Then the labeled cells were washed and incubated with anti-FITC-conjugated magnetic beads (Miltenyi Biotec). Positive cells were sorted using columns and a MACS kit (Miltenyi Biotec). Finally, the purities were tested (>90%). The purified γδ T cells were stimulated

with either IL-1β or IL-23 or the combination for 48 hours. The supernatants were collected for measurement of IL-17A. The remaining cells were directly stained for intracellular IL-17A either without additional stimulation or with phorbol-12-myristate-13-acetate (PMA, 50 ng/mL; Sigma-Aldrich), ionomycin (1 μg/mL; Sigma-Aldrich), and monensin (5 μg/mL; Sigma-Aldrich) for 5 hours. To measure IL-23 secretion by macrophages stimulated with HMGB1, peritoneal macrophages were harvested from TLR4+/+ mice or TLR4−/− mice 3 days after treatment with selleck kinase inhibitor 3% sodium thioglycolate. The cells were stimulated with HMGB1 (20 ng/mL, eBioscience) for 18 hours and the supernatant was BGB324 collected for IL-23 measurement. The concentrations of IL-17A, IL-23, IL-23p40, and HMGB1 were measured by a standard enzyme-linked immunosorbent

assay (ELISA). The following ELISA kits were used: IL-17A and IL-23p40 (Dakewe Biotech, Shenzhen, China); IL-23 (Biolegend, USA); and HMGB1 (Yanhui Biotech, Shanghai, China). To isolate hepatic leukocytes, livers were pressed through a 200G stainless steel mesh and suspended in PBS. The suspension was centrifuged at 50g for 1 minute. find more The supernatant was then transferred into a new tube and centrifuged at 800g for 10 minutes. The pellets were resuspended in 40% Percoll and centrifuged at 1,260g for 15 minutes at room temperature. The pellets were resuspended and the cell number was determined. To detect hepatic neutrophils, 1 × 106 cells were stained with specific mAb against mouse FITC-CD11b (M1/70, BD Bioscience, USA), PE-Ly6G (1A8, BD Bioscience), Percp-Cy5.5-CD45.2 (104, BD Bioscience), and APC-Gr-1 (RB6-8C5, BD Bioscience). To detect

γδ T cells, 1 × 106 cells were stained with specific mAb against mouse FITC-γδTCR (GL3, eBioscience), PE-CD3 (145-2C11, BD Bioscience), and Percp-Cy5.5-CD45.2 (104, BD Bioscience). To detect IL-17A+ cells, 1 × 106 cells were stimulated with PMA (50 ng/mL), ionomycin (1 μg/mL), and monensin (5 μg/mL) for 4 hours. The cells were stained with FITC-CD4 (RM4-5, BD Bioscience), Percp-Cy5.5-CD3 (145-2C11, BD Bioscience), APC-γδTCR (GL3, eBioscience), and PE-CY7-NK1.1 (PK136, BD Bioscience), and then intracellularly stained with PE-IL-17A (BD Bioscience) after fixation and permeabilization. Finally, the stained cells were analyzed using a FACSCalibur (BD Biosciences) or BD LSR II (BD Biosciences) flow cytometer. The acquired data were analyzed using FlowJo software. Data are presented as the mean ± standard error of the mean (SEM). The significance of differences was determined using a two-tailed unpaired t test; the significance levels are marked *P < 0.05; **P < 0.01; ***P < 0.005.

2 NKT cells are abundant in the liver. They recognize lipid antigens presented by CD1d and had different roles in liver diseases. NKT cells produce a wide range of cytokines promptly after activation.23 It is well accepted that Th1 cytokines suppress fibrosis, whereas Th2 cytokines promote fibrosis.24 In wildtype (WT) mice, it was reported that NKT cells can suppress the activation of HSC.22 But in different animal models and in human patients the conclusions were controversial.25, 26 Although the acceleration of HBV infection to liver fibrosis BYL719 have been extensively observed in clinical settings,

the immune response during this process is not clear, especially in the condition of the HBV carriers with no obvious symptoms. In this study, by using HBV transgenic mice (HBV-tg) that mimic human HBV healthy carriers,27 we found liver fibrosis spontaneously occurred in old age of HBV-tg mice, and, importantly, 5-Fluoracil ic50 HBV-tg mice were much more sensitive to the hepatotoxin CCl4-induced liver injury and liver fibrosis with the accompanied overactivation of HSCs. Further study demonstrated

that hepatic NKT cells from HBV-tg mice could directly activate HSCs and thereafter induce liver fibrosis in the experiments of cellular depletion and adoptive transfer, and IL-4 and IL-13 secreted by NKT cells were considered a crucial step for the activation of HSCs. α-SMA: α smooth muscle actin; CCl4: carbon tetrachloride; ECM: extracellular matrix; HBV: hepatitis B virus; HBV-tg: HBV transgenic mice; HSC: hepatic stellate cells; IFN-γ, interferon gamma; IL: interleukin; MMP: matrix metalloproteinase; MNC: mononuclear cell; mRNA: messenger RNA; NKT, natural killer T; qPCR: quantitative polymerase chain reaction; TIMP: tissue inhibitor of metalloproteinase. selleck chemicals HBV transgenic mice C57BL/6J-TgN (AlblHBV) 44Bri, which contains HBV genome S, pre-S, and X domains, were purchased from VITALRIVER experiment animal company (Beijing, China), who obtained the animals from Jackson Laboratory

(Bar Harbor, ME). C57BL/6 mice were also purchased from VITALRIVER experiment animal company. Rag1−/− mice were purchased from Model Animal Research Center (Nanjing, China), who obtained the mice from Jackson Laboratory. Mice were housed in a specific pathogen-free facility and used according to the regulations of animal care of University of Science and Technology of China. For chronic liver injury and fibrosis, male 7 to 10-week-old C57BL/6 and HBV-tg mice (weighing about 20-25 g) were injected (intraperitoneally, i.p., 2 times a week) with 0.5 μL per gram of body weight of pure CCl4 diluted with olive oil (Sigma). After several weeks’ injections (2, 4, 10, and 14 weeks, respectively), mice were sacrificed 72 hours following the last CCl4 injection, and liver tissues and serum were collected. For acute liver injury, both mice were injected CCl4 once and then killed and analyzed at different timepoints.

After moving to Boston for 1 year to complete my work with Dr. Zimmerman, I returned to Washington to work with Dr. Cohn on hepatic hemodynamics. At the time, it was clear to me that the circulation of a particular organ could not be isolated from the study of the systemic circulation.

Therefore, from June of 1968 to September of 1971, I became a “cardio-hepatologist” under Dr. Cohn’s tutelage.4 I worked in the arterial hypertension outpatient clinic and consulted on patients for the clinical hemodynamic section of the Department of Medicine. The patients were for the most part in cardiogenic or septic shock, but there were also many patients with cirrhosis who had advanced hemodynamic derangements, including refractory ascites and the hepatorenal syndrome. The prognosis for patients Wnt signaling with end-stage liver disease was extremely poor in the era preceding liver transplantation, but my clinical role afforded

me an important opportunity to learn to perform hemodynamic studies in patients with cirrhosis. These were very productive years because together with Dr. Cohn and collaborators, we described new techniques to measure both hepatic blood flow5 and portal systemic shunting in patients with cirrhosis,6, 7 and documented Y27632 the existence of a hyperdynamic splanchnic circulation in this group of patients.8 My collaboration with Dr. Cohn produced a series of publications, but more importantly, this experience focused my research interest on the circulatory abnormalities of patients with liver disease and portal hypertension. By 1970, I found myself at a crossroads. I had developed

a unique area of specialization and scientific interest in a field that was only practiced at a few academic medical centers. My clinical expertise did not conform to the recognized and typical clinical subspecialities, and the next steps were unclear to me. Meanwhile, my family had grown with the births of my two children. Since marrying, I had asked my wife to move four find more times in order to pursue my academic calling, but now the political situation in Argentina had improved somewhat because the military government promised to hold free democratic elections. My former medical chief and mentor, Dr. M. Royer offered me a solid academic position as a scientific investigator in the Argentine National Research Council. Aida and I acquiesced to the expressed wishes of our families and our own desire to be closer to family and old friends and we moved back to Buenos Aires in 1971. Back in Argentina, I rejoined the group that I had worked with previously at the National Institute of Gastroenterology, now renamed Policlinico A Posadas, an indication that there would be a new emphasis on clinical medicine. I was very warmly welcomed and I enjoyed the personal support of my colleagues.

After moving to Boston for 1 year to complete my work with Dr. Zimmerman, I returned to Washington to work with Dr. Cohn on hepatic hemodynamics. At the time, it was clear to me that the circulation of a particular organ could not be isolated from the study of the systemic circulation.

Therefore, from June of 1968 to September of 1971, I became a “cardio-hepatologist” under Dr. Cohn’s tutelage.4 I worked in the arterial hypertension outpatient clinic and consulted on patients for the clinical hemodynamic section of the Department of Medicine. The patients were for the most part in cardiogenic or septic shock, but there were also many patients with cirrhosis who had advanced hemodynamic derangements, including refractory ascites and the hepatorenal syndrome. The prognosis for patients click here with end-stage liver disease was extremely poor in the era preceding liver transplantation, but my clinical role afforded

me an important opportunity to learn to perform hemodynamic studies in patients with cirrhosis. These were very productive years because together with Dr. Cohn and collaborators, we described new techniques to measure both hepatic blood flow5 and portal systemic shunting in patients with cirrhosis,6, 7 and documented Veliparib cell line the existence of a hyperdynamic splanchnic circulation in this group of patients.8 My collaboration with Dr. Cohn produced a series of publications, but more importantly, this experience focused my research interest on the circulatory abnormalities of patients with liver disease and portal hypertension. By 1970, I found myself at a crossroads. I had developed

a unique area of specialization and scientific interest in a field that was only practiced at a few academic medical centers. My clinical expertise did not conform to the recognized and typical clinical subspecialities, and the next steps were unclear to me. Meanwhile, my family had grown with the births of my two children. Since marrying, I had asked my wife to move four selleck chemicals llc times in order to pursue my academic calling, but now the political situation in Argentina had improved somewhat because the military government promised to hold free democratic elections. My former medical chief and mentor, Dr. M. Royer offered me a solid academic position as a scientific investigator in the Argentine National Research Council. Aida and I acquiesced to the expressed wishes of our families and our own desire to be closer to family and old friends and we moved back to Buenos Aires in 1971. Back in Argentina, I rejoined the group that I had worked with previously at the National Institute of Gastroenterology, now renamed Policlinico A Posadas, an indication that there would be a new emphasis on clinical medicine. I was very warmly welcomed and I enjoyed the personal support of my colleagues.

Therefore, we wanted to determine whether the fatty liver index (FLI), a surrogate marker and a validated algorithm derived from the serum triglyceride level, body mass index, waist circumference, and γ-glutamyltransferase level, was associated with the prognosis in a population study. The 15-year

all-cause, hepatic-related, cardiovascular disease (CVD), and cancer mortality rates were obtained through the Regional Health Registry in 2011 for 2074 Caucasian middle-aged individuals in the Cremona study, a population study examining the prevalence of diabetes mellitus in Italy. During the 15-year observation http://www.selleckchem.com/products/z-ietd-fmk.html period, 495 deaths were registered: 34 were hepatic-related, 221 were CVD-related, 180 were cancer-related, and 60 were attributed to other causes. FLI was independently associated with the hepatic-related deaths (hazard ratio = 1.04, 95% confidence interval = 1.02-1.05, P < 0.0001). Age, sex, FLI, cigarette smoking,

and diabetes were independently associated with all-cause mortality. Age, sex, FLI, systolic blood pressure, and fibrinogen were Atezolizumab independently associated with CVD mortality; meanwhile, age, sex, FLI, and smoking were independently associated with cancer mortality. FLI correlated with the homeostasis model assessment of insulin resistance (HOMA-IR), a surrogate marker of insulin resistance (Spearman’s ρ = 0.57, P < 0.0001), and when HOMA-IR was included in the multivariate analyses, FLI retained selleck kinase inhibitor its association with hepatic-related mortality but not with all-cause, CVD, and cancer-related mortality. Conclusion: FLI is independently associated with hepatic-related mortality. It is also associated with all-cause, CVD, and cancer mortality rates, but these associations appear to be tightly interconnected with the risk conferred by the correlated insulin-resistant state. (HEPATOLOGY 2011;) Nonalcoholic fatty liver disease (NAFLD) is common in insulin-resistant subjects1 and affects 20% to 30% of the adult population and more than 50% of overweight and obese individuals.2 NAFLD

is associated with an increased risk of developing advanced fibrosis and cirrhosis3 and incident type 2 diabetes.4 Because of its association with metabolic syndrome and type 2 diabetes, it has been hypothesized that NAFLD may also be associated with increased rates of cardiovascular disease (CVD)5; in particular, patients with NAFLD have elevated levels of plasma biomarkers of inflammation, endothelial dysfunction, markers of subclinical cardiovascular risk, and a higher prevalence of clinically manifesting CVD.6 Some studies have also reported a higher incidence of major outcomes,7-10 such as nonfatal CVD events,7 deaths due to CVD,8, 9 revascularization procedures,9 and all-cause mortality.

Clinical implications: In FPDs, the morphology and type of FRC substructures might influence the shear bond strength between the FRC substructure and the indirect PI3K inhibitor veneering composite. With the proper design of these substructures, the number of veneering fractures may be decreased. “
“Purpose: The present study compared changes in CIE L*a*b* color coordinates of substrates of different colors when covered with zirconium oxide discs (Procera) and with such discs if veneered with two shades of porcelain. Material and Methods: Forty background substrates were fabricated and divided into four groups depending on

the color of the substrates: white, black, gray, and tooth-colored (Vita shade A3). The initial color of the substrates was measured using a colorimeter. The color of the substrates covered with plain zirconium oxide discs and with zirconium oxide discs veneered with porcelains of two shades (Vita shade A1 and B4) was measured. The color difference between the substrates, the substrates covered with plain discs, and the substrates covered with veneered discs was calculated, and the data were statistically analyzed with one-way ANOVA and multiple paired t-test. Results: For each group of

substrates, the resulting colors were significantly different when the substrates were covered by either plain zirconium oxide discs www.selleckchem.com/products/BEZ235.html or zirconium oxide discs veneered with Vita shade A1 or B4 porcelain. Conclusion: While zirconium oxide coping material

alone has a degree of masking ability, the resulting color of a restoration can be further modified with the veneering porcelain. “
“The aim of this study was to evaluate the amount of ions released from Ti6Al4V and Co-Cr-Mo alloys both in vivo and in vitro. Twenty-one discs of each alloy were constructed and divided into seven groups. Three specimens from each group were immersed in a buffered saline solution over a period of 1, 3, 5, 7, 14, 21, and 28 days. Twenty-eight participants were also included in the study, where the study group consisted of 14 mandibular partially edentulous patients, and the control group consisted of 14 volunteers. The study group was further divided into two equal groups: the first group received removable partial dentures (RPDs) constructed selleck inhibitor from Co-Cr-Mo alloy, while the second group received RPDs constructed from Ti6Al4V alloy. Saliva samples were collected from each participant over the same study period. The conditioning media and saliva samples were analyzed using a spectrophotometer. One-way ANOVA and Tukey tests were used for statistical analysis (p < 0.05). The concentrations of metal ions released from the studied alloys were significantly higher in the in vitro than in the in vivo study group during the follow-up periods. A statistically significant increase in ion concentrations of the different elements for both alloys was found with time (p < 0.05).

Clinical implications: In FPDs, the morphology and type of FRC substructures might influence the shear bond strength between the FRC substructure and the indirect C59 wnt concentration veneering composite. With the proper design of these substructures, the number of veneering fractures may be decreased. “
“Purpose: The present study compared changes in CIE L*a*b* color coordinates of substrates of different colors when covered with zirconium oxide discs (Procera) and with such discs if veneered with two shades of porcelain. Material and Methods: Forty background substrates were fabricated and divided into four groups depending on

the color of the substrates: white, black, gray, and tooth-colored (Vita shade A3). The initial color of the substrates was measured using a colorimeter. The color of the substrates covered with plain zirconium oxide discs and with zirconium oxide discs veneered with porcelains of two shades (Vita shade A1 and B4) was measured. The color difference between the substrates, the substrates covered with plain discs, and the substrates covered with veneered discs was calculated, and the data were statistically analyzed with one-way ANOVA and multiple paired t-test. Results: For each group of

substrates, the resulting colors were significantly different when the substrates were covered by either plain zirconium oxide discs www.selleckchem.com/screening/kinase-inhibitor-library.html or zirconium oxide discs veneered with Vita shade A1 or B4 porcelain. Conclusion: While zirconium oxide coping material

alone has a degree of masking ability, the resulting color of a restoration can be further modified with the veneering porcelain. “
“The aim of this study was to evaluate the amount of ions released from Ti6Al4V and Co-Cr-Mo alloys both in vivo and in vitro. Twenty-one discs of each alloy were constructed and divided into seven groups. Three specimens from each group were immersed in a buffered saline solution over a period of 1, 3, 5, 7, 14, 21, and 28 days. Twenty-eight participants were also included in the study, where the study group consisted of 14 mandibular partially edentulous patients, and the control group consisted of 14 volunteers. The study group was further divided into two equal groups: the first group received removable partial dentures (RPDs) constructed click here from Co-Cr-Mo alloy, while the second group received RPDs constructed from Ti6Al4V alloy. Saliva samples were collected from each participant over the same study period. The conditioning media and saliva samples were analyzed using a spectrophotometer. One-way ANOVA and Tukey tests were used for statistical analysis (p < 0.05). The concentrations of metal ions released from the studied alloys were significantly higher in the in vitro than in the in vivo study group during the follow-up periods. A statistically significant increase in ion concentrations of the different elements for both alloys was found with time (p < 0.05).

001) and positively associated with the degree of differentiation of tumor (P < 0.001) in gastric carcinoma. Each of them was have significant difference in statistically. Conclusion: The expression of PIAS3 gene is reduced in gastric cancer, which may revealed an inhibitive effect of PIAS3 on tumor growth. Key Word(s): 1. PIAS3; 2. gastric cancer; 3. non-tumor tissue; 4. immunohistochemistry; Presenting Author: LIN TAO Additional Authors: HAIXING JIANG Corresponding Author: HAIXING JIANG Affiliations: 1st Affiliated

hospital of Guangxi medical university Objective: Objective To observe the effect of Blastocystis hominis on actin cytoskeleton and its possible mechanism. Methods: Hela cells were cultured by DMEM medium in vitro, then Torin 1 purchase observed the biological characteristics; determinated MTT colorimetry OD value of the growth curve; all objecties were divided into three groups: ① blank control group: Hela cells were cultured alone; ② co-culture group: B.hominis and Hela cells were cultured at the same time; ③ co-cultured + inhibitor group:

B.hominis and Hela cells were cultured at the same time, 0.01% ammonium molybdate was added to Hela cells. Cell cultured in each experimental group were fixed under dynamic inverted phase contrast microscope after 24 h to observe living cells morphological changes. Selleckchem LDE225 Rhodamine – phalloidin was used staining actin cytoskeleton of groups of Hela check details cell. Results: 1. Hela cells were cultured in DMEM medium for adherent growth polygonal. Hela cells formed stable after the third generation, and may be formed on the cell island. 2. Hela cell growth

curve present ‘S’ shape, and went through three growth stages: incubation period, the logarithmic growth phase and stagnation. 3. Results of actin cytoskeleton of Hela cells stained by rhodamine – phalloidin after 24 h showed: ① control group, actin cytoskeleton distributed in the perinuclear area, tension wire structure was visible. ② co-culture group, the content of actin cytoskeleton became less, tension wire structure can not be founded. ③ co-cultured + inhibitor group, the content of the actin cytoskeleton was slightly less, and distributed in the perinuclear area, tension wire structure also was visible. Conclusion: DMEM medium can cultivate the Hela cells morphology, function better. Tanswell insert semi-permeable membrane can cultivate B.hominis and Hela cells better at the same time, and simulate the interaction between B.hominis and cell the in vivo environment. When the B.hominis and Hela cells were co-cultured, B.hominis may secrete acid phosphatase in growth and metabolic processes. It plays a significant role in actin cytoskeleton of Hela cells, and makes actin cytoskeleton decreased markedly and its structure abnormal. Key Word(s): 1. Blastocystis hominis; 2. Hela cells; 3. co-culture; 4.

CSF analysis for JC virus was tested negative twice. This case represents a presumptive PML after discontinuation of natalizumab treatment—similar GDC-0068 solubility dmso to the definition established for PML in HIV patients. “
“The aim of this study was to investigate whether physiological factors, including body mass index (BMI), are associated with detection of right-to-left shunt (RLS) by contrast transcranial Doppler ultrasonography (c-TCD). After prospective c-TCD for stroke patients, we compared

clinical backgrounds between patients with positive and negative results for RLS. After counting microembolic signals (MES), RLS were functionally graded as follows (grade 0 = 0 MES, grade I = 1-10 MES, grade II = 11-30 MES, grade III = 31-100 MES if countable, grade IV = over 100 MES or uncountable like a shower. Subjects comprised 584 patients (203 men, 381 women) with a mean age of 67.9 ± 11.1 years. RLS was detected in 134 of 584 patients (23%). In univariate analysis, mean BMI was 22.1 in patients with RLS and 23.3 in those without

RLS (P= .004). Mean BMI in concordance with RLS grade gradually decreased (grade 0; 22.7, grade I; 20.8, grade Trametinib II; 20.1, grade III; 19.6, P= .001). After performing the Valsalva maneuver, mean BMI in concordance with RLS grade linearly increased (grade I; 20.6, grade II; 23.2, grade III; 24.8, grade IV; 25.8, P < .001). Although smaller body size may be associated with detection of RLS, a patient with significant RLS (grade III or IV) had larger body. "
“We report the case of a 27-year-old man with a history of previously this website undiagnosed renal disease that presented with multiple cerebrovascular infarctions. Workup for

traditional causes of cerebrovascular infarction including cardiac telemetry, multiple echocardiograms, and hypercoagulative workup was negative. However, a transcranial Doppler detected circulating microemboli at the rate of 14 per hour. A serum oxalate level greater than the supersaturation point of calcium oxalate was detected, providing a potential source of the microemboli. Furthermore, serial imaging recorded rapid mineralization of the infarcted territories. In the absence of any proximal vessel irregularities, atherosclerosis, valvular abnormalities, arrhythmias, or systemic shunt as potential stroke etiology in this patient, we propose that circulating oxalate precipitate may be a potential mechanism for stroke in patients with primary oxalosis. “
“We examined the correlation of angiographic collaterals in acute stroke with the presence, extent, and distribution of white matter changes, so-called Leukoaraiosis, in an effort to determine if Leukoaraiosis indicates chronic cerebral hypoperfusion and/or is associated with the development of cerebral collateral circulation.

1B), whereas the development of anemia (hemoglobin <100

g/L) occurred gradually over the course of treatment (Fig. 1C). The baseline demographics of patients who developed anemia compared with those who did not are shown in Table 1. Patients who developed anemia were more likely to be female and significantly older with lower body weight, body mass index, creatinine clearance, hemoglobin levels, white cell counts and platelet counts than patients who did not become anemic. Patients with hemoglobin decline >30 g/L were more likely to be older, female, and with lower body weight and higher baseline 20s Proteasome activity hemoglobin than patients with a maximal hemoglobin decline ≤30 g/L (data not shown). The allocated and mean dosages received for PEG-IFN and ribavirin at weeks 12, 24, and 48 of therapy are shown in Table 2. At baseline, more patients who became anemic were allocated a lower dose of ribavirin (1,000 mg versus 1,200 mg) than patients who did not become anemic (61% versus 44%; P = 0.0002). The mean daily ribavirin dosage was significantly lower in patients who developed anemia compared with those who did not become anemic at week 12 (998 ± 143 mg/day versus 1,052 ± 152 mg/day; P = 0.0001) and week 24 (967 ± 169

mg/day versus 1030 ± 210 mg/day; P = 0.0002); there was no significant difference in ribavirin exposure at week 48. The mean weekly PEG-IFN dosage at week 48 was significantly lower in patients who did not become anemic compared with anemic patients for both standard and induction PD0325901 solubility dmso therapy arms; there was no significant difference

in PEG-IFN exposure at earlier times. Similar outcomes were observed when PEG-IFN and ribavirin exposure were analyzed as a percentage of planned target dose (data not shown). Virological responses at the end of treatment (ETR) and at the end of follow-up (SVR) were significantly different between patients with hemoglobin <100 g/L at any time during treatment compared with those with hemoglobin ≥100 g/L (ETR, 80% versus 65%, respectively, P = 0.003; SVR, 61% versus 50%, respectively, P = 0.02). Relapse rates were similar, however (Fig. 2A). Similarly, ETR and SVR rates were significantly higher in patients with hemoglobin decline >30 g/L compared with those click here with hemoglobin decline ≤30 g/L. An ETR occurred in 72% of patients with a hemoglobin decline >30 g/L compared with 52% of those without a similar change in hemoglobin (P < 0.001). Similarly, a SVR occurred in 54% with a hemoglobin decline >30 g/L compared with 46% with a hemoglobin decline ≤30 g/L (P = 0.049). Relapse rates were similar (Fig. 2B). In separate multiple logistic regression analyses, both hemoglobin <100 g/L (protocol defined anemia) and maximum hemoglobin decline >30 g/L during treatment were significantly associated with SVR rate. The odds ratio estimate for SVR for hemoglobin <100 g/L was 1.97 (95% confidence interval, 1.08-3.62; P = 0.028). The odds ratio estimate for hemoglobin decline >30 g/L was 2.17 (95% confidence interval, 1.31-3.