Precision Mass Measurements of Neutron-Rich Scandium Isotopes Refine the Evolution of N=32 and N=34 Shell Closures.

We report high-precision mass measurements of ^{50-55}Sc isotopes performed at the LEBIT facility at NSCL and at the TITAN facility at TRIUMF. Our results provide a substantial reduction of their uncertainties and indicate significant deviations, up to 0.7 MeV, from the previously recommended mass values for ^{53-55}Sc. The results of this work provide an important update to the description of emerging closed-shell phenomena at neutron numbers N=32 and N=34 above proton-magic Z=20. In particular, they finally enable a complete and precise characterization of the trends in ground state binding energies along the N=32 isotone, confirming that the empirical neutron shell gap energies peak at the doubly magic ^{52}Ca. Moreover, our data, combined with other recent measurements, do not support the existence of a closed neutron shell in ^{55}Sc at N=34. The results were compared to predictions from both ab initio and phenomenological nuclear theories, which all had success describing N=32 neutron shell gap energies but were highly disparate in the description of the N=34 isotone.

Erratum: High-Precision Mass Measurement of

This corrects the article DOI: 10.1103/PhysRevLett.120.032701.

High-Precision Mass Measurement of

We report the mass measurement of ^{56}Cu, using the LEBIT 9.4 T Penning trap mass spectrometer at the National Superconducting Cyclotron Laboratory at Michigan State University. The mass of ^{56}Cu is critical for constraining the reaction rates of the ^{55}Ni(p,γ) ^{56}Cu(p,γ) ^{57}Zn(ß^{+}) ^{57}Cu bypass around the ^{56}Ni waiting point. Previous recommended mass excess values have disagreed by several hundred keV. Our new value, ME=-38626.7(7.1) keV, is a factor of 30 more precise than the extrapolated value suggested in the 2012 atomic mass evaluation [Chin. Phys. C 36, 1603 (2012)CPCHCQ1674-113710.1088/1674-1137/36/12/003], and more than a factor of 12 more precise than values calculated using local mass extrapolations, while agreeing with the newest 2016 atomic mass evaluation value [Chin. Phys. C 41, 030003 (2017)CPCHCQ1674-113710.1088/1674-1137/41/3/030003]. The new experimental average, using our new mass and the value from AME2016, is used to calculate the astrophysical ^{55}Ni(p,γ) and ^{56}Cu(p,γ) forward and reverse rates and perform reaction network calculations of the rp process. These show that the rp-process flow redirects around the ^{56}Ni waiting point through the ^{55}Ni(p,γ) route, allowing it to proceed to higher masses more quickly and resulting in a reduction in ashes around this waiting point and an enhancement to higher-mass ashes.

High Precision Determination of the ß Decay Q(EC) Value of (11)C and Implications on the Tests of the Standard Model.

We report the determination of the Q(EC) value of the mirror transition of (11)C by measuring the atomic masses of (11)C and (11)B using Penning trap mass spectrometry. More than an order of magnitude improvement in precision is achieved as compared to the 2012 Atomic Mass Evaluation (Ame2012) [Chin. Phys. C 36, 1603 (2012)]. This leads to a factor of 3 improvement in the calculated Ft value. Using the new value, Q(EC)=1981.690(61) keV, the uncertainty on Ft is no longer dominated by the uncertainty on the Q(EC) value. Based on this measurement, we provide an updated estimate of the Gamow-Teller to Fermi mixing ratio and standard model values of the correlation coefficients.

First Direct Determination of the Superallowed ß-Decay QEC Value for (14)O.

We report the first direct measurement of the (14)O superallowed Fermi ß-decay QEC value, the last of the so-called "traditional nine" superallowed Fermi ß decays to be measured with Penning trap mass spectrometry. (14)O, along with the other low-Z superallowed ß emitter, (10)C, is crucial for setting limits on the existence of possible scalar currents. The new ground state QEC value, 5144.364(25) keV, when combined with the energy of the 0(+) daughter state, Ex(0(+))=2312.798(11) keV [F. Ajzenberg-Selove, Nucl. Phys. A523, 1 (1991)], provides a new determination of the superallowed ß-decay QEC value, QEC(sa)=2831.566(28) keV, with an order of magnitude improvement in precision, and a similar improvement to the calculated statistical rate function f. This is used to calculate an improved Ft value of 3073.8(2.8) s.

The association between the introduction of quantitative assessment of postpartum blood loss and institutional changes in clinical practice: an observational study.

BACKGROUND: Imprecise visual estimates of blood loss contribute to morbidity from postpartum hemorrhage. We examined the impact of quantitative assessment of postpartum blood loss on clinical practice and outcomes. METHODS: An observational study comparing blood loss, management and outcomes between two historical cohorts (August 2016 to January 2017 and August 2017 to January 2018) at an academic tertiary care center. Patients in the intervention group (second period) had blood loss quantified compared with visual estimation for controls. RESULTS: We included 7618 deliveries (intervention group n=3807; control group n=3811). There was an increase in the incidence of hemorrhage (blood loss >1 L) in the intervention group for both vaginal (2.2% vs 0.5%, P <0.001) and cesarean delivery (12.6% vs 6.4%, P <0.001). There was also a difference in median blood loss for vaginal (258 mL [151-384] vs 300 mL [300-350], P <0.001); and for cesarean delivery (702 mL [501-857] vs 800 mL [800-900], P <0.001). The median red blood cell units transfused was different in the intervention group having cesarean delivery (2 units [1-2] vs 2 units [2-2], P=0.043). Secondary uterotonic usage was greater in the intervention group for vaginal (22% vs 17.3%, P <0.001) but not cesarean delivery (7.0% vs 6.0%, P=0.177). Laboratory costs were different, but not the re-admission rate or length of stay. CONCLUSIONS: Quantifying blood loss may result in increased vigilance for vaginal and cesarean delivery. We identified an association between quantifying blood loss and improved identification of postpartum hemorrhage, patient management steps and cost savings.

Statistical strategies to improve the efficiency of molecular studies of colorectal cancer prognosis.

The evaluation of tumour molecular markers may be beneficial in prognosis and predictive in therapy. We develop a stopping rule approach to assist in the efficient utilisation of resources and samples involved in such evaluations. This approach has application in determining whether a specific molecular marker has sufficient variability to yield meaningful results after the evaluation of molecular markers in the first n patients in a study of sample size N (n

Elastic properties of synthetic materials for soft tissue modeling.

Mechanical models of soft tissue are useful for studying vibro-acoustic phenomena. They may be used for validating mathematical models and for testing new equipment and techniques. The objective of this study was to measure density and visco-elastic properties of synthetic materials that can be used to build such models. Samples of nine different materials were tested under dynamic (0.5 Hz) compressive loading conditions. The modulus of elasticity of the materials was varied, whenever possible, by adding a softener during manufacturing. The modulus was measured over a nine month period to quantify the effect of ageing and softener loss on material properties. Results showed that a wide range of the compression elasticity modulus (10 to 1400 kPa) and phase (3.5 degrees -16.7 degrees ) between stress and strain were possible. Some materials tended to exude softener over time, resulting in a weight loss and elastic properties change. While the weight loss under normal conditions was minimal in all materials (<3% over nine months), loss under accelerated weight-loss conditions can reach 59%. In the latter case an elasticity modulus increase of up to 500% was measured. Key advantages and limitations of candidate materials were identified and discussed.

Experimental and Computational Models for Simulating Sound Propagation Within the Lungs.

An acoustic boundary element model is used to simulate sound propagation in the lung parenchyma and surrounding chest wall. It is validated theoretically and numerically and then compared with experimental studies on lung-chest phantom models that simulate the lung pathology of pneumothorax. Studies quantify the effect of the simulated lung pathology on the resulting acoustic field measured at the phantom chest surface. This work is relevant to the development of advanced auscultatory techniques for lung, vascular, and cardiac sounds within the torso that utilize multiple noninvasive sensors to create acoustic images of the sound generation and transmission to identify certain pathologies.

Boundary element model for simulating sound propagation and source localization within the lungs.

An acoustic boundary element (BE) model is used to simulate sound propagation in the lung parenchyma. It is computationally validated and then compared with experimental studies on lung phantom models. Parametric studies quantify the effect of different model parameters on the resulting acoustic field within the lung phantoms. The BE model is then coupled with a source localization algorithm to predict the position of an acoustic source within the phantom. Experimental studies validate the BE-based source localization algorithm and show that the same algorithm does not perform as well if the BE simulation is replaced with a free field assumption that neglects reflections and standing wave patterns created within the finite-size lung phantom. The BE model and source localization procedure are then applied to actual lung geometry taken from the National Library of Medicine's Visible Human Project. These numerical studies are in agreement with the studies on simpler geometry in that use of a BE model in place of the free field assumption alters the predicted acoustic field and source localization results. This work is relevant to the development of advanced auscultatory techniques that utilize multiple noninvasive sensors to construct acoustic images of sound generation and transmission to identify pathologies.

The benefit of combination therapy depends on disease phenotype and duration in Crohn's disease.

BACKGROUND: The impact of combination therapy on disease-related morbidity in patients with established Crohn's disease (CD) or ulcerative colitis (UC) remains to be well-defined. AIM: To examine the effect of combination therapy on disease outcomes in CD and UC. METHODS: Using a multicenter prospective cohort, we classified CD and UC patients as being on monotherapy with anti-TNF or on combination with an immunomodulator. The primary outcome was a composite of new IBD-related surgery, hospitalisations, penetrating complications, need for corticosteroids or new biological at 1 year. Multivariable regression models adjusted for potential confounders. RESULTS: We included 707 patients with CD (45% combination therapy) and 164 with UC (38% combination therapy). Combination therapy was not associated with reduction in the composite outcome in either CD (OR: 0.87, 95% CI: 0.63-1.22) or UC (OR: 1.45, 95% CI: 0.63-3.38). However, while no difference was noted in those with nonstricturing, nonpenetrating CD, a significant reduction in the likelihood of the outcome was seen in those with stricturing or penetrating CD (30% vs 39%, OR: 0.58, 95% CI: 0.37-0.90). A stronger effect was also observed in those with disease duration <5 years (OR: 0.35, 95% CI: 0.14-0.87) compared to those with a longer duration (OR: 0.75, 95% CI: 0.45-1.27). A similar reduction in occurrence of composite outcome was noted with infliximab and with other anti-TNF biologics. CONCLUSION: The benefit of combination immunomodulator-biological therapy is stronger in those with complicated Crohn's disease, particularly early on in their disease course.

Cigarette smoking and the risk of colorectal cancer in women.

Colorectal cancer incidence rates for smokers, nonsmokers living with smokers (i.e., passive smokers), and nonsmokers in smoke-free households were compared in a 12-year prospective study of 25,369 women who participated in a private census conducted in Washington County, MD, in 1963. Women who smoked had a decreased relative risk of colorectal cancer compared with the risk for nonsmokers (age-adjusted relative risk, 0.76; 95% confidence interval, 0.52-1.10). The risk for passive smokers was similar to that for smokers. The relative risks were significantly reduced for older women; relative risks were 0.42 for smokers and 0.66 for passive smokers over age 65. The data suggest that older women who smoke have a lower risk of colorectal cancer than nonsmokers. The effect may be mediated by an antiestrogenic effect of smoking.

Calcium supplementation and rectal mucosal proliferation: a randomized controlled trial.

BACKGROUND: Data from studies using rodents suggest that dietary calcium inhibits bile acid-induced mucosal damage and experimental carcinogenesis in the large bowel. However, in humans, the effect of dietary calcium and calcium supplementation on proliferation and carcinogenesis in the large bowel has been unclear. PURPOSE: To assess the effect of calcium supplementation on rectal mucosal proliferation in humans, we conducted a multicenter, randomized, placebo-controlled, double-blinded trial. METHODS: Participants were part of a larger multicenter chemoprevention trial; all were at high risk for large-bowel neoplasia, with at least one large-bowel adenoma removed endoscopically within the 3 months before study entry but with no known polyps remaining. Subjects were randomly assigned to receive daily either 3000 mg of calcium carbonate (providing 1200 mg elemental calcium) or an identical-appearing placebo tablet. During a scheduled endoscopy 6-9 months after random assignment (approximately 1 year after the qualifying endoscopy), rectal mucosal samples were obtained from 333 patients (173 assigned to calcium and 160 assigned to placebo). Proliferating cell nuclear antigen (PCNA) labeling indices (LIs) were computed as the measure of proliferation in specimens from 146 patients receiving calcium and 129 patients receiving placebo. Bromodeoxyuridine (BrdU) labeling was used to measure proliferation in a smaller number of specimens (27 calcium-receiving and 31 placebo-receiving participants). For each scorable crypt having at least one labeled cell (or surrounded by crypts with at least one labeled cell), a crypt LI was calculated as the number of labeled cells divided by the total number of crypt cells. Crypt LIs were averaged to produce a participant's average LI. RESULTS: The overall unadjusted mean PCNA LIs (+/- SE) were similar in the calcium and placebo groups (3.85% +/- 0.08% versus 3.92% +/- 0.08%, respectively, P = .30). The overall unadjusted mean BrdU LIs (+/- SE) were 3.88% +/- 0.30% in the calcium group and 3.54% +/- 0.21% in the placebo group (P = .54). PCNA labeling indices in the most luminal 40% of the crypt were small but, if anything, were higher in the calcium group. There was no patient subgroup within which calcium had an antiproliferative effect; the overall findings persisted among patients with high and low calcium intake, high and low fat intake, and high and low fiber intake. CONCLUSIONS: Calcium supplementation does not decrease rectal mucosal proliferation, as measured by PCNA (and BrdU) immunohistochemistry, in patients with previous large-bowel adenomas. This study, therefore, does not provide evidence for an anticarcinogenic effect of calcium.

Diet and risk of colorectal adenomas: macronutrients, cholesterol, and fiber.

BACKGROUND: Diet is thought to be important in the etiology of colorectal cancer. Studies suggest that a diet high in red meat and saturated fat and low in dietary fiber and vegetables may increase cancer risk. Diet may also be important in the development of colorectal adenomas that are precursors of most colorectal cancers, but this hypothesis has not been well studied. PURPOSE: This case-control study was designed to examine the effects of dietary consumption of cholesterol, fiber (vegetables, fruits, beans, and grains), and macronutrients (protein, carbohydrate, and fat) on risk for colorectal adenomas. METHODS: Analyses were based on data from 236 subjects (105 men and 131 women) with histologically confirmed adenomas (cases) and 409 adenoma-free control subjects (165 men and 244 women), all of whom had had colonoscopy. Case and control subjects were similar with respect to gender, body mass, race, marital status, education, and indications for colonoscopy. Using a validated quantitative food-frequency questionnaire, an experienced graduate nutritionist interviewed each subject by telephone. Sex-specific analyses were conducted because the ranges of nutrient intake were substantially different for men and women. Odds ratios (ORs) were calculated according to quintiles of nutrient intake. RESULTS: Carbohydrate intake was inversely related to adenoma risk in women (P for trend = .002). Compared with women in the lowest quintile of carbohydrate consumption, those in the highest quintile were 60% less likely to develop adenomas (OR = 0.39; 95% confidence interval [CI] = 0.19-0.80). Intake of fruit (P for trend = .028) and intake of fiber derived from vegetables and fruits (P for trend = .012) were also inversely related to adenomas in women. Total fat showed a positive association in women (P for trend = .004), with an OR of 2.69 for the highest versus the lowest quintile (95% CI = 1.31-5.50). Results were comparable for saturated fat (P for trend = .027). The risks in men were generally similar in direction and magnitude but were not statistically significant. CONCLUSIONS: These data support the hypothesis that a diet high in fat and low in carbohydrates, fruits, and fruit and vegetable fiber increases risk not only for colorectal cancer but also for precursor colorectal adenomas. IMPLICATIONS: These results, which are consistent with findings of other investigators, suggest that environmental factors, influencing risk for colorectal cancer, such as a high-risk diet, may lead to development of the precursor adenomas.

Folate intake, alcohol consumption, cigarette smoking, and risk of colorectal adenomas.

BACKGROUND: Recent evidence suggests that folic acid (and derivatives) could contribute to the protective effect of fruits and vegetables against the risk of large-bowel cancer. Other evidence indicates that alcohol drinking and cigarette smoking may impair the biologic actions of folate. We used data from an adenoma prevention trial to investigate the occurrence of colorectal adenomas (possible precursors of colorectal cancer) in association with folate intake, alcohol consumption, and cigarette smoking. METHODS: Patients with at least one recent large-bowel adenoma were followed with colonoscopy 1 year and 4 years after their qualifying colon examinations. Adenomas detected after the year 1 examination were used as end points. A food-frequency questionnaire was administered at study entry and at study completion; nutrient intake at study entry was used in this analysis. All statistical tests were two-sided. RESULTS: After adjustment for caloric intake, dietary folate had a significant protective association with the risk of recurrence of large-bowel adenoma (P for trend = .04). However, this inverse association was attenuated by further adjustment for intake of dietary fiber and fat. Use of folate supplements was not associated with a reduction in risk. Alcohol intake (seven or more drinks/week) was associated with increased risk (odds ratio = 2.04; 95% confidence interval = 1.28-3.26). Cigarette smoking, even smoking for long duration, was not related to adenoma recurrence. CONCLUSIONS: These data provide only modest support for previous findings suggesting beneficial effects of folate on colorectal adenoma risk. We find no evidence that cigarette smoking increases risk. These findings do suggest a substantial increase in risk with alcohol consumption.

Histamine receptor antagonists and incident colorectal adenomas.

BACKGROUND: Prior studies suggest that histamines may modulate the development of colorectal neoplasia. AIM: To assess whether histamine receptor antagonist use was associated with adenoma formation. METHODS: Patients (n = 2366) were drawn from three adenoma chemoprevention trials. All underwent baseline colonoscopy with removal of adenoma(s) and were deemed free of remaining lesions; they were followed with surveillance colonoscopy. Medication use was assessed by questionnaire. Adjusted risk ratios for adenoma formation related to histamine receptor antagonist use (histamine H1 and H2 receptor, H1RA and H2RA) were determined using log linear models. RESULTS: In pooled analyses, H1RA exposure was not associated with subsequent adenoma risk (RR = 1.10; 95% CI 0.97-1.25) or multiple adenoma formation (RR = 0.85; 95% CI 0.67-1.07). H2RA use also was not associated with adenoma (RR = 0.90; 95% CI 0.77-1.06), or multiple adenoma (RR = 0.77; 95% CI 0.57-1.04) in the pooled analyses, but H2RA users in the first trial had a decreased risk of adenoma (RR = 0.70; 95% CI 0.48-1.03) and multiple adenoma (RR = 0.31; 95% CI 0.12-0.79). CONCLUSION: H2RA use was associated with reduced risk for adenoma in one trial, but not in the pooled analyses. Further study would be warranted before undertaking randomized trials of H2RAs for adenoma chemoprevention.

Variable presentation of thrombocytopenia in Graves' disease.

An association between thrombocytopenia and thyrotoxicosis has been reported but its mechanism is unclear. We describe five patients in whom thrombocytopenia accompanied Graves' disease. The thrombocytopenia resembled idiopathic thrombocytopenic purpura and responded to prednisone therapy in cases 1 and 2. In case 3, thrombocytopenia remitted with treatment of the thyrotoxicosis, while, in case 4, remission occurred despite persistent hyperthyroidism. In case 5, thrombocytopenia persisted despite correction of the hyperthyroidism but remained clinically insignificant. We conclude that there is a clear association between the two conditions but the clinical patterns of presentation and pathogenesis seem heterogenous. This variability must be considered during management.

Nephrosclerosis postpartum and in women taking oral contraceptives.

The condition of a patient with postpartum nephrosclerosis improved during heparin therapy. Review of the literature disclosed 29 other patients with the same histopathologic characteristics, eight of whom also recovered substantial renal function after anticoagulation therapy. Also reported is a patient in whom renal failure occurred while she was taking oral anovulatory agents. Renal biopsy specimen showed the same histopathologic features, which raises the question of similar factors mediating the expression of this disease. We suggest a uniform terminology for this syndrome, either postpartum nephrosclerosis or nephrosclerosis in women taking oral contraceptives.

A critical appraisal of ticlopidine, a new antiplatelet agent. Effectiveness and clinical indications for prophylaxis of atherosclerotic events.

BACKGROUND: Recommendations are broadening for the prophylaxis of atherosclerotic disorders, but aspirin is the only widely used agent. Ticlopidine hydrochloride, a new antiplatelet medication, has recently been approved for prescription in North America. We reviewed the major clinical trials of ticlopidine and derived guidelines for its use. METHODS: Studies of ticlopidine were sought through MEDLINE for 1980 to 1990 and through bibliographies of retrieved articles. All published, randomized trials of ticlopidine were appraised if they reported major morbidity and mortality as primary end points. All eligible studies were formally reviewed by an expert panel according to published principles for critical appraisal of the medical literature. Both benefits and risks were quantified. RESULTS: Four randomized trials reported major clinical end points. In these, ticlopidine was more effective than placebo for preventing recurrences after completed stroke; was more effective than aspirin for patients with transient ischemic attacks and partial strokes; and reduced vascular death and nonfatal myocardial infarction in an open trial among patients with unstable angina. For patients with intermittent claudication ticlopidine, was not significantly better than placebo for preventing myocardial infarction or stroke. Side effects were more common with ticlopidine than with aspirin or placebo. CONCLUSIONS: Ticlopidine should be prescribed in place of aspirin for stroke prophylaxis or unstable angina if the patient is unable to tolerate aspirin. Ticlopidine may also benefit patients who experience new ischemic events while taking aspirin or, probably, patients with peripheral vascular disease. A complete blood cell count should be performed every 2 weeks during the first 3 months of therapy to check for leukopenia.