The disambiguation of people names in biological collections.

Scientific collections have been built by people. For hundreds of years, people have collected, studied, identified, preserved, documented and curated collection specimens. Understanding who those people are is of interest to historians, but much more can be made of these data by other stakeholders once they have been linked to the people's identities and their biographies. Knowing who people are helps us attribute work correctly, validate data and understand the scientific contribution of people and institutions. We can evaluate the work they have done, the interests they have, the places they have worked and what they have created from the specimens they have collected. The problem is that all we know about most of the people associated with collections are their names written on specimens. Disambiguating these people is the challenge that this paper addresses. Disambiguation of people often proves difficult in isolation and can result in staff or researchers independently trying to determine the identity of specific individuals over and over again. By sharing biographical data and building an open, collectively maintained dataset with shared knowledge, expertise and resources, it is possible to collectively deduce the identities of individuals, aggregate biographical information for each person, reduce duplication of effort and share the information locally and globally. The authors of this paper aspire to disambiguate all person names efficiently and fully in all their variations across the entirety of the biological sciences, starting with collections. Towards that vision, this paper has three key aims: to improve the linking, validation, enhancement and valorisation of person-related information within and between collections, databases and publications; to suggest good practice for identifying people involved in biological collections; and to promote coordination amongst all stakeholders, including individuals, natural history collections, institutions, learned societies, government agencies and data aggregators.

People are essential to linking biodiversity data.

People are one of the best known and most stable entities in the biodiversity knowledge graph. The wealth of public information associated with people and the ability to identify them uniquely open up the possibility to make more use of these data in biodiversity science. Person data are almost always associated with entities such as specimens, molecular sequences, taxonomic names, observations, images, traits and publications. For example, the digitization and the aggregation of specimen data from museums and herbaria allow us to view a scientist's specimen collecting in conjunction with the whole corpus of their works. However, the metadata of these entities are also useful in validating data, integrating data across collections and institutional databases and can be the basis of future research into biodiversity and science. In addition, the ability to reliably credit collectors for their work has the potential to change the incentive structure to promote improved curation and maintenance of natural history collections.

Recommendations for Nuclear Medicine Technologists Drawn from an Analysis of Errors Reported in Australian Radiation Incident Registers.

When a radiation incident occurs in nuclear medicine in Australia, the incident is reported to the relevant state or territory authority, which performs an investigation and sends its findings to the Australian Radiation Protection and Nuclear Safety Agency. The agency then includes these data in its Australian Radiation Incident Register and makes them available to the public as an annual summary report on its website. The aim of this study was to analyze the radiation incidents included in these annual reports and in the publically available state and territory registers, identify any recurring themes, and make recommendations to minimize future incidents. METHODS: A multidisciplinary team comprising a nuclear medicine technologist, a radiation therapist, and a diagnostic radiographer analyzed all nuclear medicine technology-, radiation therapy-, and diagnostic radiography-related incidents recorded in the Australian Radiation Incident Register and in the registers of New South Wales, Western Australia, Victoria, South Australia, and Tasmania between 2003 and 2015. Each incident was placed into 1 of 18 categories, and each category was examined to determine any recurring causes of the incidents. RESULTS: We analyzed 209 nuclear medicine incidents. Their primary cause was failure to comply with time-out protocols (85.6%). By analyzing both the causes and the rates of radiation incidents, we were able to recommend ways to help prevent them from being repeated. CONCLUSION: Information drawn from the Australian Radiation Incident Register and 5 state registers has revealed steps that can be taken by any nuclear medicine department to prevent repetition of the incidents that have already occurred.

Hypothalamic dysfunction after chemotherapy.

Cranial irradiation with or without chemotherapy can cause hypothalamic-pituitary dysfunction. Chemotherapy without cranial irradiation has not been thought to cause such deficiency. In order to determine whether chemotherapy without cranial irradiation can lead to hormonal deficiency, we reviewed the medical records of 362 childhood cancer patients who underwent full hypothalamic-pituitary evaluation because of altered growth and development after oncological therapy (1987-2002). Of these, 31 received chemotherapy but no cranial or total body irradiation and had no CNS tumor: 18 had hematological malignancy and 13 had a solid tumor of the torso or extremity. Duration of follow-up was 13.0 +/- 4.1 years (mean +/- SD). Growth hormone deficiency (GHD) was identified in 15 (48%), central hypothyroidism (TSH-D) in 16 (52%), and pubertal abnormalities in 10 (32%). Pubertal abnormalities included precocious puberty in two (6%), gonadal failure in five of 27 who were old enough to assess puberty (19%), and gonadotropin deficiency in three of 27 (11%). GHD and TSH-D were co-existent in eight patients (26%). Overall, 81% (n = 25) had GHD, TSH-D, precocious puberty, and/or gonadotropin deficiency. None had ACTH or ADH deficiency or primary hypothyroidism. Of note, this was not a study of prevalence, but rather an evaluation of clinically referred patients. In conclusion, hypothalamic dysfunction may occur in survivors of non-CNS tumors who receive chemotherapy but do not receive cranial irradiation. We recommend at least annual observation of growth rate and pubertal development of all children treated for pediatric malignancies, with evaluation for GHD, TSH-D, pubertal abnormalities, and other hypothalamic dysfunction in all poorly-growing cancer survivors, even those not treated with cranial irradiation.

Comparative validation of online nomograms for predicting nonsentinel lymph node status in sentinel lymph node-positive breast cancer.

BACKGROUND: Completion axillary lymph node dissection is recommended for patients with metastases to the sentinel lymph node (SLN) in breast cancer although nonsentinel lymph nodes (NSLN) are often negative for tumor. Online nomograms are available to predict risk of NSLN disease. OBJECTIVE: To compare the accuracy of the Memorial Sloan-Kettering Cancer Center (MSKCC) nomogram (using 9 variables) with the Stanford nomogram (using 3 variables) in predicting NSLN metastasis. SETTING: A single academic center. PATIENTS: Prospectively maintained database of patients with breast cancer who underwent SLN biopsy from October 1, 1999, through January 31, 2008. METHODS: Risk of NSLN metastasis was calculated using each nomogram's online calculator. Results from the axillary lymph node dissection were reviewed for positive NSLNs. Nomograms were evaluated using the area under the receiver operating characteristic curve, false-negative rates, positive predictive value, and calibration plot. MAIN OUTCOME MEASURES: Nomogram scores and axillary lymph node dissection results. RESULTS: Of 579 patients who underwent SLN biopsy, 179 (30.9%) had a positive SLN. For 123 patients who underwent axillary lymph node dissection, the area under the curve for the MSKCC and Stanford nomograms was 0.72 and 0.70, respectively. False-negative rates for nomogram values of 10% or less were low (4.1% for the MSKCC and 7.8% for the Stanford). The positive predictive value for nomogram probabilities of 80% or greater was higher for MSKCC than for Stanford (90.9% vs 61.8%). The Stanford nomogram performed more accurately in low-risk patients with isolated tumor cells or micrometastatic SLN disease; however, the MSKCC nomogram more accurately predicted NSLN outcomes across the entire study population. CONCLUSION: Although the MSKCC and Stanford nomograms performed similarly on the basis of the area under the curve, the MSKCC nomogram was consistently more reliable in predicting actual NSLN outcomes.

ACTH deficiency in childhood cancer survivors.

BACKGROUND: Adrenocorticotropin deficiency (ACTHD) can be clinically subtle, but life-threatening if not recognized. We assessed the prevalence of ACTHD in survivors of childhood cancer according to tumor diagnosis/therapy. PROCEDURE: Chart review of endocrine/oncology history was performed in 310 childhood cancer survivors. Patients were referred to endocrine clinic because of slow growth, fatigue, or abnormal pubertal timing. Evaluation of growth hormone (GH), thyrotropin (TSH), ACTH, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) was performed. Low response to metyrapone and/or low dose ACTH test defined ACTHD. RESULTS: ACTHD was identified in 56 (18%), [44 of 182 (24%) central nervous system (CNS) tumors, 3 of 18 (17%) non-CNS cranial tumors, 9 of 97 (9%) hematologic malignancies]. Of the 56 with ACTHD, 53 (95%) had received cranial irradiation (mean 45.5 Gy, range 14-70 Gy); three had not: one each with craniopharyngioma, hypothalamic astrocytoma, and brain stem glioma. All but one also had GH deficiency and/or central hypothyroidism. CONCLUSIONS: Childhood cancer survivors with greatest risk for ACTHD had craniopharyngioma, other suprasellar tumor, or medulloblastoma or > or =24 Gy cranial irradiation. We recommend annual testing for ACTHD for 10-15 years and continued lifelong surveillance after CNS tumor or cranial irradiation, in patients with other hypothalamic-pituitary deficiencies or symptoms of ACTHD.