Robotic Radical Prostatectomy at a Teaching Community Hospital: Outcomes and Safety

Robotic prostatectomy was found to be a safe and successful option for prostate cancer treatment in a community teaching hospital

Ariel - Volume 10 Number 1

Executive Editors Madalyn Schaefgen David Reich Business Manager David Reich News Editors Medical College Edward Zurad CAHS John Guardiani World Mark Zwanger Features Editors Meg Trexler Jim O\u27Brien Editorials Editor Jeffrey Banyas Photography and Sports Editor Stuart Singer Commons Editor Brenda Peterso

3q26 Amplification is Rarely Present in Women Whose LSIL Cytology does not Represent CIN 2+ Disease

Comparative Medicine - OneHealth and Comparative Medicine Poster SessionObjective: 10-17% of women with LSIL cytology truly have CIN 2+ disease at colposcopically directed biopsy and 20% of the CIN 2+ lesions derive from women with LSIL cytology. No molecular marker has yet been able to triage LSIL cytology effectively. If possible, the triage would spare women the referral to colposcopy. Irreversible chromosomal damage occurs during oncogenesis. Increasing cervical dysplastic severity occurs with increasing amplification of the 3q26 chromosomal region. The purpose of this study is to evaluate the test characteristics of 3q26 amplification in women whose routine cytology is reported as LSIL with emphasis on the negative predictive value for reassurance. Methods: We conducted a retrospective study using the available SurePath™ liquid cytology LSIL archival samples from women 17-59 years old which were linked to colposcopically directed biopsy samples taken on average 36 days after cytology sampling (3-90 day range). Nuclei from the LSIL samples were hybridized with a single-copy probe for the chromosome 3q26 region and a control probe for the centromeric alpha repeat sequence of chromosome 7, using standard FISH methods. Amplification was defined as five or more signals present in at least 2 cells. Results: Of the 68 paired cytology/biopsy samples, 3q26 amplification occurred in 40% of the women with CIN 2+ disease (sensitivity 95% CI: 12, 74). There was no amplification in 91% of women with less than CIN 2 disease (specificity 95% CI: 81, 97); and the negative predictive value was 90% (79, 96). Conclusions: The lack of 3q26 amplification in women with screening cytology LSIL results offers reassurance that CIN 2+ disease has not developed. Future prospective studies are ongoing

Lassa Fever Induced Hearing Loss: The Neglected Disability of Hemorrhagic Fever.

OBJECTIVE: Lassa fever (LF) a hemorrhagic fever endemic to Western has an incidence of approximately 500,000 cases per year. Here, we evaluate hearing loss and other sequelae following LF. METHODS: This case-control study enrolled laboratory confirmed LF survivors, non-LF Febrile controls and Matched Community controls with no history of LF or recent hospitalization for a febrile illness. Study participants completed a symptom questionnaire. Pure-tone audiometry was completed by a subset of participants. RESULTS: One hundred forty-seven subjects were enrolled aged from 3-66 years (mean = 23.3). LF survivors were significantly more likely to report balance difficulties (55% vs 20%, p < 0.001), hair loss (32% vs 7%, p < 0.001), difficulty speaking (19% vs 1%, p < 0.001), social isolation (50% vs 0%, p < 0.001), and hearing loss (17% vs 1%, p = 0.002) in comparison to Matched-Community Controls. Similar trends were noted in comparison to Febrile Controls, although these findings were non-significant. Fifty subjects completed audiometry. Audiometry found that LF survivors had significantly more bilateral hearing loss in comparison to Matched-Community Controls (30% vs 4%, p = 0.029). CONCLUSION: This study characterizes the sequelae of LF and highlights the need for increased access to hearing care in West Africa

A Unified Framework for the Infection Dynamics of Zoonotic Spillover and Spread.

A considerable amount of disease is transmitted from animals to humans and many of these zoonoses are neglected tropical diseases. As outbreaks of SARS, avian influenza and Ebola have demonstrated, however, zoonotic diseases are serious threats to global public health and are not just problems confined to remote regions. There are two fundamental, and poorly studied, stages of zoonotic disease emergence: 'spillover', i.e. transmission of pathogens from animals to humans, and 'stuttering transmission', i.e. when limited human-to-human infections occur, leading to self-limiting chains of transmission. We developed a transparent, theoretical framework, based on a generalization of Poisson processes with memory of past human infections, that unifies these stages. Once we have quantified pathogen dynamics in the reservoir, with some knowledge of the mechanism of contact, the approach provides a tool to estimate the likelihood of spillover events. Comparisons with independent agent-based models demonstrates the ability of the framework to correctly estimate the relative contributions of human-to-human vs animal transmission. As an illustrative example, we applied our model to Lassa fever, a rodent-borne, viral haemorrhagic disease common in West Africa, for which data on human outbreaks were available. The approach developed here is general and applicable to a range of zoonoses. This kind of methodology is of crucial importance for the scientific, medical and public health communities working at the interface between animal and human diseases to assess the risk associated with the disease and to plan intervention and appropriate control measures. The Lassa case study revealed important knowledge gaps, and opportunities, arising from limited knowledge of the temporal patterns in reporting, abundance of and infection prevalence in, the host reservoir.Natural Environment Research Council (project no.: NEJ001570-1), Department for International Development, Economic and Social Research Council, National Institute for Health Research, Science and Technology Directorate, Department of Homeland Security, Fogarty International Center USA, European Union FP7 (project ANTIGONE (contract number 278976)), Royal Society (Wolfson Research Merit Award), Alborada Trust, US National Institute of Health (P20GM103501, BAANIAID-DAIT-NIHQI2008031, HHSN272201000022C, HHSN272200900049C, 1U19AI109762, 1R01AI104621, 2R44AI088843), USAID/NIH PEER Health grant.This is the final version of the article. It first appeared from the Public Library of Science via http://dx.doi.org/10.1371/journal.pntd.000495

Using modelling to disentangle the relative contributions of zoonotic and anthroponotic transmission: the case of lassa fever.

BACKGROUND: Zoonotic infections, which transmit from animals to humans, form the majority of new human pathogens. Following zoonotic transmission, the pathogen may already have, or may acquire, the ability to transmit from human to human. With infections such as Lassa fever (LF), an often fatal, rodent-borne, hemorrhagic fever common in areas of West Africa, rodent-to-rodent, rodent-to-human, human-to-human and even human-to-rodent transmission patterns are possible. Indeed, large hospital-related outbreaks have been reported. Estimating the proportion of transmission due to human-to-human routes and related patterns (e.g. existence of super-spreaders), in these scenarios is challenging, but essential for planned interventions. METHODOLOGY/PRINCIPAL FINDINGS: Here, we make use of an innovative modeling approach to analyze data from published outbreaks and the number of LF hospitalized patients to Kenema Government Hospital in Sierra Leone to estimate the likely contribution of human-to-human transmission. The analyses show that almost [Formula: see text] of the cases at KGH are secondary cases arising from human-to-human transmission. However, we found much of this transmission is associated with a disproportionally large impact of a few individuals ('super-spreaders'), as we found only [Formula: see text] of human cases result in an effective reproduction number (i.e. the average number of secondary cases per infectious case) [Formula: see text], with a maximum value up to [Formula: see text]. CONCLUSIONS/SIGNIFICANCE: This work explains the discrepancy between the sizes of reported LF outbreaks and a clinical perception that human-to-human transmission is low. Future assessment of risks of LF and infection control guidelines should take into account the potentially large impact of super-spreaders in human-to-human transmission. Our work highlights several neglected topics in LF research, the occurrence and nature of super-spreading events and aspects of social behavior in transmission and detection.This work for the Dynamic Drivers of Disease in Africa Consortium, NERC project no. NE-J001570-1, was funded with support from the Ecosystem Services for Poverty Alleviation (ESPA) programme. The ESPA programme is funded by the Department for International Development (DFID), the Economic and Social Research Council (ESRC) and the Natural Environment Research Council (NERC). See more at: http://www.espa.ac.uk/about/identity/acknowledging-espafunding# sthash.UivKPObf.dpuf. GL, JLNW, AAC, CTW and EFC also benefit from the support of the small mammal disease working group, funded by the Research and Policy for Infectious Disease Dynamics (RAPIDD) programme of the Science and Technology Directorate, Department of Homeland Security, and Fogarty International Center, USA. JLNW and AC were also supported by the European Union FP7 project ANTIGONE (contract number 278976). AAC is supported by a Royal Society Wolfson Reearch Merit Award. JLNW is also supported by the Alborada Trust. JSS, LM, RG, and JGS were supported by the US National Institute of Health (JSS: NIH grant P20GM103501; LM, RG, JGS: NIH grant BAA-NIAID-DAIT-NIHQI2008031).This is the final published version. It first appeared at http://www.plosntds.org/article/info%3Adoi%2F10.1371%2Fjournal.pntd.0003398

Expanding the clinical phenotype of the 3q29 microdeletion syndrome and characterization of the reciprocal microduplication

<p>Abstract</p> <p>Background</p> <p>Interstitial deletions of 3q29 have been recently described as a microdeletion syndrome mediated by nonallelic homologous recombination between low-copy repeats resulting in an ~1.6 Mb common-sized deletion. Given the molecular mechanism causing the deletion, the reciprocal duplication is anticipated to occur with equal frequency, although only one family with this duplication has been reported.</p> <p>Results</p> <p>In this study we describe 14 individuals with microdeletions of 3q29, including one family with a mildly affected mother and two affected children, identified among 14,698 individuals with idiopathic mental retardation who were analyzed by array CGH. Eleven individuals had typical 1.6-Mb deletions. Three individuals had deletions that flank, span, or partially overlap the commonly deleted region. Although the clinical presentations of individuals with typical-sized deletions varied, several features were present in multiple individuals, including mental retardation and microcephaly. We also identified 19 individuals with duplications of 3q29, five of which appear to be the reciprocal duplication product of the 3q29 microdeletion and 14 of which flank, span, or partially overlap the common deletion region. The clinical features of individuals with microduplications of 3q29 also varied with few common features. <it>De novo </it>and inherited abnormalities were found in both the microdeletion and microduplication cohorts illustrating the need for parental samples to fully characterize these abnormalities.</p> <p>Conclusion</p> <p>Our report demonstrates that array CGH is especially suited to identify chromosome abnormalities with unclear or variable presentations.</p

Short-course Benznidazole treatment to reduce Trypanosoma cruzi parasitic load in women of reproductive age (BETTY): A non-inferiority randomized controlled trial study protocol

Background: Retrospective observational studies suggest that transmission of Trypanosoma cruzi does not occur in treated women when pregnant later in life. The level of parasitemia is a known risk factor for congenital transmission. Benznidazole (BZN) is the drug of choice for Preconceptional treatment to reduce parasitic load.The fear of treatment-related side effects limits the implementation of the Argentine guideline recommending BZN 60d/300 mg (or equivalent) treatment of T. cruzi seropositive women during the postpartum period to prevent transmission in a future pregnancy. A short and low dose BZN treatment might reduce major side effects and increase compliance, but its efficacy to reduce T. cruzi parasitic load compared to the standard 60d/300 mg course is not yet established. Clinical trials testing alternative BZN courses among women of reproductive age are urgently needed.Methods and design: We are proposing to perform a double-blinded, non-inferiority randomized controlled trial comparing a short low dose 30-day treatment with BZN 150 mg/day (30d/150 mg) vs. BZN 60d/300 mg. We will recruit not previously treated T. cruzi seropositive women with a live birth during the postpartum period in Argentina, randomize them at 6 months postpartum, and follow them up with the following specific aims:Specific aim 1: to measure the effect of BZN 30d/150 mg compared to 60d/300 mg preconceptional treatment on parasitic load measured by the frequency of positive Polymerase Chain Reaction (PCR) (primary outcome) and by real-time quantitative PCR (qPCR), immediately and 10 months after treatment.Specific aim 2: to measure the frequency of serious adverse events and/or any adverse event leading to treatment interruption.Fil: Cafferata, María L.. Instituto de Efectividad Clínica y Sanitaria; Argentina. Unicem; UruguayFil: Toscani, María A.. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Althabe, Fernando. Organizacion Mundial de la Salud; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones en Epidemiología y Salud Pública. Instituto de Efectividad Clínica y Sanitaria. Centro de Investigaciones en Epidemiología y Salud Pública; ArgentinaFil: Belizan, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones en Epidemiología y Salud Pública. Instituto de Efectividad Clínica y Sanitaria. Centro de Investigaciones en Epidemiología y Salud Pública; ArgentinaFil: Bergel, Eduardo. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Berrueta, Mabel. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Capparelli, Edmund V.. University of California; Estados UnidosFil: Ciganda, Álvaro. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Danesi, Emmaría. Dirección Nacional de Institutos de Investigación. Administración Nacional de Laboratorios e Institutos de Salud. Centro Nacional de Diagnóstico e Investigaciones Endemo-epidémicas; ArgentinaFil: Dumonteil, Eric. University of Tulane; Estados UnidosFil: Gibbons, Luz. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Gulayin, Pablo Elías. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Herrera, Claudia. University of Tulane; Estados UnidosFil: Momper, Jeremiah D.. University of California; Estados UnidosFil: Rossi, Steven. University of California; Estados UnidosFil: Shaffer, Jeffrey G.. University of Tulane; Estados UnidosFil: Schijman, Alejandro Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Sosa-Estani, Sergio Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones en Epidemiología y Salud Pública. Instituto de Efectividad Clínica y Sanitaria. Centro de Investigaciones en Epidemiología y Salud Pública; ArgentinaFil: Stella, Candela B.. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Klein, Karen. Instituto de Efectividad Clínica y Sanitaria; ArgentinaFil: Buekens, Pierre. University of Tulane; Estados Unido