autoimmune diseases, and symptoms associated with liver injury and cirrhosis. Prevention and management of these symptoms are required.

4B). Therefore, Gal-1 promotes HepG2 cell adhesion through an integrin-mediated process involving PI3K and/or ERK1/2 signaling routes. To determine whether Gal-1 plays additional roles in liver physiology, we further determined its ability to modulate BC formation. When HepG2 cells, which represent a model of differentiated HCC cells for studying hepatocyte polarization, were cultured on coverslips, they acquired the polarized phenotype characterized by the appearance of BC between adjacent cells

in a time-dependent manner (Fig.5A,B). Notably, this effect was substantially enhanced after plating the cells for 24 hours in the presence of rGal-1 (7 μM). In fact, cell polarization significantly increased, GSK126 manufacturer reaching considerable click here levels after exposure to exogenous rGal-1 (15 ± 1 BC/100 cells versus control: 9 ± 1) for 48 hours. Moreover, maximal cell polarization was reached following exposure to rGal-1 for 72 hours, a time point that did not differ from control cell polarization. This effect also involved the carbohydrate recognition domain of Gal-1, because it was significantly prevented by pretreatment with 10 mM thiodigalactoside (TDG)

(Fig. 5C). However, when cells were cultured in the presence of rGal-3 (7 μM) for 48 hours, cell polarization was not significantly different with respect to controls, indicating that acceleration of cell polarization is a Gal-1–specific effect (Fig. 5C). To determine whether endogenous Gal-1 regulates the function of HCC cells, we assessed the

effects of Gal-1 overexpression this website on HepG2 cell polarization. Interestingly, HepG2-G2 cells showed an increase in cell polarization (153 ± 8%), which was considerably inhibited in the presence of TDG (Fig. 5C). These findings imply a novel unrecognized role for Gal-1 in accelerating HepG2 cell polarization and promoting BC development. To evaluate whether Gal-1–induced cell polarization is secondary to the observed effect on cell adhesion or, to the contrary, these are two separate effects, we first allowed cells adhere to coverslips for 4 hours. Then, we added exogenous rGal-1 or knocked down Gal-1 expression by way of siRNA-mediated silencing. After 48 hours, cell polarization was analyzed. When rGal-1 was added 4 hours after cell adhesion, no significant differences (120 ± 8%) were observed in cell polarization with respect to control cells (in the absence of rGal-1; 94 ± 15%) (Fig. 5D), suggesting that the presence of rGal-1 at the time of cell plating was necessary to promote cell polarization (156 ± 5%). On the other hand, siRNA-mediated Gal-1 silencing resulted in no significant differences in cell polarization (90 ± 5%) with respect to cells transfected with scrambled siRNA (104 ± 15%).

4B). Therefore, Gal-1 promotes HepG2 cell adhesion through an integrin-mediated process involving PI3K and/or ERK1/2 signaling routes. To determine whether Gal-1 plays additional roles in liver physiology, we further determined its ability to modulate BC formation. When HepG2 cells, which represent a model of differentiated HCC cells for studying hepatocyte polarization, were cultured on coverslips, they acquired the polarized phenotype characterized by the appearance of BC between adjacent cells

in a time-dependent manner (Fig.5A,B). Notably, this effect was substantially enhanced after plating the cells for 24 hours in the presence of rGal-1 (7 μM). In fact, cell polarization significantly increased, Selleckchem Target Selective Inhibitor Library reaching considerable GSI-IX chemical structure levels after exposure to exogenous rGal-1 (15 ± 1 BC/100 cells versus control: 9 ± 1) for 48 hours. Moreover, maximal cell polarization was reached following exposure to rGal-1 for 72 hours, a time point that did not differ from control cell polarization. This effect also involved the carbohydrate recognition domain of Gal-1, because it was significantly prevented by pretreatment with 10 mM thiodigalactoside (TDG)

(Fig. 5C). However, when cells were cultured in the presence of rGal-3 (7 μM) for 48 hours, cell polarization was not significantly different with respect to controls, indicating that acceleration of cell polarization is a Gal-1–specific effect (Fig. 5C). To determine whether endogenous Gal-1 regulates the function of HCC cells, we assessed the

effects of Gal-1 overexpression this website on HepG2 cell polarization. Interestingly, HepG2-G2 cells showed an increase in cell polarization (153 ± 8%), which was considerably inhibited in the presence of TDG (Fig. 5C). These findings imply a novel unrecognized role for Gal-1 in accelerating HepG2 cell polarization and promoting BC development. To evaluate whether Gal-1–induced cell polarization is secondary to the observed effect on cell adhesion or, to the contrary, these are two separate effects, we first allowed cells adhere to coverslips for 4 hours. Then, we added exogenous rGal-1 or knocked down Gal-1 expression by way of siRNA-mediated silencing. After 48 hours, cell polarization was analyzed. When rGal-1 was added 4 hours after cell adhesion, no significant differences (120 ± 8%) were observed in cell polarization with respect to control cells (in the absence of rGal-1; 94 ± 15%) (Fig. 5D), suggesting that the presence of rGal-1 at the time of cell plating was necessary to promote cell polarization (156 ± 5%). On the other hand, siRNA-mediated Gal-1 silencing resulted in no significant differences in cell polarization (90 ± 5%) with respect to cells transfected with scrambled siRNA (104 ± 15%).