29% (n = 24) had low Vit D at 12 months of whom 58% (n-14) were deficient at baseline. Surprisingly, only 10/30 patients with initial deficient Vit D reported adherence with Vit D supplementation and 8/10 (80%) achieved Vit D sufficiency. In the remaining 20, Vit D remained deficient at follow up in 13 (65%) and had become sufficient in 7 without supplementation. The mean IBDQ scores did not change over the 12 months in either those who achieved sufficiency or remained deficient (became sufficient 48–50 cf remained deficient 48–49). In those who took AZD1208 the Vitamin D and became replete, only one had a significant increase in

IBDQ (>17 point increase). Of patients with Vit D sufficiency at baseline (n = 50), by 12 months 80%

(n = 40) remained Vit D sufficient while 20% (n = 10) had become Vit D deficient. Over the 12 months, neither patients who maintained sufficient vitamin D levels nor those who subsequently developed Vit D deficiency had any significant change in mean IBDQ Selleck Cisplatin score (remained sufficient: 52–54 cf became deficient: 52–48). By 12 months, of the 28 subjects with baseline abnormal BMD, 15 remained osteopenic/osteoporotic while 10/28 had normal BMD. Of those with normal baseline BMD, only 1/47 subsequently became osteopenic. Of note, in this patient, initial and follow-up Vit D measures were low (20 and 21 respectively). Conclusion: Vit D deficiency is highly prevalent, despite this being a predominantly ambulant outpatient sample. Impaired bone health, was also surprisingly common (>1/3 of the cohort), despite an average age of ∼32. Despite advice, Vit D therapy was poorly adopted, but biochemically successful when taken. As yet, the relationships amongst disease activity, QoL and Vit D and the role of supplementation are unclear, however, for prevention of future osteoporosis alone, it may be justified given the prevalence of deficiency we have discovered. 1. Mouli, VP and Ananthakrishnan, AN. Review article: vitamin D and inflammatory bowel diseases. Aliment Pharmacol Ther. 2014. Volume 39:2 pp 125–136. 2. Nowson CA, McGrath JJ, Ebeling PR, et al. 上海皓元 Vitamin

D and health in adults in Australia and New Zealand: a position statement. Med J Aust. 2012 Jun 18; 196(11): 686–687. PubMed PMID: 22708765. Epub 2012/06/20. eng. 3. Guyatt G, Mitchell A, Irvine EJ, Singer J, Williams N, Goodacre R, Tompkins C. A new measure of health status for clinical trials in inflammatory bowel disease. Gastroenterology. 1989; 96: 804–810. CHAMARA BASNAYAKE,1 GREGORY MOORE2 1Gastroenterology Registrar, Monash Health; 2Head of Inflammatory Bowel diseases Monash Health Introduction: Magnetic Resonance Enterography (MRE) is an increasingly used diagnostic imaging test in patients with either suspected or known IBD. We sought to determine the clinical utility of MRE in a tertiary referral center and compare it with other factors that influence diagnosis and management.

29% (n = 24) had low Vit D at 12 months of whom 58% (n-14) were deficient at baseline. Surprisingly, only 10/30 patients with initial deficient Vit D reported adherence with Vit D supplementation and 8/10 (80%) achieved Vit D sufficiency. In the remaining 20, Vit D remained deficient at follow up in 13 (65%) and had become sufficient in 7 without supplementation. The mean IBDQ scores did not change over the 12 months in either those who achieved sufficiency or remained deficient (became sufficient 48–50 cf remained deficient 48–49). In those who took Lumacaftor the Vitamin D and became replete, only one had a significant increase in

IBDQ (>17 point increase). Of patients with Vit D sufficiency at baseline (n = 50), by 12 months 80%

(n = 40) remained Vit D sufficient while 20% (n = 10) had become Vit D deficient. Over the 12 months, neither patients who maintained sufficient vitamin D levels nor those who subsequently developed Vit D deficiency had any significant change in mean IBDQ selleck inhibitor score (remained sufficient: 52–54 cf became deficient: 52–48). By 12 months, of the 28 subjects with baseline abnormal BMD, 15 remained osteopenic/osteoporotic while 10/28 had normal BMD. Of those with normal baseline BMD, only 1/47 subsequently became osteopenic. Of note, in this patient, initial and follow-up Vit D measures were low (20 and 21 respectively). Conclusion: Vit D deficiency is highly prevalent, despite this being a predominantly ambulant outpatient sample. Impaired bone health, was also surprisingly common (>1/3 of the cohort), despite an average age of ∼32. Despite advice, Vit D therapy was poorly adopted, but biochemically successful when taken. As yet, the relationships amongst disease activity, QoL and Vit D and the role of supplementation are unclear, however, for prevention of future osteoporosis alone, it may be justified given the prevalence of deficiency we have discovered. 1. Mouli, VP and Ananthakrishnan, AN. Review article: vitamin D and inflammatory bowel diseases. Aliment Pharmacol Ther. 2014. Volume 39:2 pp 125–136. 2. Nowson CA, McGrath JJ, Ebeling PR, et al. 上海皓元 Vitamin

D and health in adults in Australia and New Zealand: a position statement. Med J Aust. 2012 Jun 18; 196(11): 686–687. PubMed PMID: 22708765. Epub 2012/06/20. eng. 3. Guyatt G, Mitchell A, Irvine EJ, Singer J, Williams N, Goodacre R, Tompkins C. A new measure of health status for clinical trials in inflammatory bowel disease. Gastroenterology. 1989; 96: 804–810. CHAMARA BASNAYAKE,1 GREGORY MOORE2 1Gastroenterology Registrar, Monash Health; 2Head of Inflammatory Bowel diseases Monash Health Introduction: Magnetic Resonance Enterography (MRE) is an increasingly used diagnostic imaging test in patients with either suspected or known IBD. We sought to determine the clinical utility of MRE in a tertiary referral center and compare it with other factors that influence diagnosis and management.

Choice of treatment is strongly dependent on antibiotic resistance rates. In some countries, triple therapy with a proton-pump inhibitor, amoxicillin, and clarithromycin is still the best option, but eradication results fall short of what would be desired (90–95%) in countries with clarithromycin resistance >20%, bismuth-containing quadruple therapy, or nonbismuth sequential or concomitant therapies may then be the preferred option. Newer antibiotic regimens are awaited. Vaccination would be the best option, especially for developing countries, but little progress has been

made in designing a vaccine. A considerable amount of work has been conducted over the last year assessing many issues around Helicobacter pylori eradication therapy. These focussed primarily on assessing the efficacy selleck chemicals llc of current standard triple

therapy and exploring new first-line treatments. There was also progress in investigating antibiotic resistance rates, and the rescue therapies required to deal with ensuing treatment failures. There has also been an evolution in the use of adjunctive therapies. This article will address the published literature over the last year pertaining to these topics. Numerous studies over the last year have assessed the efficacy of standard triple therapy with amoxicillin, clarithromycin, and a proton-pump inhibitor buy Ceritinib for the eradication of H. pylori, which have been perceived to be in decline in recent years. One such study looked at cure rates reported in all published literature from Spain between 1997 and 2008 and found that while cure rates have in fact been stable over that period, they remain inadequate with a mean cure rate of 80% by intention-to-treat and 83% by per-protocol [1]. Similar results were obtained from a multicenter study in Japan that revealed an eradication rate

of 80.7% with an incidence of adverse drug reactions of 4.4% [2]. Other studies have looked at whether the efficacy of triple therapy can be improved by prolonging the course of therapy. In China, a study of shorter regimens showed eradication rates of 76, 89, and 91% for 3-day, 5-day, and 7-day regimens, respectively [3]. Increasing efficacy by prolongation of therapy was also noted in Greek patients, 上海皓元 with eradication rates of 74.5% for 7 days, 80.6% for 10 days, and 90.2% for 14 days of therapy [4]. Another study showed that efficacy could be maintained when lower doses of medications were given, which reduced costs and side effects with cure rates of 77.2% for 10 mg rabeprazole, 500 mg amoxicillin, and 250 mg clarithromycin vs 78.9% for the standard 20 mg, 1 g, and 500 mg doses of these drugs [5]. Regardless of the type of therapy used, study from Canada showed widespread failure to comply with test and treat in up to 10% of cases and a failure to confirm eradication in 32% [6].

Choice of treatment is strongly dependent on antibiotic resistance rates. In some countries, triple therapy with a proton-pump inhibitor, amoxicillin, and clarithromycin is still the best option, but eradication results fall short of what would be desired (90–95%) in countries with clarithromycin resistance >20%, bismuth-containing quadruple therapy, or nonbismuth sequential or concomitant therapies may then be the preferred option. Newer antibiotic regimens are awaited. Vaccination would be the best option, especially for developing countries, but little progress has been

made in designing a vaccine. A considerable amount of work has been conducted over the last year assessing many issues around Helicobacter pylori eradication therapy. These focussed primarily on assessing the efficacy beta-catenin inhibitor of current standard triple

therapy and exploring new first-line treatments. There was also progress in investigating antibiotic resistance rates, and the rescue therapies required to deal with ensuing treatment failures. There has also been an evolution in the use of adjunctive therapies. This article will address the published literature over the last year pertaining to these topics. Numerous studies over the last year have assessed the efficacy of standard triple therapy with amoxicillin, clarithromycin, and a proton-pump inhibitor selleck chemicals llc for the eradication of H. pylori, which have been perceived to be in decline in recent years. One such study looked at cure rates reported in all published literature from Spain between 1997 and 2008 and found that while cure rates have in fact been stable over that period, they remain inadequate with a mean cure rate of 80% by intention-to-treat and 83% by per-protocol [1]. Similar results were obtained from a multicenter study in Japan that revealed an eradication rate

of 80.7% with an incidence of adverse drug reactions of 4.4% [2]. Other studies have looked at whether the efficacy of triple therapy can be improved by prolonging the course of therapy. In China, a study of shorter regimens showed eradication rates of 76, 89, and 91% for 3-day, 5-day, and 7-day regimens, respectively [3]. Increasing efficacy by prolongation of therapy was also noted in Greek patients, MCE with eradication rates of 74.5% for 7 days, 80.6% for 10 days, and 90.2% for 14 days of therapy [4]. Another study showed that efficacy could be maintained when lower doses of medications were given, which reduced costs and side effects with cure rates of 77.2% for 10 mg rabeprazole, 500 mg amoxicillin, and 250 mg clarithromycin vs 78.9% for the standard 20 mg, 1 g, and 500 mg doses of these drugs [5]. Regardless of the type of therapy used, study from Canada showed widespread failure to comply with test and treat in up to 10% of cases and a failure to confirm eradication in 32% [6].

15, 16 (3) Besides preS1, another essential element of HBV/HDV infectivity has been assigned to the antigenic loop (AGL) of the S-domain.17 Replacement of cysteine residues in the AGL rendered HDV and HBV (Yi Ni, unpubl. results) noninfectious. Since some of these cysteines (e.g., Cys-124)

participate in intramolecular disulfide bonds, the sensitivity against reducing agents hints at the involvement of disulfide-bridge rearrangements during virus entry.18 Since only L-protein containing SVPs are able to bind hepatocytes from Tupaia belangeri the S-protein/domain is probably not essential for hepatocyte-specific binding.19 Consistent with the selleck screening library results of the mutational analyses, HBV preS1-derived lipopeptides,

mimicking the myristoylated N-terminal preS1-infectivity domain, efficiently inhibit HBV and HDV infection of HepaRG cells, PHH, and PTH.7, 20-23 The activity of the peptides requires myristoylation and the integrity of an internal sequence (9-NPLGFFP-15) which is highly conserved between primate hepadnaviruses.21 Since their inhibitory effect remains for several hours after preincubation they probably inactivate a cellular receptor.24 In the present study we used fluorescently labeled, myristoylated HBVpreS1-peptides to analyze the presence and turnover kinetics of this HBVpreS1-specific receptor on hepatocytes from different species. ACP-196 We investigated

whether receptor expression coincides with the species specificity of HBV and demonstrate highly specific binding of the preS1-lipopeptide to permissive cells (PHH, PTH, HepaRG). Unexpectedly, we detected specific binding to hepatocytes from non-susceptible species such as mouse, rat, rabbit, and dog, but not pig, cynomolgus, or rhesus monkey. Expression of a functional HBVpreS1-receptor was associated with the differentiation state of the hepatocyte: MCE No binding was observed in undifferentiated HepaRG cells or dedifferentiated PMH and PHH. HepG2 and HuH7 cells were unable to bind the peptide even after dimethyl sulfoxide (DMSO)-induced differentiation. Kinetic studies demonstrated a slow turnover and a constrained lateral movement of the receptor complex at the plasma membrane (PM), possibly due to a cytoskeleton interaction. DIPEA, N,N-Diisopropylethylamine; DMSO, dimethyl sulfoxide; FITC, fluorescein isothiocyanate; ge, genome equivalent; HBTU, O-(benzotriazol-1-yl)-N,N,N ′,N ′-tetramethyluronium hexafluorophosphate; HSPG, heparan sulfate proteoglycan; L-protein, hepatitis B virus large surface protein; PBS, phosphate-buffered saline; PEG, polyethylene glycol; PHH, primary human hepatocytes; PMH, primary mouse hepatocytes; PTH, primary Tupaia belangeri hepatocytes.

15, 16 (3) Besides preS1, another essential element of HBV/HDV infectivity has been assigned to the antigenic loop (AGL) of the S-domain.17 Replacement of cysteine residues in the AGL rendered HDV and HBV (Yi Ni, unpubl. results) noninfectious. Since some of these cysteines (e.g., Cys-124)

participate in intramolecular disulfide bonds, the sensitivity against reducing agents hints at the involvement of disulfide-bridge rearrangements during virus entry.18 Since only L-protein containing SVPs are able to bind hepatocytes from Tupaia belangeri the S-protein/domain is probably not essential for hepatocyte-specific binding.19 Consistent with the DNA Damage inhibitor results of the mutational analyses, HBV preS1-derived lipopeptides,

mimicking the myristoylated N-terminal preS1-infectivity domain, efficiently inhibit HBV and HDV infection of HepaRG cells, PHH, and PTH.7, 20-23 The activity of the peptides requires myristoylation and the integrity of an internal sequence (9-NPLGFFP-15) which is highly conserved between primate hepadnaviruses.21 Since their inhibitory effect remains for several hours after preincubation they probably inactivate a cellular receptor.24 In the present study we used fluorescently labeled, myristoylated HBVpreS1-peptides to analyze the presence and turnover kinetics of this HBVpreS1-specific receptor on hepatocytes from different species. EX527 We investigated

whether receptor expression coincides with the species specificity of HBV and demonstrate highly specific binding of the preS1-lipopeptide to permissive cells (PHH, PTH, HepaRG). Unexpectedly, we detected specific binding to hepatocytes from non-susceptible species such as mouse, rat, rabbit, and dog, but not pig, cynomolgus, or rhesus monkey. Expression of a functional HBVpreS1-receptor was associated with the differentiation state of the hepatocyte: 上海皓元医药股份有限公司 No binding was observed in undifferentiated HepaRG cells or dedifferentiated PMH and PHH. HepG2 and HuH7 cells were unable to bind the peptide even after dimethyl sulfoxide (DMSO)-induced differentiation. Kinetic studies demonstrated a slow turnover and a constrained lateral movement of the receptor complex at the plasma membrane (PM), possibly due to a cytoskeleton interaction. DIPEA, N,N-Diisopropylethylamine; DMSO, dimethyl sulfoxide; FITC, fluorescein isothiocyanate; ge, genome equivalent; HBTU, O-(benzotriazol-1-yl)-N,N,N ′,N ′-tetramethyluronium hexafluorophosphate; HSPG, heparan sulfate proteoglycan; L-protein, hepatitis B virus large surface protein; PBS, phosphate-buffered saline; PEG, polyethylene glycol; PHH, primary human hepatocytes; PMH, primary mouse hepatocytes; PTH, primary Tupaia belangeri hepatocytes.

We evaluated the ability of novel global assays to better understand clinical bleeding severity in congenital FVII deficiency. Subjects underwent PI3K Inhibitor Library high throughput central determination of factor VII activity (FVII:C) as well as clot formation and lysis (CloFAL) and simultaneous thrombin and plasmin generation (STP) global assay analysis. A bleeding score was assigned to each subject through medical chart review. Global assay parameters were analysed with respect to bleeding score and FVII:C. Subgroup analyses

were performed on paediatric subjects and subjects with FVII ≥1 IU dL−1. CloFAL fibrinolytic index (FI2) inversely correlated with FVII:C while CloFAL maximum amplitude (MA) and STP maximum velocity of thrombin generation (VT max) varied directly with FVII:C. CloFAL FI2 directly correlated with bleeding score among subjects in both the total cohort and paediatric subcohort, but not among subjects with FVII ≥1 IU dL−1. Among subjects with FVII ≥1 IU dL−1, STP time to maximum velocity of thrombin generation

and Nivolumab datasheet time to maximum velocity of plasmin generation inversely correlated with bleeding score. These preliminary findings suggest a novel potential link between a hyperfibrinolytic state in bleeding severity and congenital FVII deficiency, an observation that should be further explored. “
“Summary.  Prophylaxis is recommended as preventive therapy for young boys with severe haemophilia in countries where safe factor concentrates are available. This recommendation 上海皓元医药股份有限公司 is supported by results from a randomized, controlled study that compared on-demand therapy with full-dose prophylaxis (Manco-Johnson MJ, Abshire TC, Shapiro AD et al. N Engl J Med 2007;357:535). It is important to distinguish primary vs. secondary prophylaxis. Primary prophylaxis refers to preventive treatment started before the onset of joint damage, whereas secondary prophylaxis refers to treatment started after joint damage has occurred. Whereas the benefits of primary prophylaxis are well documented, data relating

to secondary prophylaxis are limited, especially in the adolescent/adult haemophilia population. Failure of prophylaxis may relate to several variables, including: (i) underlying status of the joints; (ii) poor compliance; (iii) participation in high-risk activities and (iv) unfavourable pharmacokinetics (PK), i.e., too rapid elimination of infused coagulation factors. There is evidence that the risk of joint bleeding in individuals with severe haemophilia A relates to time spent with factor levels < 1% (Collins PW, Blanchette VS, Fischer K et al. J Thromb Haemost 2009;7:413); this variable is strongly influenced by frequency of factor infusions and the individual’s PK profile.

e. during the first interval and the two infusions) were the thalamus, insula, cingulated gyri, temporal pole and some parts of the frontal, parietal, temporal and occipital lobes (Table 1). Activation of the postcentral and precentral gyri occurred during the saline and HCl infusions, but not during the first interval (Figs 1,2). There were no distinct differences between the two infusions in the activated cerebral regions. Visceral sensory and motor abnormalities are often seen in functional gastrointestinal disorders (FGIDs) and the brain–gut interaction plays an important role in the development of these abnormalities. Recently, brain imaging techniques, such as positron emission

tomography and fMRI, have been used to examine this interaction.1,8 Many studies that have investigated brain responses Opaganib in vivo during visceral stimulation in FGID patients or healthy volunteers have been published. Because the results have often been contradictory, Derbyshire systematically reviewed the published studies as a critical appraisal and revealed that during visceral stimulation key regions, including the insula, and prefrontal, anterior cingulate and

primary sensory cortices, were activated in the majority of studies.1 In most of these published studies, balloon distension was used for visceral stimulation and the responses of the lower gastrointestinal LEE011 concentration tract were examined. There are few studies of the regional activation during esophageal acid exposure.9,10 In the case of acid stimulation

of the esophagus, the task model is unclear and so contradictory results may be acquired when using model-based techniques for the analysis. Independent component analysis is a method of identifying a single source from mixed independent sources, and does not need a priori information of the task, namely a task model. Moreover, group ICA is used to study specific conditions among subjects to hide individual differences, which ICA preserves.11 In our study, fMRI data were analyzed using group ICA, which revealed that several common cerebral regions were activated under three of the study conditions: during the first interval, the saline infusion, and the HCl infusion. Activated regions included the insula and cingulate gyri, which have been reported as activated during visceral stimulation. These regions were activated during MCE公司 the first interval as well as during the two infusions. It may have been caused by inserting the multi-lumen catheter transnasally, although there is a possibility that activity seen in those areas was background brain activity. Acid and saline infusion into the esophagus did not cause heartburn, whereas activation of the postcentral and precentral gyri was detected during liquid infusion. Although the subjects other than two subjects did not feel the liquid infusion, their brain might recognize the existence of liquid in the esophagus, thereby leading to possible swallowing.

This behavior limits the ability of shallow-diving predators to track Blainville’s acoustically and may provide a striking example of the evolutionary influence of the risk of predation on animal communication. “
“Understanding the population structure of a species is critical to its effective management and conservation. The humpback whale (Megaptera novaeangliae) has been the target of numerous research projects in several ocean basins, but no clear picture of its population structure has emerged. In the North Atlantic Ocean, genetic analyses and photo-identification movements have shown significant heterogeneity

among the summer feeding grounds. Building on this knowledge, we test the hypothesis that the feeding grounds represent distinct populations by analyzing the spatial pattern of summer humpback whale sightings and survey effort. Controlling

for the spatial pattern of effort, sightings are clustered, with learn more peaks at radial distances of 300 km, 600 km, and 1,500 km. These results provide insight into the spatial extent of the summer population structure of humpback whales in the North Atlantic Ocean. Fine-scale clustering at distances of 300 km and 600 km is compatible with multiple populations consisting of the Gulf of Maine, eastern Canada, Napabucasin chemical structure western Greenland, and Iceland. Broad-scale clustering at distances of 1,500 km may represent divisions between the western and eastern North

Atlantic populations. These results provide spatial bounds to the feeding grounds of humpback whales and emphasize their distinct nature as management units. “
“Quantifying the vocal repertoire of a species is critical for subsequent analysis of signal functionality, geographic variation, and social relevance. However, the vocalizations of free-ranging common dolphins (Delphinus sp.) have not previously been described from New Zealand waters. We present the first quantitative analysis of whistle characteristics to be undertaken on the medchemexpress New Zealand population. Acoustic data were collected in the Hauraki Gulf, North Island from 28 independent dolphin group encounters. A total of 11,715 whistles were collected from 105.1 min of recordings. Seven whistle contours were identified containing 29 subtypes. Vocalizations spanned from 3.2 to 23 kHz, with most whistles occurring between 11 and 13 kHz. Whistle duration ranged from 0.01 to 4.00 s (mean ± SD; 0.27 ± 0.32). Of the 2,663 whistles analyzed, 82% have previously been identified within U.K. populations. An additional six contours, apparently unique to New Zealand Delphinus were also identified. Data presented here offer a first insight into the whistle characteristics of New Zealand Delphinus. Comparisons with previously studied populations reveal marked differences in the whistle frequency and modulation of the New Zealand population.

From 1992 to 2008, the incidence rate of histologically unconfirmed HCC increased 2.5 times more rapidly than the incidence rate of confirmed HCC (Fig. 1). The APC in incidence rates for these two groups Selleckchem CP 690550 were 7.9 and 3.2, respectively (both statistically significant: P < 0.05). Between 1992 and 2008, incidence rates of localized stage HCC increased

nearly twice as rapidly as rates of regional and distant stage HCC combined (Fig. 2) and surpassed regional and distant stage incidence rates during 2006-2008. The APC in incidence rates for the two groups were 8.1 and 4.2, respectively (both statistically significant: P < 0.05, as were APCs for regional and distant stage alone, data not shown). The APC for unstaged HCC was −2.6 (P < 0.05). Incidence rates of reported invasive liver surgery or ablation (Fig. 3) increased significantly from 1992 to 2008 (APC = 10.7; P < 0.05). Incidence rates of HCC receiving no surgical intervention also increased significantly from 1992 to 2008 (APC = 7.2; P < 0.05). During 1998-2008, most HCC cases with reported first-course surgery or ablation had localized stage HCC (Fig. 4), including cases receiving transplantation (77%), resection (75%), and local tumor destruction (70%). Overall, 41% of cases had localized-stage HCC. One third of cases with no reported surgery or local tumor

destruction had localized-stage HCC. Among HCC cases diagnosed during 1998-2007 and followed for vital status through 2008, transplant recipients experienced 84% 5-year survival (Fig. 5). Cases with http://www.selleckchem.com/products/MG132.html local tumors less than 3 cm that received RFA had 5-year survival of 53%, whereas cases undergoing liver resection had 5-year survival of 47%. Among cases with reported local tumor destruction, 5-year survival was 35%. Compared to the 3% 5-year cause-specific survival in SEER-9 during 1975-1977 (data not shown), overall HCC survival during 1998-2007 was

18%, whereas survival was 8% among cases without reported invasive surgery or local tumor destruction. 5-year survival exceeded 75% among transplant recipients in all non-Hispanic racial and Hispanic ethnic groups with informative data (Fig. 5). Results were suppressed when there were fewer than 16 cases. 上海皓元 Among cases with reported liver resection, Asians or Pacific Islanders experienced significantly better 5-year survival (52%) than Hispanics (35%) and blacks (33%). American Indian/Alaska Native cases had 63% survival after resection, with wide CIs. 5-year survival after local tumor destruction was significantly higher among Asians or Pacific Islanders (43%) than black (21%) cases. Overall 5-year cause-specific survival among Asians or Pacific Islanders (23%) was significantly better than among white (18%), Hispanic (15%), or black cases (12%). White cases (18%) and American Indian/Alaska Native cases (20%) had significantly better survival than black cases (12%).