diabetes decreases the overall life expectancy and cause a heavy burden on public health. moreover, the asia - pacific region is considered to be on the verge of an emerging diabetes epidemic. the development of type 2 diabetes is affected by genetic and environmental determinants. recently, one study investigated whether common variants of functional and positional candidate genes, including adrb3, pparg, enpp1 and capn10, were determinants of type 2 diabetes. enpp1, also called k121q, has a glutamine substitution for lysine at codon 121. type 2 diabetes is characterized by insulin resistance, and enpp1 plays an important role in insulin resistance. enpp1 interacts with -subunit of the insulin receptor to interrupt signaling. in previous studies, the k121q polymorphism of the human pc-1 gene was strongly associated with insulin resistance. however, there was no association between insulin resistance and the k121q variant. in addition, there were discrepancies for the impact of enpp1 polymorphism on obesity between ethnic groups. obesity increases the concentration of insulin in plasma and is the major contributor of insulin resistance. obesity appears to be an effect modifier of type 2 diabetes in d1057 carriers. the association of obesity with the genetic variant of the insulin receptor substrate was identified in other studies. in the chinese han population, the pc-1 q121 allele was associated with insulin resistance. in women, carriers of the q allele had an increased risk for obesity development. in caucasians and african - americans, 121q carriers had an association with increased body mass index (bmi), and the three - allele risk type haploid qdeltg with the q allele increased the risk for obesity however, in the danish population, there were no differences in the distribution of frequencies of dominant types (kk wild type and kq / qq variant type) and alleles. the complexity of type 2 diabetes is related to factors such as genetic heterogeneity, interactions between genes, and the modulating role played by the environment. in spite of these limitations, studies of type 2 diabetes and genetic factors of obesity can predict the risks for development of both type 2 diabetes and obesity in order to assist primary prevention, and korea is an appropriate country for such studies because of the homogeneity of racial composition and lifestyle. therefore, the aim of this study was to analyze the presence of the enpp1 polymorphism, not studied yet in korean population, to identify the association between genotypes and allele with type 2 diabetes and obesity. this company is an electric power company located at kori, yonggwang, ulchin, wolsung, and seoul in korea. there were 195 male workers (age 48.26.7 yr, bmi 24.672.64 kg / m) who were diagnosed as diabetics during medical examinations conducted from march 2004 to october. the 1,750 male workers (age 45.27.7 yr, bmi 24.772.64 kg / m) in the control group were selected randomly. subjects were included if they met one of the criteria below and their onset age was older than 20 yr old to exclude type 1 diabetes: 1 ) blood - sugar level before a meal exceeded 126 mg / dl twice or more; 2 ) blood - sugar level before a meal exceeded 126 mg / dl once or more and blood - sugar level two hours after a meal exceeded 200 mg / dl; 3 ) those who reported that he had a history of diabetes in the questionnaire and being taken oral hypoglycemic agents. the workers included in the obesity group were those whose bmi was 25 kg / m or more. after collecting a blood sample from vein in fasting (8 hr) status, we measured the blood - sugar level, insulin, and lipid profile. we also measured height and weight to calculate bmi. if fasting glucose levels were greater than 126 mg / dl , we checked the 2 hr post - prandial plasma glucose level at each site within 1 month. height and weight were measured by autoanalyzer (health guard, fanics, seoul, korea). the fasting blood level was analyzed by glucose - oxidase assay using an autochemistry analyzer. to determine the lipid profile, total cholesterol was analyzed by enzyme assay using cholesterol oxidase (cod), high density lipoprotein (hdl) cholesterol by glycerol phosphate oxidase assay, low density lipoprotein (ldl) cholesterol by direct surfactant assay. we carried out this study under the approval by the ethnics committee of the asan medical center, and obtained written consent from all subjects, providing subjects with sufficient explanation to obtain informed consent. we extracted genomic dna from buffy coats using the generall blood sv kit (general biosystem, seoul, korea) and following the instructions suggested by the manufacturer. the method of genotyping used to identify the k121q polymorphism in enpp1 exon 4 was polymerase chain reaction - restriction fragment length polymorphism (pcr - rflp), using dna treated with a restriction enzyme after pcr, based on the paper reported by abate et al. we carried out student's t - test to analyze the effects of genotypes on biochemical parameters using genotypes as factors. the hardy - weinberg equilibrium was computed based on the goodness - of - fit test. we also investigated the differences in frequencies of genotypes between type 2 diabetic and normal groups, and between obesity and normal groups by fisher's exact test. the spss 12.0 (for window) statistical software package was used for statistical analysis. this company is an electric power company located at kori, yonggwang, ulchin, wolsung, and seoul in korea. there were 195 male workers (age 48.26.7 yr, bmi 24.672.64 kg / m) who were diagnosed as diabetics during medical examinations conducted from march 2004 to october. the 1,750 male workers (age 45.27.7 yr, bmi 24.772.64 kg / m) in the control group were selected randomly. subjects were included if they met one of the criteria below and their onset age was older than 20 yr old to exclude type 1 diabetes: 1 ) blood - sugar level before a meal exceeded 126 mg / dl twice or more; 2 ) blood - sugar level before a meal exceeded 126 mg / dl once or more and blood - sugar level two hours after a meal exceeded 200 mg / dl; 3 ) those who reported that he had a history of diabetes in the questionnaire and being taken oral hypoglycemic agents. the workers included in the obesity group were those whose bmi was 25 kg / m or more. after collecting a blood sample from vein in fasting (8 hr) status, we measured the blood - sugar level, insulin, and lipid profile. we also measured height and weight to calculate bmi. if fasting glucose levels were greater than 126 mg / dl , we checked the 2 hr post - prandial plasma glucose level at each site within 1 month. height and weight were measured by autoanalyzer (health guard, fanics, seoul, korea). the fasting blood level was analyzed by glucose - oxidase assay using an autochemistry analyzer. to determine the lipid profile, total cholesterol was analyzed by enzyme assay using cholesterol oxidase (cod), high density lipoprotein (hdl) cholesterol by glycerol phosphate oxidase assay, low density lipoprotein (ldl) cholesterol by direct surfactant assay. we carried out this study under the approval by the ethnics committee of the asan medical center, and obtained written consent from all subjects, providing subjects with sufficient explanation to obtain informed consent. we extracted genomic dna from buffy coats using the generall blood sv kit (general biosystem, seoul, korea) and following the instructions suggested by the manufacturer. the method of genotyping used to identify the k121q polymorphism in enpp1 exon 4 was polymerase chain reaction - restriction fragment length polymorphism (pcr - rflp), using dna treated with a restriction enzyme after pcr, based on the paper reported by abate et al. we carried out student's t - test to analyze the effects of genotypes on biochemical parameters using genotypes as factors. the hardy - weinberg equilibrium was computed based on the goodness - of - fit test. we also investigated the differences in frequencies of genotypes between type 2 diabetic and normal groups, and between obesity and normal groups by fisher's exact test. the spss 12.0 (for window) statistical software package was used for statistical analysis. the frequencies of the kk type, kq type, and qq type in enpp1 k121q were 82.1%, 17% and 0.9%, respectively. the homozygous type of q carrier (qq type) was added to the heterozygous type (kq type) because the frequency of qq type was very low (0.9%). we investigated the differences in age, blood pressure, bmi, and of clinical examinations according to genotypes of enpp1 k121q between the type 2 diabetic and non - diabetic groups (table 1). when type 2 diabetics and non - diabetics were pooled (n=1,945), there were no significant differences in bmi, systolic pressure, diastolic pressure, glucose value in fasting status, total cholesterol, ldl cholesterol, hdl cholesterol, triglyceride, c - reactive protein, and homa - ir between the kk type and kq+qq type. in addition, there were no significant differences in the same characteristics above between type 2 diabetic group and non - diabetic groups (table1), and between the obese group and non - obese groups (table2). the frequencies of genotypes were in accordance with the hardy - weinberg equilibrium (p=0.85). the odds ratio of having a kq+qq genotype was 0.85 for diabetics versus non - diabetics. the odds ratio of having a q allele was 0.91 for diabetics versus non - diabetics. however, there was no significant difference in the genotypic and allelic distribution between type 2 diabetics and non - diabetics (table3). the odds of a kq+qq genotype were 0.93 for obese versus non - obese subjects. furthermore, the odds of having a q allele were 0.96 for obese versus non - obese subjects. however, there was no significant difference in the genotypic and allelic distribution between obese and non - obese (table4). the frequency of the kk type in enpp1 k121q genotypes was 82.1%, that of kq+qq type was 17.9% and that of q allele was 9.4%. there was no statistically significant difference in the distribution among these genotypes and alleles (p=0.81, p=0.89, respectively), although the 121q carrier and q allele in obese and/or diabetics seemed to differ slightly from those in the non - obese non - diabetics (reference group). in determining the prevalence of the q allele carriers (kq and qq subjects) and q allele , there were no significant differences in the genotypic and allelic distribution with the respect to any phenotypes (data not shown). after adjusting for the effects of obesity, the probability of type 2 diabetes in kq+qq type was 0.858 (data not shown) and that in q allele was 1.095, showing no significant difference (table 5). moreover, after adjusting for the effects of type 2 diabetes, the probability of developing obesity in the kq+qq type was 0.936 (data not shown) and that in the q allele was 1.038, showing no significant difference (table 6). the of studies of the association between enpp1 k121q variants and both type 2 diabetes and obesity in several races are disparate. we carried out this study to investigate the association of k121q variants with type 2 diabetes and obesity in korean male workers. insulin resistance is a major component of the pathogenesis of type 2 diabetes, and insulin receptor kinase activity is impaired in muscle and other insulin - sensitive tissue of many type 2 diabetic patients, and then a potential inhibitor of the insulin receptor tyrosine kinase is identified as the plasma - cell membrane differentiation antigen-1 (pc-1). therefore, it is significant to analyze enpp1 (pc-1) polymorphism. in the previous studies of the association between type 2 diabetes and polymorphism in enpp1, the k121q missense mutation increased the odds ratio (or) for type 2 diabetes in dominican, south asian, caucasian, finnish, and french populations. moreover, according to a meta - analysis of the association between enpp1 k121q variant and type 2 diabetes, the odds ratios were 1.30 (95% confidence interval , 1.13 - 1.50) and 1.17 (95% ci, 1.10 - 1.25), showing significant association. in this study, 121q was not associated with type 2 diabetes, showing consistent with those in the japanese population, danish caucasians, oji - cree population, finnish population, and danish white subjects. most type 2 diabetes in koreans is characterized by non - obesity, thus the enpp1 k121q mutant relevant to insulin resistance possibly could be a candidate gene that is not appropriate to explain susceptibility to type 2 diabetes. this can be a possible explanation for the lack of association between enpp1 121q carrier and type 2 diabetes in this study. obesity is a main risk factor for the development of type 2 diabetes and there is linear association between obesity and type 2 diabetes. in previous studies of the association between obesity and polymorphism in enpp1, 121q carriers and/or q allele were associated with obesity in the chinese han population (bmi of obesity group 27 kg / m), caucasians (bmi of obesity group > 90th percentile), african - american adults (bmi of obesity group > 80th percentile), french population (bmi of obesity group 95th percentile), and dominican population (bmi of obesity group 30 kg / m). however, in this study (bmi of obesity group 25 kg / m), there was no difference in distribution between obesity and 121q carriers and presence of the q allele. this was consistent with those from a study of 7,333 danes and a spanish population in which the bmi of the obesity group was 25 kg / m or higher. on the other hand, in matsuoka's study, the percentage of subjects whose bmi was 30 kg / m or higher was too low (2.5%) to investigate the effect of k121q genotype on obesity. the of the present study showed that the frequencies of the q allele was 8.7% in the type 2 diabetic group and 9.2% in the obesity group, which was lower than those in finnish and swedish populations (12.9 - 15.1%), danish caucasians (14 - 16%), south asians in chennai (14%), caucasians in dallas (16%), south asians in dallas (19%), the dominican population (54.2%) and, black children (77%). the frequencies of the q allele investigated in this study might have a smaller statistical power to explain any association with either type 2 diabetes or obesity with 121q carriers (kq+qq) and/or the q allele. in , the present study suggests that the enpp1 k121q polymorphism was not associated with type 2 diabetes and obesity. the of negative associations in this study might be attributable to the low prevalence of obesity, relatively younger age, and low frequencies of the 121q carriers. large and prospective studies are needed to confirm this preliminary observation in the korean population.

Abstract: type 2 diabetes is characterized by insulin resistance, and enpp1 plays an important role in insulin resistance. we investigated the association of the enpp1 k121q polymorphism with both diabetes and obesity (body mass index) in korean male workers. the study design was case - control. subjects were 1,945 male workers (type 2 diabetes, 195 ; non - diabetes, 1,750) of nuclear power plants who received examinations from march to october in 2004. we collected venous blood samples under fasting (8 hr) conditions, calculated bmi by height and weight, and assessed relevant biochemical factors. the of this study demonstrated that the enpp1 121q genotype (kq+qq types) was not associated with type 2 diabetes (odds ratios , 0.854 ; 95% confidence interval , 0.571 - 1.278) or obesity (or, 0.933 ; 95% ci, 0.731 - 1.190). in addition, the frequency of the q allele was not related to type 2 diabetes (or, 0.911 ; 95% ci, 0.630 - 1.319) or obesity (or, 0.962 ; 95% ci, 0.767 - 1.205). we concluded that the enpp1 121q allele is not a critical determinant for either diabetes or obesity in korean males. the discordance between the of this study and those derived from studies of dominican, south asian, caucasian, finnish, and french populations might be due to differences in genetic s between these populations.


lipid apheresis provides a safe and effective means of treating patients with severe hyperlipidemia. it functions by first separating plasma from blood cells with a cell separator and then using either the adsorption of apolipoprotein b by affinity columns containing anti - apolipoprotein b antibodies or dextran sulphate, or their precipitation at low ph by heparin. lipid apheresis allows patients to attain lower levels of low - density lipoprotein (ldl), which are usually not attainable with traditional drug therapy alone, while leaving high - density lipoprotein (hdl) levels generally unaffected. when used in conjunction with statins and other lipid - lowering drugs , lipid apheresis may also induce the regression of coronary atherosclerotic plaque in familial hypercholesterolemia (fh) patients. fh is a group of autosomal dominant genetic defects ing in elevated serum (ldl) cholesterol levels. in the heterozygous state, fh is a relatively common but serious genetic disorder, with an incidence of about 1 in 500 persons in the general population. fh has been associated with an increased risk for atherosclerosis, premature coronary heart disease, and heart failure. fh is caused by a mutation affecting apolipoprotein b, proprotein convertase subtilisin kexin type 9 (pcsk9 ; an enzyme involved in ldl receptor degradation), or, most commonly, the ldl receptor gene, ing in defective ldl receptors and/or a diminished number of ldl receptors. these mutations cause ldl to be catabolized at a slower rate and thus accumulate in the circulation. currently, fh is treated using a variety of cholesterol - lowering drugs, most notably statins or hmg - coa reductase inhibitors. for many patients, however, statins are not a viable treatment option, because of either intolerance or ineffectiveness. lipid apheresis is an alternative form of treatment for these fh patients as well as those who have persistently elevated ldl levels despite treatment. because apheresis is performed at only a few highly specialized centers in relatively low volume, there is very little literature discussing the effectiveness of lipid apheresis on the reduction of lipid profiles and the prevention of future cardiac events. this study, therefore, reports the experience in a single metropolitan center of treating patients with hyperlipidemia with lipid apheresis. retrospective chart reviews were performed and questionnaire surveys were given to active lipid apheresis patients at the minneapolis heart institute (mhi) at abbott northwestern hospital (anw), minneapolis, minnesota. mhi and anw are divisions of allina health, a large healthcare provider in minnesota and western wisconsin. patients were identified through an electronic health record (ehr) screen of ambulatory patients representing all patients seen at all allina health metro area and regional locations between 2009 and 2012 (epic systems, verona wi). of these patients, criteria to qualify for apheresis were based on the united states food and drug administration (fda) approval recommendations. currently, the fda supports ldl apheresis for patients who, after six months, do not have an adequate response to diet therapy and maximum drug therapy, due to either ineffectiveness or intolerance, and meet the following criteria: functional homozygotes with an ldl cholesterol > 500 mg / dl without cad, functional heterozygotes with ldl cholesterol > 300 mg / dl without cad, functional heterozygotes with ldl cholesterol > 200 mg / dl with documented coronary heart disease. functional homozygotes with an ldl cholesterol > 500 mg / dl without cad, functional heterozygotes with ldl cholesterol > 300 mg / dl without cad, functional heterozygotes with ldl cholesterol > 200 mg / dl with documented coronary heart disease. the date of birth, gender, date of apheresis initiation, lipid disorder diagnosis, apheresis frequency, and family history of cardiac events were recorded. patients were noted as having fh if the active problem list contained a diagnosis of fh. to determine which patients had fh, we used the national lipid association (nla) criteria for an 80% probable fh diagnosis, using the highest ldl recorded in the patient chart as follows: age < 20 and ldl > 190 mg / dl, age 2029 and ldl > 220 mg / dl, and age 30 and ldl > 250 mg / dl. potential homozygous fh (hofh) patients were defined as having an untreated ldl > 500 mg / dl or a treated (on statin) ldl over > 300 mg / dl, in addition to clinical evidence of xanthomas before age of 10 years or having two parents with heart disease or high lipids. identifiable secondary causes for marked hyperlipidemia were excluded from the analysis by examining the ehr chart of each potential homozygote. current cholesterol lowering medications were also recorded, focusing on the use of statins, colesevelam (welchol), ezetimibe (zetia), niacin, and aspirin. a significant cardiovascular event was defined as a myocardial infarction (mi), a percutaneous transluminal coronary angioplasty (ptca) or stenting procedure, or a coronary artery bypass graft (cabg) using ehr documented icd-9 criteria. cardiac events were separated by their occurrence before or after the patient began apheresis, and the total number of events was recorded for each group. multiple cardiac events occurring at the same hospitalization, such as mi followed by ptca, were counted as a single event for cardiac event rate calculation. pre- and postapheresis cardiac event rates were calculated by adding the total number of cardiac events and dividing by the total person years during each time period. the preapheresis time period describes the time from the first documented ehr visit to the date of apheresis initiation. the postapheresis time period describes the time from the date of apheresis initiation to the study date. unverifiable events noted in the ehr but occurring prior to the first documented ehr visit were noted but excluded from the cardiac event rate calculation. mean acute ldl reductions were calculated by averaging all recorded ldl values prior to and immediately after the treatment sessions. mean acute total cholesterol, hdl cholesterol, and triglyceride reductions were calculated by using lipid profile from the most recent treatment session. ldl apheresis was performed at abbott northwestern hospital using the kaneka liposorber la-15 system (kaneka medical products). the system consists of the kaneka ma-03 machine, the integrated sulflux kp-05 plasma separator, which consists of porous hollow fibers, to separate the plasma from the whole blood, and two disposable liposorber la-15 adsorption columns to adsorb apolipoprotein b - containing lipoproteins from patient plasma. patients confirmed information in their ehr such as risk factors, answered questions relating to their awareness of fh and if their family had been previously tested for it, provided their level of satisfaction with their apheresis program, and indicated their interest in learning more about alternative treatments. the data from the questionnaires was cross - referenced with the data from the patient charts to ensure accuracy. descriptive statistics are displayed as means and sds for continuous variables; number and percentage with characteristic are given for categorical variables. categorical variables were analyzed using pearson's chi - square or fisher's exact tests. continuous variables were analyzed using student's t - test. a value of p < 0.05 was considered significant, and p values are two - sided where possible. all statistical calculations and plots were done with stata 11.2 (college station, tx). institutional review board approval was obtained for data collection, follow - up, and data analysis. of these, 8 (72.7%) were male, 10 (90.9%) were caucasian, 1 (9.1%) was african american, 10 (90.9%) carried the diagnosis of fh, with 2 (18.2%) patients identified as probable homozygotes, and 1 (9.1%) was diagnosed as having familial combined hyperlipidemia. the average age of patients was 65.6 9.3 years, and patients had been on apheresis for an average of 6.2 7.0 years. four (36.4%) patients were currently on statins while the other 7 (63.6%) had a history of statin intolerance. five of 11 (45.5%) patients were on a nonstatin cholesterol lowering medications, including 1 (9.1%) on colesevelam (welchol), 3 (27.3%) on ezetimibe (zetia), and 1 (9.1%) on niacin. maximum ldl levels ranged from 211 to 448 mg / dl with a mean (sd) value of 298 80.7 mg / dl in the study group. since our ehr was implemented in 2005, it is possible we may be underestimating the highest lifetime ldl for each patient. of the 11 participants, 9 completed the questionnaire in its entirety; 1 patient provided answers to all questions but did not disclose risk factors and 1 patient did not complete the questionnaire. all of the patients indicated that they were aware that they likely had fh and 7 patients indicated that their immediate family had been tested for fh. the patients self - reported a total of 44 cardiac events before apheresis and 8 cardiac events after apheresis. of the 10 patients that completed the questionnaire, 4 patients were currently on statins while the other 6 were statin intolerant. eight patients (72.7%) had a cardiac event documented by ehr, with 43 cardiac events occurring overall (table 4). self - reported events which were unable to be verified via the ehr were excluded from the cardiac event rate analysis. thirty - four cardiac events were documented before apheresis in 8 patients compared with 9 events in 5 patients after apheresis. after excluding cardiac events that were unverifiable, 14 cardiac events were documented in the preapheresis time period and 7 were documented in the postapheresis time period. the cardiac event rates were calculated to be 0.23 (0.13, 0.39) events per person year in the preapheresis group and 0.10 (0.041, 0.21) events per person year in the postapheresis group (p = 0.064). patients were observed for an average of 7.6 5.9 years before apheresis and 6.2 4.7 years after apheresis, with 60.6 total patient years before apheresis and 67.8 patient years after apheresis. this study was conducted to gain more information on lipid apheresis and evaluate the effectiveness in lowering lipid values. in addition , through chart review and patient survey, we attempted to gain a greater understanding of this patient population in terms of traditional risk factors, family awareness and screening, statin and other cholesterol medication uses, desire for additional treatment options, and ultimately cardiac events. our study shows that apheresis markedly lowers total cholesterol, ldl cholesterol, triglycerides and, to a much lesser degree, hdl cholesterol. there was a small, but statistically significant, reduction in hdl values after apheresis. many of these patients were statin intolerant and some had been using nonstatin cholesterol medications. importantly, 10/11 (90.9%) participants indicated a desire to learn more about other potential treatment options, indicating that this population may indeed experience fatigue of this procedure. although taken from a small study population, our data suggests a reduction in cardiac event rate after apheresis. while not statistically significant, our data shows a strong trend towards event rate reduction. this statistical insignificance is likely explained by the study's small sample size. with a larger population it is also important to note that the risk for cardiac events increases with age. ldl apheresis has been shown to improve endothelium dependent vasodilation , microvascular flow, and myocardial perfusion. some studies have also shown a significant reduction in angiographic cad, but others have not. these studies have been small, primarily nonrandomized trials. the ldl - apheresis atherosclerosis regression study (laars) looked at the change in plaque characteristics of patients undergoing apheresis compared to drug therapy over a period of two years. in that period, 7 out of 21 patients on apheresis had a cardiac event compared with 3 out of 21 on medication only. while this study found that apheresis arrested the progression of atherosclerosis the fh regression study found that ldl apheresis combined with simvastatin was more effective than colestipol plus simvastatin in reducing ldl cholesterol and lipoprotein (a) but was less effective at influencing coronary atherosclerosis. another study found that, out of 18 patients, 3 had myocardial infarctions, 1 underwent a cabg, and 12 needed coronary angioplasties within two years of beginning a combination therapy of apheresis, statins, and probucol. before beginning the combination therapy, 11 had experienced a mi, 5 had undergone a cabg, and 13 had undergone an angioplasty. the heparin - induced extracorporeal ldl precipitation (help) study found that help is suitable for reducing ldl concentrations and may work to reduce the burden of atherosclerosis, as there were no myocardial infarctions and a low coronary intervention rate in patients who began apheresis. due to the expensive nature of apheresis, a randomized, controlled clinical trial is needed to truly gauge the effectiveness of apheresis in reducing the occurrence of cardiac events. if apheresis is not deemed effective or is minimally effective, as some of these studies suggest, other types of treatment, such as lomitapide, mipomersen, or pcsk9 inhibitors, should be pursued. while satisfaction was generally high in our survey, patients specifically cited that this satisfaction was based on the of apheresis and not on the process itself. many patients complained about the invasive nature of apheresis, citing bruises from the procedure and the inconvenience of reporting for treatment every two weeks. additionally, almost all patients were interested in learning more about alternative treatments, suggesting that they would prefer an alternative treatment which could match the provided by apheresis. this study had several limitations. since lipid apheresis is an advanced treatment for an uncommon genetic disease, the limited number of patients available to participate in the study led to a small sample size. the event rate reduction was not statistically significant but showed a strong trend toward cardiac event rate reduction before and after apheresis. by defining the observational period initial time point as the first documented ehr visit , we excluded 20 events before apheresis and 2 events after apheresis from the cardiac event rate calculation. the lipid - lowering effects of apheresis are best expressed as reductions in interval means. although lipid apheresis was performed every two weeks, ldl values were not measured ever two weeks due to clinical practices. this inconsistency in measurement intervals prevents the use of more advanced measures to accurately track the effect apheresis has on ldl measurements. finally, this study focused on active apheresis patients and therefore did not include patients who had stopped apheresis or were deceased. lipid apheresis can reliably reduce ldl, non - hdl cholesterol, triglyceride, and total cholesterol levels in fh patients. our data suggest that lipid apheresis shows a strong, but not statistically significant, trend towards the reduction of cardiac events. apheresis is a viable treatment for fh patients, especially those that are statin - intolerant, due to its lipid lowering nature and its apparent reduction of cardiac events. however, there is a need for alternative treatments which are less invasive and provide easier patient access.

Abstract: lipid apheresis is used to treat patients with severe hyperlipidemia by reducing low - density lipoprotein cholesterol (ldl - c). this study examines the effect of apheresis on the lipid panel and cardiac event rates before and after apheresis. an electronic health record screen of ambulatory patients identified 11 active patients undergoing lipid apheresis with 10/11 carrying a diagnosis of fh. baseline demographics, pre- and postapheresis lipid levels, highest recorded ldl - c, cardiac events, current medications, and first apheresis treatment were recorded. patients completed a questionnaire and self - reported risk factors and interest in alternative treatment. there were significant reductions in mean total cholesterol (58.4%), ldl - c (71.9%), triglycerides (51%), high - density lipoprotein (hdl) cholesterol (9.3%), and non - hdl (68.2%) values. thirty - four cardiac events were documented in 8 patients before apheresis, compared with 9 events in 5 patients after apheresis. our survey showed a high prevalence of statin intolerance (64%), with the majority (90%) of participants indicating an interest in alternative treatment options. our have shown that lipid apheresis primary effect is a marked reduction in ldl - c cholesterol levels and may reduce the recurrence of cardiac events. apheresis should be compared to the newer alternative treatment modalities in a randomized fashion due to patient interest in alternative options.


agenesis of the inferior vena cava (ivc) as a cause of recurrent deep vein thrombosis (dvt) is uncommon. a 33-year - old male with no family history of thrombophilia, who had experienced multiple recurrent episodes of dvt over a 15-year period of unknown cause, was admitted into our hospital because of cellulitis in the right leg. congenital absence of the ivc could be a rare risk factor for idiopathic dvt, especially in young individuals. venous thromboembolism (vte), which includes deep vein thrombosis (dvt) and pulmonary embolism, has an incidence of 1 to 3 per 1000 individuals per year in western populations.1 congenital anomalies of the inferior vena cava (ivc) are uncommon, and have been associated with the development of venous thrombosis of the lower limbs.2 congenital anomalies of the ivc has been reported as a risk factor for dvt, especially in individuals < 30 years old, and a concomitant thrombophilic disorder has been found in such individuals.3 we report a case of recurrent dvt in a 33-year - old man with agenesis of the ivc. the patient had experienced recurring episodes of idiopathic dvt in the right leg for 15 years. a 33-year - old man was admitted to the internal medicine department, holy family hospital, nazareth, israel, because of cellulitis in the right leg. one week prior to his admission, he complained about pain and increased local heat in the left ankle and thumb of the right leg. the patient had no history of previous trauma, surgery, insect bites, dysuria, or joint symptoms, and no family history of thrombophilia. he reported that he had (a) rheumatic fever without any complications when he was 19 years old, which was treated with penicillin, (b) been hospitalized when he was 23 years old because of infected skin ulcers on the right calf, for which he was treated by parenteral antibiotics, and (c) recurrent episodes of idiopathic dvt for the last 15 years. he also reported that he had not been treated with warfarin, but he had been on prophylactic enoxaparin therapy for dvt some years ago which has since been stopped and that he had been recently treated with allopurinol and colchicine for a presumed diagnosis of gout. he had been investigated several times for a primary hypercoagulability state, and the were negative. on examination, the most outstanding clinical findings were swelling of ankles, mild edema, redness, and increased temperature of the right ankle and calf with trophic skin changes (skin discoloration with ulcers), and superficial varicose veins in the lower abdomen (figure 1). the clinical laboratory findings (erythrocyte sedimentation rate, leukocyte and platelet counts, and plasma hemoglobulin, plasma protein c, plasma protein s, fibrinogen, and antithrombin iii levels), the of the kidney and liver function tests, and resistance to activated protein c were all normal. polymorphisms of the genes that encode for methylenetetrahydrofolate reductase were not detected, and the factor v leiden and prothrombin mutations g20210a were absent. the of the clinical immunological studies for complement c3 and c4 and rheumatoid factor were negative, and no circulating titers for antinuclear antibody, antineutrophil cytoplasmic antibody, and cardiolipin antibody were found. cultures from the infected skin ulcers of the right leg were positive for methicillin - resistant staphylococcus aureus (mrsa). ultrasound imaging of the leg veins showed a previous dvt in the right common femoral vein, and dilated superficial inguinal veins. computer tomography with contrast of the abdomen showed agenesis of the infrarenal segment of the ivc (figure 2) with dilated azygos and hemiazygos veins (figure 3). there were also varicose veins in the abdominal wall and right groin, which were associated with dilated superficial and collateral veins (figure 4). transthoracic echocardiography of the patient s heart revealed mild atrial enlargement and good systolic function of the left ventricle, and no pathological valvular flows. the patient was diagnosed as having agenesis of the infrarenal segment of the ivc and dvt of the right leg without concomitant risk factors for vte. since we attributed the agenesis of the ivc to be the underlying cause of the recurrent episodes of the dvts, the patient was started on anticoagulant therapy (subcutaneous enoxaparin 160 mg / day) for dvt, antibiotic therapy (intravenous vancomycin 1.5 g / day for mrsa skin infection), and referred to a vascular surgeon specialist but the patient refused. at follow - up in the internal medicine clinic, the most outstanding clinical findings were swelling of left ankle, redness, with trophic skin changes, and a mild improvement of the skin ulcers. despite several phone calls for follow - up the normal ivc is composed of 4 segments: hepatic, suprarenal, renal, and infrarenal. since many transformations can occur during the formation of the ivc such anomalies occur in 0.3% of otherwise healthy individuals, and in 0.6% to 2% of patients with other cardiovascular anomalies.4 ruggeri et al reported 10 years ago 4 cases of congenital absence of the ivc in 75 young patients with idiopathic dvt over a 5-year period, and estimated that 5% of young patients with dvt had an anomaly of the ivc.5 venous thrombosis is caused by the presence of isolated or combined risk factors. almost 150 years ago, the nineteenth century pathologist rudolf virchow described 3 critically important causes of venous thrombosis: venous damage, coagulation defect(s), and venous stasis.6 individuals with a congenital anomaly of the ivc are typically asymptomatic, and the anomaly is usually detected incidentally during radiological or abdominal procedures. congenital absence of the ivc is infrequently associated with thromboembolic events.5 patients who suffer from congenital anomalies of the ivc usually develop a compensatory circulation through the azygos veins or collateral abdominal veins in order to keep the venous return near normal levels.7 most reported cases of congenital anomalies of ivc cases have been linked to thrombophilia disorders.3,5,7 however, the true prevalence of thrombophilia in congenital anomalies of the ivc is unknown because the screening for thrombophilia in patients with an ivc anomaly was usually incomplete.3 anticoagulants, but not thrombolytic therapy, are usually prescribed for venous thrombosis, but the duration of the anticoagulant therapy is not well established. hence, anticoagulant therapy for an indefinite duration will probably be prescribed, unless vascular reconstructive surgery is done on the anomalous ivc. such surgery has been rarely reported, and its long - term outcome is undetermined.8 congenital anomalies of the ivc may cause recurrent dvt, especially in young individuals.

Abstract: : agenesis of the inferior vena cava (ivc) as a cause of recurrent deep vein thrombosis (dvt) is uncommon.case:a 33-year - old male with no family history of thrombophilia, who had experienced multiple recurrent episodes of dvt over a 15-year period of unknown cause, was admitted into our hospital because of cellulitis in the right leg. computer tomography with contrast of the abdomen showed an absence of ivc.:congenital absence of the ivc could be a rare risk factor for idiopathic dvt, especially in young individuals.


The counselor helped the laborer because

he is a very kind person.
she is a very kind person.


The lawyer talked with the counselor because

she needed to gather additional evidence for the case.


The driver offered a ride to the teacher but

he refused the offer.
she refused the offer.


The cleaner got mad at the farmer because

she brought lots of dirt.
he brought lots of dirt.


The carpenter met with the teacher so that

she could fix the cabinets in the classroom.


The salesperson met with the counselor because


The receptionist reminded the cook to wear suits because


The sheriff told the counselor that

he was under investigation.
she was under investigation.


The supervisor was impressed by the tailor because

she is easily impressed.
he is easily impressed.


The driver picked up bread from the baker because


Youre so shiny
Stuck on the outside
Youre so pretty
Stuck on the outside
In denial
Stuck on the outside, in
Shut em out, Shut em out
Youre so with it
Stuck on the outside
Youre so without it
Stuck on the outside
Hot streak over
And now youre lying face down
Youre not the biggest shot around
So youre lying face down
You let your karma crash down
Whats upstairs, nothings there
Nothing is nothing squared
Whats upstairs, nothings there
Freeze, squeeze on your knees
You better walkabout
Youre so rigid
Stuck on the outside
You just dont get it
Stuck on the outside
So frustrated
Stuck on the outside, in
Shut em out, Shut em out
Youre so fetish
Stuck on the outside
So pathetic
Stuck on the outside
Hot streak over
And now youre lying face down
Youre not the biggest shot around
So youre lying face down
You let your karma crash down
Whats upstairs, nothings there
Nothing is nothing squared
Whats upstairs, nothings there
Freeze, squeeze on your knees
You better walkabout
Whats upstairs, nothings there
Nothing is nothing squared
Whats upstairs, nothings there
Freeze, squeeze on your knees
You better walkabout
You gave the hipper than hip
Something to talk about
Theyre shooting straight from the hip
And youre the sucker out
All of the statements that
Made this an A list
Felony squeeze on your knees
You better walkabout
The final blow
To your favorite show
And your fancy friends agree
When you test the ground
That youre standing on
Now youre sinking way ahead of me
Whats upstairs, nothings there
Nothing is nothing squared
Whats upstairs, nothings there
Freeze, squeeze on your knees
You better walkabout
Whats upstairs, nothings there
Nothing is nothing squared
Whats upstairs, nothings there
Freeze, squeeze on your knees
You better walkabout
You better walkabout
You better walkabout
You better walkabout


Longing for those days of wonder
Dredging up yesterday
You try omitting the cheese factor
But it rarely ever really looks the same
When colours of the others fade to grey
Hey Steve
When you gonna leave
Hanging all your hopes in syndicated cheese
Hey Steve
Million dollar freak
Jamie Summers screams out
Here today, gone later today
Jumping on the next big thing
But when the wagon starts to waver
We scramble off and resurrect the dead
And take our fill until were retro-fed
Jamie Summers
Bionic cover
In a fast based tech based
Psychedelic foot race
Over the mountain
Faster than a stopwatch
Up on the hillside
A bionic sasquatch


Buy a burger
So I jumped in my car
And I drove through the drivethrough
I got desperate
And I got lied to
Its another double cheese
Burger and fries
Youre gonna kill the cow
Just to eat the thighs
Chicken pick a nugget
Gonna puke in the bucket
Get a fat stack heart attack
Clogging up your power pack
Separated chicken
Pick and eat your meat
Youre gonna chuck it up
Because its beaks and feet
Ronald is killing me
A billion served, a billion die
Mickey D gonna break-a
The bricks with your thighs
Lean you mean, theres less
Grease than a piece of fat
Yeah right, come on, youre gonna buy that
Break for milkshake
Make way for outbreak
Pop the pimple of pus on the late great
Food, folks and fun in the sun
Grab the kids and youd better run
Serial killer, came back with the filler
Grown full of steroids, eat em
Make you strong
But it wont last long
Whats your swan song
Pick it up, big smack to the head
Two shots to the dome
And now youre dead
Oh what a rough time
Aint no rewind
Theyre selling death
And youre standing in line
Drive ahead please


If ignorance is this
Eyes wide open faking the trip
Automatic, so synthetic watch your step
You small pathetic man
The ultimate sin
Is thinking youre in
Youre so unsure
The one to be so lost in static
Oh so tragic
Its fun to be pistol whip
The chronic ultra tonic
Youre bleeding straight from the hip
The brass is counting on it
Its fun to be pistol whip
Out, censored, quite platonic
All the rage, out of phase
Everyone is scheming ways
Thanks for taking the time
To choke down someones being point of view
A tough pill to swallow
All the rage, out of phase
Everyone is scheming ways
Casualties of inner battles, scars remain
Rise to face the day
Dont waste away, so hollow
So hollow
Misguided logic
Track it dodge it
Someone stop it
Falling on deaf ears


Rippin up a pension cheque and tired
Sick and tired, sick
Hey old lady on the 7th floor balcony
Looking down on me like Im
Some kind of disrespectful being
Why dont you open up your mind
And give me a break
Loosen up
You say I dont respect your way
Rippin up a pension cheque and tired
Sick and tired, sick
Try to steal my mind
Stop blue haired crime
You are what I dont want to become
So numb
Rippin up a blue hair crime
We dont want or need no blue hair crime
Why dont you just loosen up


Jump back from where youre standing
Forget about it, get about it, get about it dont be late
Ive got to stop pretending
Ive thought about it, thought about it, thought about it
I want to stay....hey
Let me share your misery
Carnage makes me happy
Showing tacts beyond me
I cant take my eyes off you
Firmly planted in the avenue
I cant take my eyes off you
Rubber necking breaks your neck in two
Accident waiting to happen
Dont think about it, think about it, think about
Its someone else
You find it fascinating
The trick about it, trick about it, trick about it
Could be you
Beyond understanding
Let em seek it, let em seek it
Beyond comprehension
Let em feed it, bottom feed it
I swear your droolings hard to take
I sometimes make the same mistake
Your smiling face
Your smashed in face
Cant explain it, now Im captivated


Little twitches got me wondering
Darting eyes that peer away
Youre stuttering, it must be something
You said, you said, you say
But I doubt you saw it coming
Where were you with all the answers?
You lie, you lie, deny, so lie
Interest feigned but Im not listening
Minced your words about your history
Sell your stories, still you try to
Stare me down
But Im not buying
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Naivety has taught you one thing
The gilded lily blooms for you
But doubting eyes forgot to conceal
The truth, the truth, so true
But I doubt you saw it coming
Where were you with all the answers?
You lie, you lie, deny, so lie
Interest feigned but Im not listening
Minced your words about your history
Sell your stories, still you try to
Stare me down
But Im not buying
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Then I sense youre after something
And I see through your scam
You cannot pull wool over my eyes
Cause Im see into yours
Save your breath its all semantics
To tell the truth would breach your ethics
You lie, you lie, deny, so lie
Interest feigned but Im not listening
Minced your words about your history
Sell your stories, still you try to
Stare me down
But Im not buying
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector
Im turning on my lie detector


the half-ling book one in the fall of igneeria series kaylee soderburg copyright 2013 kaylee soderburg all rights reserved .


isbn : 1492913731 isbn-13 : 978-1492913733 for my family , who encouraged me to never stop fighting for my dreams chapter 1 summer vacations supposed to be fun , right ?


i wish i had a better answer to that question .


starlings , new york is not the place youd expect much to happen .


its a small quiet town , the kind where everyone knows your name .


its a place where your parents wouldnt even care if you stayed out late biking with your friends .


only because everyone felt so safe , so comfy .


they dont know the half of it .


i know it all and starlings is not the place where you want to be after dark .


My boyfriend did n't pay for this so I 'm not sure I will be able to do it . He booked as a surprise but did n't pay


FUCK OFF MACHINE !


it all . )


Good Morning !


Which Saturday ? What time ?


Thank you for the reminder . We will be there .


I am interested in Korean style Microblading eyebrow as below photo


Hi there . I 'm going to have to change my appt . I thought my flight got in tonight at {time} but I do n't arrive until 5:53 . That was a complete miss on my part .


I 'm running 8 minutes late . I 'm sorry my previous appointment ran longer than scheduled . Be there shortly


Cassie do you have any openings next week for a hair cut


(CNN) -- Shelling hit areas near two key cities in eastern Ukraine on Sunday morning, intensifying fears that a ceasefire that took effect less than two days ago may be falling apart. Why is the ceasefire under strain? A variety of fighting factions in the conflict zone -- on both sides -- may not fall directly under a military chain of command. The pro-Russian rebels are mostly volunteer militias; fighting against them on the Ukrainian side are at least some far-right nationalist militias. Controlling these groups is difficult and some may have different aims, including sabotaging the truce. At this point it's been nearly impossible to figure out who's doing the firing and why. The conditions of the ceasefire agreement don't help either. The conditions are vague and at this point there doesn't seem to be an effective mechanism in place inside the conflict zone to monitor and enforce the agreement. Why can't the two sides' leaders control their forces? It's unclear if Kiev has control over all of the fighting forces in eastern Ukraine. Some of the volunteer militias fighting alongside Ukrainian soldiers are far-right nationalists who've been critical of the current government in Kiev, but they're still fighting because they feel Ukraine is under attack by Russia. And who controls the pro-Russian rebels? Is it the local commanders? Is it Russian President Vladimir Putin? None of that is clear. Which side has the most to gain from the truce? If the truce leads to good-faith negotiations and a compromise, then both sides can gain. A compromise could look like something like this: The pro-Russian region of Donbas gets autonomy and self-determination under a federalized Ukrainian government, and in return the rebels drop their demand for independence and Kiev gets to protect Ukraine's sovereignty and territorial integrity. There are elements on both sides that don't want a compromise, and they could certainly have the potential of undermining the truce. What happens next? We wait to see if the overnight shellings and firings are an anomaly or if they're a sign of more violence and more fighting. If the ceasefire sticks, both sides have agreed to hold talks that will address the core issues and demands on both sides that are still unresolved -- including the disarming of the rebels, a guarantee of self-determination for the pro-Russian Donbas region, the fate of Russian-annexed Crimea, constitutional reform, and a solution to the humanitarian crisis in the conflict zone. Obviously if the fighting continues, all bets are off. What effect does this have on the rest of the world? What happens in the coming days will determine the next move by NATO and Western leaders. If the ceasefire falls apart, the West will likely turn up the pressure by following through with sanctions and bolstering Western forces in NATO's Baltic-member states. Moscow has already threatened to respond if that happens. The bottom line is, the conflict will escalate and so will the prospects of a regional conflict -- although at this point that seems unlikely.

Shelling in eastern Ukraine raises fears that a ceasefire may fall apart .
Reza Sayah: It's been nearly impossible to say who's doing firing and why .
It's unclear who has control over fighting forces on either side in east Ukraine .
There are elements on both sides that don't want a compromise .


(CNN) -- Remember when oil giant BP paid billions of dollars to clean up its own mess from the 2010 Gulf oil spill? Then the company agreed to plead guilty to criminal charges and pay an unprecedented $4 billion fine for the spill. In the latest development, Wednesday, BP was essentially told to stand in the corner when it comes to winning new federal contracts -- a potentially huge blow to the company's bottom line. And it's still likely on the hook for civil penalties the federal government hopes to recover for environmental damages. So, is BP being punished enough for the deadly and destructive Deepwater Horizon spill, or too much? It depends on who you ask. This matters. BP says it supports nearly a quarter of a million American jobs and has invested $52 billion in the United States since 2007. Experts suggest punishments ranging from massive fines to banning the company from offshore drilling. However this all shakes out, it likely will send a powerful message to the industry. Families of killed rig workers react to BP settlement . First, here's what happened Wednesday: . The U.S. Environmental Protection Agency said it will block BP from new government contracts due to its "lack of business integrity" stemming from the 2010 explosion and oil spill. It was a tragedy that killed 11 oil workers and dumped 205 million gallons of oil into the Gulf in a slow-moving, 85-day national drama that prosecutors called the worst environmental disaster in U.S. history. This month hasn't been good to BP. The decision follows the London-based company's agreement November 15 to plead guilty to criminal charges including manslaughter, obstruction of Congress and environmental violations related to the explosion and spill -- an agreement that still requires a judge's approval. What it means . Wednesday's EPA decision means BP won't be allowed to compete for new contracts, grants or other business until the company shows it meets federal business standards. As of February, BP had $9 billion in contracts to supply the U.S. government with fuel, most of it destined for military users, said Christine Tiscareno, a London-based analyst with S&P Capital IQ. Those contracts aren't affected by the EPA decision, the agency said. BP said it's already filed paperwork to get back in good graces with the EPA, said the agency is already preparing an administrative agreement to lift the suspension and highlighted what the company says it's done to rectify the situation. "As BP's submissions to the EPA have made clear, the company has made significant enhancements since the accident," the company said in a statement. "The company launched an internal investigation immediately after the accident, publicly released the results, and has been implementing all 26 of the investigation's recommendations." What's ahead . The next big step in the case comes in February, when a civil trial is expected to begin over the government's demand for civil damages under the Clean Water Act. That case could draw huge new fines for the company. The disaster, in addition to claiming 11 lives, caused disruption to countless residents and businesses, many of whom counted on the Gulf for their livelihoods, whether in the oil fields, fishing grounds or tourist beaches. For some, including environmentalists, the company couldn't be fined enough or spend enough money to get back on their good side. "Well, you know, we're discussing the worst environmental disaster in U.S. history," said Matt Dundas, acting campaign director at the environmental group Oceana. "The punishment needs to fit the crime." But, he said, the record $4 billion fine BP is expected to pay as a result of the criminal case is a tenth of the maximum it could have faced, making it small consolation to BP's harshest critics. The fine, while a record for the U.S. justice system, represents less than three months worth of profits for BP. The company reported $5.2 billion in profits in the quarter that ended September 30. Dundas is now rooting for the maximum possible verdict in the civil case -- $50 billion in fines. But he says there's only one punishment that would really get BP and other oil companies to sit up and take steps to prevent what Dundas says is the overwhelming risk of another large oil spill: being kicked out of the game entirely. "I think a terrific minimum would be to bar them from offshore drilling," he said. "That's really the only standard that's going to get oil companies to pay attention." The head of a trade association representing BP and other oil and gas operators in Louisiana and the Gulf of Mexico said Wednesday that BP has already complied with government requirements. "BP has done everything that the federal government has asked and more. ... This new EPA designation is another layer," said Chris John, president of the Louisiana Mid-Continent Oil and Gas Association. "How much is enough, when the economy in America is trying to dig out of the recession, and energy ... is a very important component to getting Americans back to work?" The EPA's decision could have a negative impact beyond BP, he said, affecting other companies in the industry who have also complied with regulators. "The companies that operate out in the Gulf of Mexico, they can go anywhere, they're global. They can drill anywhere in the world," John said. "They have chosen to come back to the Gulf in the past few years. ... This additional statement and designation by the EPA has to play into their decision of where to put their capital." BP didn't directly address whether it believes it has paid enough for the disaster, but noted Wednesday that it has spent $14 billion in response and cleanup costs, $1 million on restoration projects and $9 billion in compensation and expects to spend $7.8 billion more to resolve the majority of outstanding claims. Owning up . The company also pointed out it has acknowledged criminal responsibility, carried out recommendations made by investigators who studied the incident and has taken actions to strengthen safety and drilling standards that exceed federal regulations. Tiscareno, the oil analyst, said that while the costs to BP have been steep, they are bearable for the company. The big question is what happens in February, when the civil case goes to trial. Tiscareno said she expects BP, which has taken a long-term approach to recovering from the spill, will recover financially unless the civil trial nets an "irrational" decision. A huge verdict could pose problems for BP, Tiscareno said, but she said the government can't go too far in gutting the firm because of all the jobs and tax revenues the company provides. BP has invested $52 billion in the U.S. in the last five years, employs 23,000 U.S. residents and indirectly supports nearly 250,000 jobs, the company said Wednesday. "The U.S. needs BP as much as BP needs the U.S.," Tiscareno said. CNN's Kendra Wates and Catherine E. Shoichet contributed to this report.

NEW: Trade association: "BP has done everything that the federal government has asked"
Two years after the oil spill, experts weigh in on possible punishments for BP .
BP says it expects the temporary ban will be lifted soon .
The EPA says the oil giant showed a "lack of business integrity"


Adel Taarabt appeared for QPR for the first time since his public fall-out with Harry Redknapp in Monday afternoon's reserve game against Ipswich Town. The Moroccan's days at Loftus Road appeared to be numbered after his extraordinary spat with Redknapp last month. Taarabt claimed his manager never takes a training session after Redknapp had accused the midfielder of being 'three stone overweight' following the 3-2 defeat to Liverpool. VIDEO Scroll down to watch Harry Redknapp say  Taarabt's camp have told blatant lies . Adel Taarabt has played just three first-team games for QPR this season after returning from loan at AC Milan . Taarabt laughed off claims by QPR manager Harry Redknapp that the midfielder was 'three stone overweight' The 25-year-old was due to play for the club's Under 21s last week, but wasn't included in the draw against Swansea. However, Taarabt came through 90 minutes in the 3-0 win against Ipswich Town as he tries to prove his fitness to his boss. The former Spurs man, who has been hampered by an ankle injury, has been limited to just three appearances for the R's this season after returning from a loan spell at AC Milan. Taarabt hit back at Redknapp during an exclusive interview with Sportsmail last month . Taarabt spent last campaign on loan at Fulham and then Serie A side AC Milan .

Moroccan played 90 minutes for Under 21s in 3-0 win against Ipswich Town .
Taarabt has made just three first-team appearances for the R's this season .
Midfielder was accused of being 'overweight' by manager Harry Redknapp .
Taarabt hit back and claimed Redknapp never took training sessions .


By . Wills Robinson . PUBLISHED: . 11:14 EST, 6 March 2014 . | . UPDATED: . 12:19 EST, 6 March 2014 . Members of the feminist punk group Pussy Riot have been attacked by a gang of men inside a Russian McDonalds. Nadya Tolokonnikova and Masha Alyokhina were covered in paint while they sat and had breakfast in the city of Nizhny Novgorod. The pair, who were jailed for hooliganism in 2012, also had pepper spray, green antispetic and metal thrown in their faces during the assault. Scroll down for video . Attacked: Nadya Tolokonnikova and Masha Alyokhina were covered in paint during the assault while they sat and had breakfast in the city of Nizhny Novgorod . Distressed: The pair spoke directly into the camera after the incident . They were visiting the area to inspect a local prison with Peter Verzilov and members of NGO 'Zone of the Rights'. Tolonnikova allegedly left the restaurant with a 'cut forehead' and the group have complained to the police. She was seen getting up from her seat and clutching her face during the incident. while the gang of men continually shouted abuse. When the attack eventually stopped, one of the men held up a sign to the camera while another was seen shouting down the lens. At around 7.00 am the group barged into the fast food restaurant where the musicians and their crew were eating. Gang: They were covered in paint, antiseptic and pepper spray by the group of men . Prolonged: The gang shouted abuse while they continued to launch the liquids at the members of the feminist band . Close: One of the attackers faced up to Nadya Tolokonnikova, preparing to throw something at her . Abuse: The individuals continued to shout at the musicians while a crowd built up behind them . It is not the first time the group have been targeted by members of the public. At the start of the Sochi winter . Olympics, members of the group were whipped and tackled to the ground by Cossacks as . they sang in protest. The . band started to perform an anti-Putin song under a sign advertising the . Winter Olympics. But singer Tolokonnikova was brutally whipped . in the attack and the guitarist was left bloodied and bruised. Last month, Tolokonnikova was filmed saying the anti-government protests in Ukraine were an 'inspiation'. She was also among those arrested during protests outside a Moscow courthouse. Tolokonnikova and Alyokhina were released from seperate prisons on December 23, 2013 after the Russian State Duma approved an amnesty. Speech: An attacker spoke into a camera owned by the NGO 'Zone of the Rights' in the aftermath of the assault . Slogan: One man holds up a sign to the camera before the group leave the restaurant .

Nadya Tolokonnikova and Masha Alyokhina were also pepper sprayed .
The pair were in city of Nizhny Novgorod visiting a local prison .
Alyokhina reportedly left the fast food restaurant with a 'cut forehead'


check if details are parsed . concode_field_sep Container parent concode_elem_sep boolean isParsed concode_elem_sep long offset concode_elem_sep long contentStartPosition concode_elem_sep ByteBuffer deadBytes concode_elem_sep boolean isRead concode_elem_sep long memMapSize concode_elem_sep Logger LOG concode_elem_sep byte[] userType concode_elem_sep String type concode_elem_sep ByteBuffer content concode_elem_sep FileChannel fileChannel concode_field_sep Container getParent concode_elem_sep byte[] getUserType concode_elem_sep void readContent concode_elem_sep long getOffset concode_elem_sep long getContentSize concode_elem_sep void getContent concode_elem_sep void setDeadBytes concode_elem_sep void parse concode_elem_sep void getHeader concode_elem_sep long getSize concode_elem_sep void parseDetails concode_elem_sep String getType concode_elem_sep void _parseDetails concode_elem_sep String getPath concode_elem_sep boolean verify concode_elem_sep void setParent concode_elem_sep void getBox concode_elem_sep boolean isSmallBox

boolean function ( ) { return isParsed ; }


answer the library file defining the library containing the compilation unit to be indexed or null if the library is not on disk concode_field_sep IndexStore indexStore concode_elem_sep IndexPerformanceRecorder performanceRecorder concode_elem_sep DartUnit unit concode_elem_sep CompilationUnit compilationUnit concode_elem_sep Resource resource concode_elem_sep File libraryFile concode_field_sep boolean removeWhenResourceRemoved concode_elem_sep CompilationUnit getCompilationUnit concode_elem_sep boolean isQuery concode_elem_sep String toString concode_elem_sep void performOperation

File function ( ) { return libraryFile ; }


this method deletes index files of the @linkplain indexcommit for the specified generation number . concode_field_sep Logger log concode_field_sep void deleteNonSnapshotIndexFiles concode_elem_sep Map<String,Integer> buildRefCounts

void function ( Directory arg0 , Collection < SnapshotMetaData > arg1 , long arg2 ) { List < IndexCommit > loc0 = DirectoryReader . listCommits ( arg0 ) ; Map < String , Integer > loc1 = buildRefCounts ( arg1 , loc0 ) ; for ( IndexCommit loc2 : loc0 ) { if ( loc2 . getGeneration ( ) == arg2 ) { deleteIndexFiles ( arg0 , loc1 , loc2 ) ; break ; } } }


do n't use this . no , really , do n't use this . you already have an authenticationtoken with org.apache.accumulo.core.client.mapreduce.lib.impl.configuratorbase #getauthenticationtoken class , configuration . you do n't need to construct it yourself . gets the password from the configuration . warning : the password is stored in the configuration and shared with all mapreduce tasks ; it is base64 encoded to provide a charset safe conversion to a string , and is not intended to be secure . concode_field_sep PlaceHolder placeHolder concode_field_sep String getPrincipal concode_elem_sep void setLogLevel concode_elem_sep Level getLogLevel concode_elem_sep Boolean isConnectorInfoSet concode_elem_sep String getTokenClass concode_elem_sep void setZooKeeperInstance concode_elem_sep void setMockInstance concode_elem_sep Instance getInstance concode_elem_sep String enumToConfKey concode_elem_sep void setConnectorInfo

byte [ ] function ( Class < ? > arg0 , Configuration arg1 ) { return AuthenticationTokenSerializer . serialize ( org . apache . accumulo . core . client . mapreduce . lib . impl . ConfiguratorBase . getAuthenticationToken ( arg0 , arg1 ) ) ; }


force the eventbus from ambarieventpublisher to be serialand synchronous . concode_field_sep PlaceHolder placeHolder concode_field_sep void registerAlertListeners concode_elem_sep EventBus synchronizeAlertEventPublisher concode_elem_sep void replaceEventBus concode_elem_sep void registerAmbariListeners

void function ( Binder arg0 ) { EventBus loc0 = new EventBus ( ) ; AmbariEventPublisher loc1 = new AmbariEventPublisher ( ) ; replaceEventBus ( AmbariEventPublisher . class , loc1 , loc0 ) ; arg0 . bind ( AmbariEventPublisher . class ) . toInstance ( loc1 ) ; }


returns the id used by the client to authenticate itself when authentication is enabled . concode_field_sep TransportResponseHandler handler concode_elem_sep Logger logger concode_elem_sep String clientId concode_elem_sep Channel channel concode_field_sep byte[] sendRpcSync concode_elem_sep SocketAddress getSocketAddress concode_elem_sep String toString concode_elem_sep boolean isActive concode_elem_sep void close concode_elem_sep void fetchChunk concode_elem_sep void setClientId concode_elem_sep void sendRpc

String function ( ) { return clientId ; }


get the score . concode_field_sep int score concode_elem_sep Id3Tag id3Tag concode_elem_sep Comparator<SuggestionItem> comparator concode_elem_sep boolean isSelected concode_field_sep String getTrack concode_elem_sep int compare concode_elem_sep String getTitle concode_elem_sep String getYear concode_elem_sep String getGenre concode_elem_sep void setSelected concode_elem_sep String getArtist concode_elem_sep boolean isSelected concode_elem_sep Id3Tag getTag concode_elem_sep String getTAlbum concode_elem_sep void setScore


the aws support case id requested or returned in the call . the case id is an alphanumeric string formatted as shown in this example : case-12345678910-2013-c4c1d2bf33c5cf47 concode_field_sep String caseId concode_field_sep void setCaseId concode_elem_sep int hashCode concode_elem_sep CreateCaseResult withCaseId concode_elem_sep boolean equals concode_elem_sep CreateCaseResult clone concode_elem_sep String toString

String function ( ) { return this . caseId ; }


Kelly: Oh! Oh! Can I pick the first question?
Jessica: Sure. Go for it!
Kelly: What's the scariest place you've been to!
Jessica: I'll start: Palermo in Italy.
Mickey: And what's so scary about that? Did you break your nail? :P
Jessica: Shut it, Mickey! No, there are the Capuchin Catacombs with 8000 corpses!
Kelly: Ewwww! Corpses? Rly?
Jessica: Yeah! And you can look at them like museum exhibits. I think they're divided somehow, but have no clue how!
Ollie: That's so cool! Do you get to see the bones or are they covered up?
Jessica: Well, partly. Most of them were exhibited in their clothes. Basically only skulls and hands.
Mickey: I'm writing this one down! That's so precious!
Ollie: Me too!

The scariest place for Jessica was the Capuchin Catacombs in Palermo.


Carrie: Just back from Fantastic Beast :)
Gina: and what do you think?
Carrie: generally good - as usual nice special effect and visuals, an ok plot, a glimpse of the wizarding community in the US.
Alex: Sounds cool. I was thinking of going this weekend with Lane, but I've seen some bad reviews.
Carrie: Depends on what you expect really - I have a lot of sentiment towards Harry Potter so, I'm gonna like everything the do. But seriously the movie was decent. However, if you're expecting to have your mind blown, then no, it's not THAT good.
Gina: I agree. I saw it last week and basically I'm satisfied.
Alex: No spoilers, girls.
Carrie: no worries ;)
Carrie: And Gina, what do you think about Eddie Redmayne as Newt?
Gina: I loved him <3 I loved how introverted and awkward he was and how caring he was towards the animals. And with all that he showed a lot of confidence in his beliefs and was a genuinely compassionate character
Carrie: not your standard protagonist, that's for sure
Gina: and that's what I liked about him
Alex: Maybe I'll go and see it sooner so we can all talk about it.
Carrie: go see it. If' you're not expecting god-knows-what you're going to enjoy it ;)

Carrie and Gina saw "Fantastic Beast" and liked it. Ginna loved Eddie Redmayne as Newt.


Samantha: How are you doing today?
Robyn: better, but I really exaggerated with bier last night
Samantha: was it really only bier?
Robyn: sure, why?
Samantha: I don't know, your eyes, behaviour
Robyn: you want to say I took drugs?
Samantha: I'm only asking, I don't have anything against drugs
Robyn: but I have and I never take them
Samantha: ok, sorry, I didn't intend to offend you
Robyn: I just drank too much, that's eat
Samantha: much too much
Robyn: yes, I lost control a bit
Robyn: I am sorry for that
Samantha: important that you feel better today

Robyn drank too much beer last night and lost control. She is feeling better today.


Peyton: I have been asking you to bring that video game for me
Cameron: Honey, I am not having enough time to come home
Peyton: When would you come home?
Cameron: I will have to stay out of town for another week i guess
Peyton: Cant you just deliver that game through the courier? :P
Cameron: Dont be mean :/
Peyton: Get the job done and come to home then. ASAP :P

Peyton is expecting Cameron to bring the video game. Cameron will probably be out for another week.


Gene: Did you get the package I sent you
Jack: No, when did you send it?
Gene: on Friday
Jack: shit I should have gotten it by now
Jack: send me the tracking umber I;ll check whats up
Gene: 12345678900

Jack has not received yet the package Gene had sent him on Friday. She sent him the tracking number, so he could check the status of the shipment.


Russ: Hi Gurdun, are you feeling better?
Gurdun: Hi Ross, a little bit better, yes, thank you.
Russ: Do you think you'll be back at the uni this week?
Gurdun: Not tomorrow for sure, but I hope Wednesday maybe.
Russ: Oh, that's fine.
Gurdun: Yeah. I'm feeling a bit weak still
Russ: I guess that's pretty normal at this stage.
Gurdun: I believe so. And the muscle pain.
Russ: I know what you mean. I had flu like that three months ago.
Gurdun: Luckily the headache's gone. It was absolutely awful.
Russ: True enough. I had the same.
Gurdun: Anyway, how are things with you?
Russ: Same old, same old, you know. Not much happening in the middle of term.
Gurdun: And the team?
Russ: Oh yeah, we won the last match. It was a good game.
Gurdun: Great. Listen Russ, I need to run. Catch up later.
Russ: OK, talk to you later.

Gurdun has the flu. He is feeling better. Gurdun hopes he'll be back at the uni on Wednesday. Russ and his team won the last match.


Susan: Will you be home tomorrow?
Rob: Why do you ask?
Susan: We could have dinner together if you have time after work
Rob: Sure! Sounds great
Susan: Fantastic! I will cook something special then!

Rob will be home tomorrow. Rob and Susan will have dinner together after Rob's work. Susan will cook something special.


Evan: Hi Dennis, I need to cancel my lesson tomorrow, sorry.
Dennis: Fine, what's up?
Evan: Oh, got the flu, been off college since Tuesday. Should be ok for next Thurs.
Dennis: OK, just tell me in good time if you can't make it. Hope you feel better soon.
Evan: Bye, Den! Thanks.

Evan can't come to his lesson tomorrow, because he's got the flu.


Lorena: Hi, can you help me with something?
Martin: Well, I can try.
Martin: Depends what it is?
Lorena: I got a new desk and it comes with assembly instructions but I give up, I just can't do it.
Lorena: I'm illiterate when it comes to instructions, haha.
Lorena: So I could really use some help...
Martin: Hmm, I can't today, but how about tomorrow? Shouldn't take long anyway.
Lorena: Yeah, it's fine! I just need it for the weekend, but tomorrow's great! Sorry for troubling you again.
Martin: Don't mention it, we've known each other for so long it's almost like we're siblings, haha.
Lorena: Thanks a lot! I should be home by 6, so let me know when you can.

Martin is going to help Lorena assemble a new desk. He is coming to her house tomorrow.


Joanna: They are sending emails about Lewandowska.
Merve: What happened?
Joanna: <file_photo>
Merve: Wooow!
Joanna: She is hospitalized because she has measles.
Merve: She had what?
Joanna: Anyone who had contact with her within the last couple of days must get vaccinated.
Merve: Luckily I didn't see her since the last semester...
Joanna: I did, she is my thesis mentor :(
Merve: What will you do?
Joanna: They are organizing vaccinations in the main building from 17th until 19th.
Merve: You have to go!
Joanna: I know... And I just started working so I really don't have a lot of time.
Merve: Come on, this is really important.
Joanna: I will try to do it before work on 18th, hopefully I won't lose the entire day...

Lewandowska has measles. There are vaccinations in the main building from 17th until 19th for everyone who had contact with her.


Baghdad blasts kills at least 16 Insurgents have detonated two bombs near a convoy of US military vehicles in southern Baghdad, killing at least 16 people, Iraqi police say.


Immoral, unjust, oppressive dictatorship. . . and then there #39;s <b>...</b> ROBERT MUGABES Government is pushing through legislation designed to prevent human rights organisations from operating in Zimbabwe.


Ford to Cut 1,150 Jobs At British Jaguar Unit Ford Motor Co. announced Friday that it would eliminate 1,150 jobs in England to streamline its Jaguar Cars Ltd. unit, where weak sales have failed to offset spending on new products and other parts of the business.


Palestinian gunmen kidnap CNN producer GAZA CITY, Gaza Strip -- Palestinian gunmen abducted a CNN producer in Gaza City on Monday, the network said. The network said Riyadh Ali was taken away at gunpoint from a CNN van.


Bomb Blasts in Baghdad Kill at Least 35, Wound 120 Insurgents detonated three car bombs near a US military convoy in southern Baghdad on Thursday, killing at least 35 people and wounding around 120, many of them children, officials and doctors said.


Marine Wives Rally A group of Marine wives are running for the family of a Marine Corps officer who was killed in Iraq.


Auto Stocks Fall Despite Ford Outlook Despite a strong profit outlook from Ford Motor Co., shares of automotive stocks moved mostly lower Friday on concerns sales for the industry might not be as strong as previously expected.


Mladin Release From Road Atlanta Australia #39;s Mat Mladin completed a winning double at the penultimate round of this year #39;s American AMA Chevrolet Superbike Championship after taking


Suicide Bombings Kill 10 in Green Zone Insurgents hand-carried explosives into the most fortified section of Baghdad Thursday and detonated them within seconds of each other, killing 10 people and wounding 20.


Lightning Strike Injures 40 on Texas Field (AP) AP - About 40 players and coaches with the Grapeland High School football team in East Texas were injured, two of them critically, when lightning struck near their practice field Tuesday evening, authorities said.


help me find a new position as a programmer


plug used in china


what's the exhange rate between mxn and gbp


let me know what ingredients i need to make pasta


tell me what pokemon is


i was in thailand and i could not use my card to buy snacks


i want to reserve table for 5 at red robin under the name sara at 5


my check engine light is on so is anyone available to check it out for me


i need more checkbooks mailed as soon as possible


i watched "were the millers" on netflix last night


Silver-coloured gift box with white interior and silver logo. No exchanges or returns are accepted.


Collared dress featuring sleeveslling below the elbow with cuffs and pleats. Front patch pockets with flaps. Gathering at the waist. Button-up front.


Midi dress with a lapel collar and crossover V-neckline, long sleeves, an adjustable waistband with matching drawstrings. Asymmetric hem with side vents and a front slit.


Round neck midi dress with long sleeves. Featuring interior lining with adjustable straps and buttonstening at the back with an opening.


Flowing midi dress with a Johnny collar. Short sleeves. Polo-style buttonstening on the front.


Oversized collared shirt. Long cuffed sleeves with pleats. Dart detail in the back. Asymmetric hem. Polo-style buttonstening in the front.


Long sleeve bodysuit with a sweetheart neckline. Back zip and snap-buttonstening at the bottom.


Long sleeve sweatshirt with a high neck. Polo-stylestening with snap buttons.


Collared shirt with long cuffed sleeves. In-seam pockets on the sides, an asymmetric hem with side vents and frontstening with hidden buttons.


Round neck top with thin straps and a knot detail at the back.


Premise: Conceptually cream skimming has two basic dimensions - product and geography.

( ( Conceptually ( cream skimming ) ) ( ( has ( ( ( two ( basic dimensions ) ) - ) ( ( product and ) geography ) ) ) . ) )

(ROOT (S (NP (JJ Conceptually) (NN cream) (NN skimming)) (VP (VBZ has) (NP (NP (CD two) (JJ basic) (NNS dimensions)) (: -) (NP (NN product) (CC and) (NN geography)))) (. .)))

Hypothesis: Product and geography are what make cream skimming work.

( ( ( Product and ) geography ) ( ( are ( what ( make ( cream ( skimming work ) ) ) ) ) . ) )

(ROOT (S (NP (NN Product) (CC and) (NN geography)) (VP (VBP are) (SBAR (WHNP (WP what)) (S (VP (VBP make) (NP (NP (NN cream)) (VP (VBG skimming) (NP (NN work)))))))) (. .)))


Premise: you know during the season and i guess at at your level uh you lose them to the next level if if they decide to recall the the parent team the Braves decide to call to recall a guy from triple A then a double A guy goes up to replace him and a single A guy goes up to replace him

( you ( ( know ( during ( ( ( the season ) and ) ( i guess ) ) ) ) ( at ( at ( ( your level ) ( uh ( you ( ( ( lose them ) ( to ( the ( next level ) ) ) ) ( if ( ( if ( they ( decide ( to ( recall ( the ( the ( parent team ) ) ) ) ) ) ) ) ( ( the Braves ) ( decide ( to ( call ( to ( ( recall ( a guy ) ) ( from ( ( triple A ) ( ( ( then ( ( a ( double ( A guy ) ) ) ( ( goes up ) ( to ( replace him ) ) ) ) ) and ) ( ( a ( single ( A guy ) ) ) ( ( goes up ) ( to ( replace him ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) )

(ROOT (S (NP (PRP you)) (VP (VBP know) (PP (IN during) (NP (NP (DT the) (NN season)) (CC and) (NP (FW i) (FW guess)))) (PP (IN at) (IN at) (NP (NP (PRP$ your) (NN level)) (SBAR (S (INTJ (UH uh)) (NP (PRP you)) (VP (VBP lose) (NP (PRP them)) (PP (TO to) (NP (DT the) (JJ next) (NN level))) (SBAR (IN if) (S (SBAR (IN if) (S (NP (PRP they)) (VP (VBP decide) (S (VP (TO to) (VP (VB recall) (NP (DT the) (DT the) (NN parent) (NN team)))))))) (NP (DT the) (NNPS Braves)) (VP (VBP decide) (S (VP (TO to) (VP (VB call) (S (VP (TO to) (VP (VB recall) (NP (DT a) (NN guy)) (PP (IN from) (NP (NP (RB triple) (DT A)) (SBAR (S (S (ADVP (RB then)) (NP (DT a) (JJ double) (NNP A) (NN guy)) (VP (VBZ goes) (PRT (RP up)) (S (VP (TO to) (VP (VB replace) (NP (PRP him))))))) (CC and) (S (NP (DT a) (JJ single) (NNP A) (NN guy)) (VP (VBZ goes) (PRT (RP up)) (S (VP (TO to) (VP (VB replace) (NP (PRP him))))))))))))))))))))))))))))

Hypothesis: You lose the things to the following level if the people recall.

( You ( ( ( ( lose ( the things ) ) ( to ( the ( following level ) ) ) ) ( if ( ( the people ) recall ) ) ) . ) )

(ROOT (S (NP (PRP You)) (VP (VBP lose) (NP (DT the) (NNS things)) (PP (TO to) (NP (DT the) (JJ following) (NN level))) (SBAR (IN if) (S (NP (DT the) (NNS people)) (VP (VBP recall))))) (. .)))


Premise: One of our number will carry out your instructions minutely.

( ( One ( of ( our number ) ) ) ( ( will ( ( ( carry out ) ( your instructions ) ) minutely ) ) . ) )

(ROOT (S (NP (NP (CD One)) (PP (IN of) (NP (PRP$ our) (NN number)))) (VP (MD will) (VP (VB carry) (PRT (RP out)) (NP (PRP$ your) (NNS instructions)) (ADVP (RB minutely)))) (. .)))

Hypothesis: A member of my team will execute your orders with immense precision.

( ( ( A member ) ( of ( my team ) ) ) ( ( will ( ( execute ( your orders ) ) ( with ( immense precision ) ) ) ) . ) )

(ROOT (S (NP (NP (DT A) (NN member)) (PP (IN of) (NP (PRP$ my) (NN team)))) (VP (MD will) (VP (VB execute) (NP (PRP$ your) (NNS orders)) (PP (IN with) (NP (JJ immense) (NN precision))))) (. .)))


Premise: How do you know? All this is their information again.

( ( How ( ( ( do you ) know ) ? ) ) ( ( All this ) ( ( ( is ( their information ) ) again ) . ) ) )

(ROOT (S (SBARQ (WHADVP (WRB How)) (SQ (VBP do) (NP (PRP you)) (VP (VB know))) (. ?)) (NP (PDT All) (DT this)) (VP (VBZ is) (NP (PRP$ their) (NN information)) (ADVP (RB again))) (. .)))

Hypothesis: This information belongs to them.

( ( This information ) ( ( belongs ( to them ) ) . ) )

(ROOT (S (NP (DT This) (NN information)) (VP (VBZ belongs) (PP (TO to) (NP (PRP them)))) (. .)))


Premise: yeah i tell you what though if you go price some of those tennis shoes i can see why now you know they're getting up in the hundred dollar range

( yeah ( i ( ( tell you ) ( what ( ( though ( if ( you ( go ( price ( some ( of ( those ( tennis shoes ) ) ) ) ) ) ) ) ) ( i ( can ( see ( why ( now ( you ( know ( they ( 're ( ( getting up ) ( in ( the ( hundred ( dollar range ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) ) )

(ROOT (S (VP (VB yeah) (S (NP (FW i)) (VP (VB tell) (NP (PRP you)) (SBAR (WHNP (WP what)) (S (SBAR (RB though) (IN if) (S (NP (PRP you)) (VP (VBP go) (VP (VB price) (NP (NP (DT some)) (PP (IN of) (NP (DT those) (NN tennis) (NNS shoes)))))))) (NP (FW i)) (VP (MD can) (VP (VB see) (SBAR (WHADVP (WRB why)) (S (ADVP (RB now)) (NP (PRP you)) (VP (VBP know) (SBAR (S (NP (PRP they)) (VP (VBP 're) (VP (VBG getting) (PRT (RP up)) (PP (IN in) (NP (DT the) (CD hundred) (NN dollar) (NN range)))))))))))))))))))

Hypothesis: The tennis shoes have a range of prices.

( ( The ( tennis shoes ) ) ( ( have ( ( a range ) ( of prices ) ) ) . ) )

(ROOT (S (NP (DT The) (NN tennis) (NNS shoes)) (VP (VBP have) (NP (NP (DT a) (NN range)) (PP (IN of) (NP (NNS prices))))) (. .)))


Premise: my walkman broke so i'm upset now i just have to turn the stereo up real loud

( ( my walkman ) ( broke ( so ( i ( 'm ( upset ( now ( i ( just ( have ( to ( ( turn ( the stereo ) ) ( up ( real loud ) ) ) ) ) ) ) ) ) ) ) ) ) )

(ROOT (S (NP (PRP$ my) (NN walkman)) (VP (VBD broke) (SBAR (IN so) (S (NP (FW i)) (VP (VBP 'm) (ADJP (VBN upset) (SBAR (RB now) (S (NP (FW i)) (ADVP (RB just)) (VP (VBP have) (S (VP (TO to) (VP (VB turn) (NP (DT the) (NN stereo)) (ADVP (RB up) (RB real) (JJ loud)))))))))))))))

Hypothesis: I'm upset that my walkman broke and now I have to turn the stereo up really loud.

( ( ( ( I ( 'm ( upset ( that ( ( my walkman ) broke ) ) ) ) ) and ) ( now ( I ( have ( to ( ( turn ( the stereo ) ) ( up ( really loud ) ) ) ) ) ) ) ) . )

(ROOT (S (S (NP (PRP I)) (VP (VBP 'm) (ADJP (VBN upset) (SBAR (IN that) (S (NP (PRP$ my) (NN walkman)) (VP (VBD broke))))))) (CC and) (S (ADVP (RB now)) (NP (PRP I)) (VP (VBP have) (S (VP (TO to) (VP (VB turn) (NP (DT the) (NN stereo)) (ADVP (RB up) (RB really) (JJ loud))))))) (. .)))


Premise: But a few Christian mosaics survive above the apse is the Virgin with the infant Jesus, with the Archangel Gabriel to the right (his companion Michael, to the left, has vanished save for a few feathers from his wings).

( But ( ( a ( few ( Christian mosaics ) ) ) ( ( survive ( above ( ( the apse ) ( ( ( is ( ( the Virgin ) ( with ( the ( infant Jesus ) ) ) ) ) , ) ( with ( ( ( the ( Archangel Gabriel ) ) ( to ( the right ) ) ) ( -LRB- ( ( ( his companion ) ( ( ( ( Michael , ) ( to ( the left ) ) ) , ) ( has ( vanished ( save ( for ( ( a ( few feathers ) ) ( from ( his wings ) ) ) ) ) ) ) ) ) -RRB- ) ) ) ) ) ) ) ) . ) ) )

(ROOT (S (CC But) (NP (DT a) (JJ few) (JJ Christian) (NNS mosaics)) (VP (VBP survive) (PP (IN above) (NP (NP (DT the) (NN apse)) (SBAR (S (VP (VBZ is) (NP (NP (DT the) (NN Virgin)) (PP (IN with) (NP (DT the) (JJ infant) (NN Jesus)))) (, ,) (PP (IN with) (NP (NP (DT the) (NNP Archangel) (NNP Gabriel)) (PP (TO to) (NP (DT the) (NN right))) (PRN (-LRB- -LRB-) (NP (NP (PRP$ his) (NN companion)) (SBAR (S (NP (NP (NNP Michael)) (, ,) (PP (TO to) (NP (DT the) (NN left))) (, ,)) (VP (VBZ has) (VP (VBN vanished) (S (VP (VB save) (PP (IN for) (NP (NP (DT a) (JJ few) (NNS feathers)) (PP (IN from) (NP (PRP$ his) (NNS wings)))))))))))) (-RRB- -RRB-)))))))))) (. .)))

Hypothesis: Most of the Christian mosaics were destroyed by Muslims.

( ( Most ( of ( the ( Christian mosaics ) ) ) ) ( ( were ( destroyed ( by Muslims ) ) ) . ) )

(ROOT (S (NP (NP (JJS Most)) (PP (IN of) (NP (DT the) (JJ Christian) (NNS mosaics)))) (VP (VBD were) (VP (VBN destroyed) (PP (IN by) (NP (NNPS Muslims))))) (. .)))


Premise: (Read  for Slate 's take on Jackson's findings.)

( -LRB- ( ( ( Read ( for ( ( ( Slate 's ) take ) ( on ( ( Jackson 's ) findings ) ) ) ) ) . ) -RRB- ) )

(ROOT (S (-LRB- -LRB-) (VP (VB Read) (PP (IN for) (NP (NP (NP (NNP Slate) (POS 's)) (NN take)) (PP (IN on) (NP (NP (NNP Jackson) (POS 's)) (NNS findings)))))) (. .) (-RRB- -RRB-)))

Hypothesis: Slate had an opinion on Jackson's findings.

( Slate ( ( had ( ( an opinion ) ( on ( ( Jackson 's ) findings ) ) ) ) . ) )

(ROOT (S (NP (NNP Slate)) (VP (VBD had) (NP (NP (DT an) (NN opinion)) (PP (IN on) (NP (NP (NNP Jackson) (POS 's)) (NNS findings))))) (. .)))


Premise: Gays and lesbians.

(ROOT (NP (NP (NP (NNS Gays)) (CC and) (NP (NNS lesbians))) (. .)))

Hypothesis: Heterosexuals.


Premise: At the end of Rue des Francs-Bourgeois is what many consider to be the city's most handsome residential square, the Place des Vosges, with its stone and red brick facades.

( ( At ( ( the end ) ( of Rue ) ) ) ( ( des Francs-Bourgeois ) ( ( is ( what ( many ( consider ( to ( ( be ( ( ( ( ( the ( city 's ) ) ( ( most handsome ) ( residential square ) ) ) , ) ( the ( Place ( des Vosges ) ) ) ) , ) ) ( with ( its ( stone ( and ( red ( brick facades ) ) ) ) ) ) ) ) ) ) ) ) . ) ) )

(ROOT (S (PP (IN At) (NP (NP (DT the) (NN end)) (PP (IN of) (NP (NNP Rue))))) (NP (NNP des) (NNP Francs-Bourgeois)) (VP (VBZ is) (SBAR (WHNP (WP what)) (S (NP (DT many)) (VP (VBP consider) (S (VP (TO to) (VP (VB be) (NP (NP (NP (DT the) (NN city) (POS 's)) (ADJP (RBS most) (JJ handsome)) (JJ residential) (NN square)) (, ,) (NP (DT the) (NNP Place) (NNP des) (NNPS Vosges)) (, ,)) (PP (IN with) (NP (PRP$ its) (NN stone) (CC and) (JJ red) (NN brick) (NNS facades)))))))))) (. .)))

Hypothesis: Place des Vosges is constructed entirely of gray marble.

( ( Place ( des Vosges ) ) ( ( is ( ( constructed entirely ) ( of ( gray marble ) ) ) ) . ) )

(ROOT (S (NP (NNP Place) (FW des) (NNP Vosges)) (VP (VBZ is) (VP (VBN constructed) (ADVP (RB entirely)) (PP (IN of) (NP (JJ gray) (NN marble))))) (. .)))


Generate and show all primes with strictly ascending decimal digits.

Aside: Try solving without peeking at existing solutions. I had a weird idea for generating
a prime sieve faster, which needless to say didn't pan out. The solution may be p(r)etty trivial
but generating them quickly is at least mildly interesting.
Tip: filtering all 7,027,260 primes below 123,456,789 probably won't kill you, but there is
at least one significantly better and much faster way, needing a mere 511 odd/prime tests.

See also
 OEIS:A052015 - Primes with distinct digits in ascending order

Related

Primes with digits in nondecreasing order (infinite series allowing duplicate digits, whereas this isn't and doesn't)
Pandigital prime (whereas this is the smallest, with gaps in the used digits being permitted)

BEGIN # find all primes with strictly increasing digits                      #
    PR read "primes.incl.a68" PR                   # include prime utilities #
    PR read "rows.incl.a68"   PR                   # include array utilities #
    [ 1 : 512 ]INT primes;         # there will be at most 512 (2^9) primes  #
    INT p count := 0;                        # number of primes found so far #
    FOR d1 FROM 0 TO 1 DO
        INT n1 = d1;
        FOR d2 FROM 0 TO 1 DO
            INT n2 = IF d2 = 1 THEN ( n1 * 10 ) + 2 ELSE n1 FI;
            FOR d3 FROM 0 TO 1 DO
                INT n3 = IF d3 = 1 THEN ( n2 * 10 ) + 3 ELSE n2 FI;
                FOR d4 FROM 0 TO 1 DO
                    INT n4 = IF d4 = 1 THEN ( n3 * 10 ) + 4 ELSE n3 FI;
                    FOR d5 FROM 0 TO 1 DO
                        INT n5 = IF d5 = 1 THEN ( n4 * 10 ) + 5 ELSE n4 FI;
                        FOR d6 FROM 0 TO 1 DO
                            INT n6 = IF d6 = 1 THEN ( n5 * 10 ) + 6 ELSE n5 FI;
                            FOR d7 FROM 0 TO 1 DO
                                INT n7 = IF d7 = 1 THEN ( n6 * 10 ) + 7 ELSE n6 FI;
                                FOR d8 FROM 0 TO 1 DO
                                    INT n8 = IF d8 = 1 THEN ( n7 * 10 ) + 8 ELSE n7 FI;
                                    FOR d9 FROM 0 TO 1 DO
                                        INT n9 = IF d9 = 1 THEN ( n8 * 10 ) + 9 ELSE n8 FI;
                                        IF n9 > 0 THEN
                                            IF is probably prime( n9 ) THEN
                                                # have a prime with strictly ascending digits #
                                                primes[ p count +:= 1 ] := n9
                                            FI
                                        FI
                                    OD
                                OD
                            OD
                        OD
                    OD
                OD
            OD
        OD
    OD;
    QUICKSORT primes FROMELEMENT 1 TOELEMENT p count;     # sort the primes #
    FOR i TO p count DO                                # display the primes #
        print( ( "  ", whole( primes[ i ], -8 ) ) );
        IF i MOD 10 = 0 THEN print( ( newline ) ) FI
    OD
END