Adjuvant chemotherapy vs radiotherapy in high-risk endometrial carcinoma: results of a randomised trial

Patients with high-risk endometrial carcinoma (stage IcG3, IIG3 with myometrial invasion >50%, and III) receive adjuvant therapy after surgery but it is not clear whether radiotherapy (RT) or chemotherapy (CT) is better. We randomly assigned 345 patients with high-risk endometrial carcinoma to adjuvant CT (cisplatin (50 mg m−2), doxorubicin (45 mg m−2), cyclophosphamide (600 mg m−2) every 28 days for five cycles, or external RT (45–50 Gy on a 5 days week−1 schedule). The primary end points were overall and progression-free survival. After a median follow-up of 95.5 months women in the CT group as compared with the RT group, had a no significant hazard ratio (HR) for death of 0.95 (95% confidence interval (CI), 0.66–1.36; P=0.77) and a nonsignificant HR for event of 0.88 (95% CI, 0.63–1.23; P=0.45). The 3, 5 and 7-year overall survivals were 78, 69 and 62% in the RT group and 76, 66 and 62% in the CT group. The 3, 5 and 7-year progression-free survivals were, respectively, 69, 63 and 56 and 68, 63 and 60%. Radiotherapy delayed local relapses and CT delayed metastases but these trends did not achieve statistical significance. Overall, both treatments were well tolerated. This trial failed to show any improvement in survival of patients treated with CT or the standard adjuvant radiation therapy. Randomised trials of pelvic RT combined with adjuvant cytotoxic therapy compared with RT alone are eagerly awaited

Bringing Information Literacy (IL) into the First-Year College Science Curriculum: Expanding a Faculty/Librarian Partnership to Develop Chemical IL Modules for Freshmen Lecture and Laboratory Courses

Information literacy skills, both general and discipline-specific, are widely recognized by college faculty and librarians as necessary for supporting critical thinking and communication. Starting in first year, these skills are most effectively developed as part of a course curriculum rather than in a one-time visit to the library. However, integrating information literacy instruction in freshmen-level courses can be a challenge as instructors and librarians both must consider scalability for the large class sizes, relevance to the coursework, and difficulties in giving up class time. A recent library reorganization at UC San Diego and creation of a new, instruction-focused program offered us the opportunity to build upon previous efforts to embed chemical information literacy (CIL) in a third quarter introductory chemistry lecture course for science and engineering majors, as well as a new introductory laboratory course for chemistry majors. The chemistry professor and three librarians (chemistry, instructional design, and instructional technologies) successfully collaborated to create a series of online tutorials and in-person activities that addressed the scalability and relevancy issues, while minimizing the impact on regular class time. In this presentation, we will share how we revised a list of CIL undergraduate learning outcomes, mapped outcomes to the specific courses, and developed curricular materials to support the outcomes. We will also highlight logistics like technology and communication workflows, what was successful and what needs improvement, and how this can inform future information literacy partnerships between our librarians and faculty, as well as potential CIL integration into other courses

Surfactant dysfunction after inhalation of nitric oxide

To study whether nitric oxide (NO) affects surfactant function, 36 young rats inhaled one of the following humidified environments for 24 h: 1) air; 2) 95% O2; 3) air and 100 parts/million (ppm) NO; and 4) 95% O2 and 100 ppm NO. The treatments did not change the recovery of phospholipid from bronchoalveolar lavage (BAL). Exposure to NO of animals that breathed either air or 95% O2 increased the minimum surface tension of surfactant from BAL at low (1.5 mumol/ml), but not at high (4 mumol/ml), phosphatidylcholine concentration. After inhaled NO, the nonsedimentable protein of BAL decreased the surface activity of surfactant (1 mumol phosphatidylcholine/ml) more than the protein from the controls. NO treatment of animals that breathed either air or 95% O2 affected neither the quantity nor the molecular weight distribution of nonsedimentable protein. Hyperoxia increased the amount of the nonsedimentable protein, whereas NO increased the iron saturation of transferrin. The surfactant fraction and the nonsedimentable protein from BAL were separately exposed to 80 ppm NO in vitro. NO exposure had no effect on the surface activity of surfactant fraction. NO exposure of nonsedimentable protein from the control animals (no NO) increased the inhibition of the surface activity and changed the adsorption spectrum of the protein, suggesting conversion of hemoglobin to methemoglobin. Nonsedimentable protein from NO-exposed animals contained methemoglobin. We propose that surfactant dysfunction caused by inhaled NO is in part due to alteration of protein(s) in epithelial lining fluid that in turn inactivates surfactant

Surfactant dysfunction after inhalation of nitric oxide.

To study whether nitric oxide (NO) affects surfactant function, 36 young rats inhaled one of the following humidified environments for 24 h: 1) air; 2) 95% O2; 3) air and 100 parts/million (ppm) NO; and 4) 95% O2 and 100 ppm NO. The treatments did not change the recovery of phospholipid from bronchoalveolar lavage (BAL). Exposure to NO of animals that breathed either air or 95% O2 increased the minimum surface tension of surfactant from BAL at low (1.5 mumol/ml), but not at high (4 mumol/ml), phosphatidylcholine concentration. After inhaled NO, the nonsedimentable protein of BAL decreased the surface activity of surfactant (1 mumol phosphatidylcholine/ml) more than the protein from the controls. NO treatment of animals that breathed either air or 95% O2 affected neither the quantity nor the molecular weight distribution of nonsedimentable protein. Hyperoxia increased the amount of the nonsedimentable protein, whereas NO increased the iron saturation of transferrin. The surfactant fraction and the nonsedimentable protein from BAL were separately exposed to 80 ppm NO in vitro. NO exposure had no effect on the surface activity of surfactant fraction. NO exposure of nonsedimentable protein from the control animals (no NO) increased the inhibition of the surface activity and changed the adsorption spectrum of the protein, suggesting conversion of hemoglobin to methemoglobin. Nonsedimentable protein from NO-exposed animals contained methemoglobin. We propose that surfactant dysfunction caused by inhaled NO is in part due to alteration of protein(s) in epithelial lining fluid that in turn inactivates surfactant

Cerebral Metabolism during Cord Occlusion and Hypoxia in the Fetal Sheep: A Novel Method of Continuous Measurement Based on Heat Production

This study was undertaken to validate a new method of measuring cerebral metabolic rate in the fetal sheep based on heat production in a local region of the brain. Heat production was compared to oxygen use in 20 near-term fetuses during basal conditions, moderate hypoxia and cord occlusion. Thermocouples were placed to measure core and brain temperature and a composite probe placed in the parietal cortex to measure changes in cortical blood flow (CBF) using laser Doppler flowmetry and tissue PO2 using fluorescent decay. Catheters were inserted in a brachiocephalic artery and sagittal sinus for blood sampling. With moderate hypoxia, induced by administering 10−12 % oxygen to the ewes, fetal arterial PO2 declined from 23 ± 1 to 11 ± 1 Torr and brain tissue PO2 fell from 7.6± 0.7 to a nadir of 0.8 ± 0.4 Torr, while CBF increased to 139 ± 5 % of baseline. Cortical heat production, calculated as the product of CBF, the temperature gain from artery to brain tissue, and the specific heat of blood, decreased by 45 ± 11 % in parallel to similar declines in oxygen uptake. With severe asphyxia induced by complete cord occlusion for 10 min, fetal arterial PO2 declined from 23 ± 1 to 9 ± 2 Torr and brain tissue PO2 fell from 7.0 ± 0.7 to essentially 0 Torr while CBF decreased 40 ± 5 %. Cortical heat production decreased by 78 ± 6 % while oxygen use declined by 90 ± 3 %. Glucose uptake increased significantly relative to oxygen use and lactate concentration increased in sagittal sinus blood. We conclude that local measurements of heat production in the brain provide a useful index of overall metabolic rate, closely reflecting oxygen use in moderate hypoxia and indicating a significant contribution from anaerobic metabolism during severe asphyxia