The top 100 cited papers in the field of iron deficiency in humans: A bibliometric study

Worldwide, iron deficiency is a common form of micronutrient deficiency with a high individual and societal cost. There are considerable knowledge and practice gaps in the diagnosis and treatment of iron deficiency. Bibliometric analysis examines the published body of knowledge of a subject in an objective fashion. The Web of Science Core Collection was searched to retrieve the 100 most cited papers on the topic of iron deficiency, and the key metrics of each paper were extracted. A keyword study was performed using VOSviewer 1.6.10 software, which provided a visual mapping of the network of keyword cooccurrences. The papers were published between 1964 and 2017 and were cited an average of 636 times. They were contributed by authors from 119 different countries/regions, with the largest contributing country being the United States. 29 institutions contributed at least 6 publications each, and 4 researchers authored or coauthored at least 5 papers. Keyword analysis suggests that the most cited topics could be grouped into 4 categories: (1) epidemiologic research of the global burden of iron deficiency, (2) clinical aspects of iron deficiency anemia, (3) iron metabolism, and (4) the impact of iron deficiency on children. Identification of the most impactful studies in the field of iron deficiency may be helpful to practitioners interested in improving their knowledge base. Compared to bibliometric studies performed on other topics, the medical literature of iron deficiency is mature, as evidenced by the high citation rate of the top 100 papers. Despite the high worldwide prevalence of iron deficiency, the top cited papers are dominated by a relatively small number of countries and institutions. Interestingly, however, the most cited authors in this study do not overlap with the most cited institutions

Mast cell leukemia with prolonged survival on PKC412/midostaurin

Mast cell leukemia (MCL) is a rare and aggressive form of systemic mastocytosis. There are approximately 50 reported cases since 1950s. MCL is refractory to cytoreduction chemotherapy and the average survival is only six months. We report a MCL case in a 71 year-old woman with high tumor load at the initial presentation in 2005, who did not respond to either interleukin-2 or dasatinib therapy. After enrolled in a clinical trial of PKC412 (or Midostaurin) with a daily dose of 100 mg, the patient responded well to PKC412 and became transfusion independent in three months. Since then, her disease had been stably controlled. This is the first report of a high-tumor-load MCL case which achieved prolonged survival (101 months) by PKC 412. The 101-month overall survival is the longest among reported MCL cases in the English literature

A transient benign lymph node-based proliferation of T-cells simulating non-Hodgkin lymphoma in a patient with psoriasis treated with tumor necrosis factor alpha and CD11a antagonists

<p>Abstract</p> <p>Background</p> <p>Therapeutic biologic agents are uncommonly associated with lymphoma.</p> <p>Case presentation</p> <p>We report a patient with psoriasis treated with the biologic agents efalizumab (Raptiva^®) and etanercept (Enbrel^®), who developed painless lymphadenopathy with peripheral lymphocytosis during treatment, simulating a non-Hodgkin lymphoma clinically and pathologically. Lymphocytosis and lymphadenopathy spontaneously remitted following cessation of etanercept therapy and have not recurred.</p> <p>Conclusion</p> <p>Distinction between clinically benign lymphoid proliferations related to antipsoriasis therapy and malignant lymphoma avoids the unnecessary use of anti-lymphoma chemotherapy.</p

Acute EBV infection masquerading as "In-situ Follicular Lymphoma": a pitfall in the differential diagnosis of this entity

We present the case of a 30 year-old man who was referred for evaluation of diffuse lymphadenopathy. Six weeks prior, he noticed darkening of his urine associated with pale stools, nausea and an eventual 30 lb weight loss within a month. The initial laboratory findings showed elevation of the liver enzymes. A CT scan showed mesenteric and periaortic lymphadenopathy with the largest lymph node measuring 2.8 cm. Other laboratory results were otherwise unremarkable (including a normal LDH) with the exception of positive serum antibodies against Epstein-Barr virus (EBV) associated antigens (IgM+ and IgG+). An excisional biopsy of 4 of the small neck lymph nodes showed a normal architecture with prominent follicles and an intact capsule. But, by immunohistochemistry two of the follicles showed aberrant coexpression of BCL-2, in addition to CD10 and BCL-6. In-situ hybridization for early Epstein-Barr virus mRNA (EBER) and immunohistochemistry for latent membrane protein-1 (LMP-1) stained both scattered positive cells, as well as BCL-2 positive B-cells. Although an original diagnosis of in-situ follicular lymphoma was favored at an outside facility, additional interphase fluorescence in situ hybridization (FISH) studies for t(14;18);(IGH-BCL2) rearrangement (performed on the BCL-2 + follicles microdissected from the tissue block; Abott probe dual colour fusion) and molecular studies (IGH gene rearrangement by PCR, also performed on the microdissected follicles) were negative. Serologic studies (positive EBV antibodies) and immunostains in conjunction with the molecular studies confirmed the reactive nature of the changes. Our case also shows direct immunopathogenic evidence of BCL-2 expression among the EBV-infected cells, which has to our knowledge not been previously documented in vivo. A diagnosis of EBV infection should, therefore, be considered when confronted with BCL-2 expression in germinal centers, particularly in younger individuals, as the diagnosis of FLIS may lead to extensive and invasive haematologic work-ups. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/132365631894006

Congenital acute myeloid leukemia with unique translocation t(11;19)(q23;p13.3)

Congenital leukemia is rarely encountered in clinical practice, even in tertiary children's hospitals. Leukemia may cause significant coagulopathy, putting the patient at risk of intracranial hemorrhage. In this case, the authors present a female infant with a unique mixed phenotypic congenital acute myeloid leukemia showing mixed-lineage leukemia (MLL) rearrangement and severe coagulopathy resulting in a large subdural hematoma. Despite the fatal outcome in this case, neurosurgical treatment of patients with acute myeloid leukemia should be considered if coagulopathy and the clinical scenario allow

The Southern Galactic Plane Survey: The Test Region

The Southern Galactic Plane Survey (SGPS) is a project to image the HI line emission and 1.4 GHz continuum in the fourth quadrant of the Milky Way at high resolution using the Australia Telescope Compact Array (ATCA) and the Parkes Radio Telescope. In this paper we describe the survey details and goals, present lambda 21-cm continuum data, and discuss HI absorption and emission characteristics of the SGPS Test Region (325.5 deg < l < 333.5 deg; -0.5 deg < b < +3.5 deg). We explore the effects of massive stars on the interstellar medium (ISM) through a study of HI shells and the HI environments of HII regions and supernova remnants. We find an HI shell surrounding the HII region RCW 94 which indicates that the region is embedded in a molecular cloud. We give lower limits for the kinematic distances to SNRs G327.4+0.4 and G330.2+1.0 of 4.3 kpc and 4.9 kpc, respectively. We find evidence of interaction with the surrounding HI for both of these remnants. We also present images of a possible new SNR G328.6-0.0. Additionally, we have discovered two small HI shells with no counterparts in continuum emission.Comment: 17 pages, 7 embedded EPS figures, 10 low-res jpeg figures, uses emulateapj5.sty. Accepted for publication in the Astrophysical Journal. Version with all full resolution figures embedded is available at http://www.astro.umn.edu/~naomi/sgps/papers/SGPS.ps.g

G313.3+00.3: A New Planetary Nebula discovered by the Australia Telescope Compact Array and the Spitzer Space Telescope

We present a new planetary nebula, first identified in images from the Australia Telescope Compact Array, although not recognized at that time. Recent observations with the Spitzer Space Telescope during the GLIMPSE Legacy program have rediscovered the object. The high-resolution radio and infrared images enable the identification of the central star or its wind, the recognition of the radio emission as thermal, and the probable presence of polycylic aromatic hydrocarbons in and around the source. These lead to the conclusion that G313.3+00.3 is a planetary nebula. This object is of particular interest because it was discovered solely through radio and mid-infrared imaging, without any optical (or near-infrared) confirmation, and acts as a proof of concept for the discovery of many more highly extinguished planetary nebulae. G313.3+00.3 is well-resolved by both the instruments with which it was identified, and suffers extreme reddening due to its location in the Scutum-Crux spiral arm.Comment: 18 pages, LaTeX (aastex), incl. 8 PostScript (eps) figures and 1 table. Accepted by ApJ (Part 1

Radio Emission from the Composite Supernova Remnant G326.3-1.8 (MSH15-56)

High resolution radio observations of the composite supernova remnant (SNR) G326.3-1.8 or MSH 15-56 with the Australia Telescope Compact Array show details of both the shell and the bright plerion which is offset about 1/3 of the distance from the center of the SNR to the shell. The shell appears to be composed of thin filaments, typical of older shell SNRs. The central part of the elongated plerion is composed of a bundle of parallel ridges which bulge out at the ends and form a distinct ring structure on the northwestern end. The magnetic field with a strength of order 45 microGauss, is directed along the axis of the ridges but circles around the northwestern ring. This plerion is large and bright in the radio but is not detected in x-ray or optical wavelengths. There is, however, a faint hard x-ray feature closer to the shell outside the plerion. Perhaps if the supernova explosion left a rapidly moving magnetar with large energy input but initially rapid decay of both relativistic particles and magnetic field, the observed differences with wavelength could be explained.Comment: 15 pages, 10 figures, accepted by Ap

Distinct clonal identities of B-ALLs arising after lenolidomide therapy for multiple myeloma

Patients with multiple myeloma (MM) who are treated with lenalidomide rarely develop a secondary B-cell acute lymphoblastic leukemia (B-ALL). The clonal and biological relationship between these sequential malignancies is not yet clear. We identified 17 patients with MM treated with lenalidomide, who subsequently developed B-ALL. Patient samples were evaluated through sequencing, cytogenetics/fluorescence in situ hybridization (FISH), immunohistochemical (IHC) staining, and immunoglobulin heavy chain (IgH) clonality assessment. Samples were assessed for shared mutations and recurrently mutated genes. Through whole exome sequencing and cytogenetics/FISH analysis of 7 paired samples (MM vs matched B-ALL), no mutational overlap between samples was observed. Unique dominant IgH clonotypes between the tumors were observed in 5 paired MM/B-ALL samples. Across all 17 B-ALL samples, 14 (83%) had a TP53 variant detected. Three MM samples with sufficient sequencing depth (\u3e500×) revealed rare cells (average of 0.6% variant allele frequency, or 1.2% of cells) with the same TP53 variant identified in the subsequent B-ALL sample. A lack of mutational overlap between MM and B-ALL samples shows that B-ALL developed as a second malignancy arising from a founding population of cells that likely represented unrelated clonal hematopoiesis caused by a TP53 mutation. The recurrent variants in TP53 in the B-ALL samples suggest a common path for malignant transformation that may be similar to that of TP53-mutant, treatment-related acute myeloid leukemia. The presence of rare cells containing TP53 variants in bone marrow at the initiation of lenalidomide treatment suggests that cellular populations containing TP53 variants expand in the presence of lenalidomide to increase the likelihood of B-ALL development