tbuckley/cabot-search huggingface dataset:
Surveillance of travel-associated gastrointestinal infections in Norway, 2009–2010: are they all actually imported?
Authors: B Guzman-Herrador, L Vold, K Nygård
Journal: Eurosurveillance (2012)

The Norwegian Surveillance System for Communicable Diseases (MSIS) includes variables related to travel for clinicians to fill when notifying travel-associated infections. We measured the completeness and validated the travel-history information for salmonellosis, campylobacteriosis, giardiasis and shigellosis reported in 2009-2010. Of all 8,978 selected infections in MSIS, 8,122 (91%) were reported with place of infection of which 5,236 (65%) were notified as acquired abroad, including 5,017 with symptoms. Of these, 2,972 (59%) notifications had information on both date of arrival in Norway and date of symptom onset, so time between travel and illness onset could be assessed. Taking in account the incubation period, of the 1,435 infections reported as travel-associated and for which symptom onset occurred after return to Norway, 1,404 (98%) would have indeed been acquired abroad. We found a high level of completeness for the variable 'place of infection'. Our evaluation suggests that the validity of this information is high. However, incomplete data in the variables 'return date to Norway' and 'date of symptoms onset', only allowed assessment of the biological plausibility of being infected abroad for 59% of the cases. We encourage clinicians to report more complete travel information. High quality information on travel-associated gastrointestinal infections is crucial for understanding trends in domestic and imported cases and evaluating implemented control measures.
Neuroprotection After Traumatic Brain Injury
Authors: Ralf Watzlawick, David W. Howells, Jan M. Schwab
Journal: JAMA Neurology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
pVAX14DNA-mediated add-on immunotherapy combined with arsenic trioxide and all-trans retinoic acid targeted therapy effectively increases the survival of acute promyelocytic leukemia mice
Authors: S Patel, L Guerenne, P Gorombei, N Omidvar, M-H Schlageter, A A Alex, S Ganesan, R West, L Adès, V Mathews, P Krief, M Pla, P Fenaux, C Chomienne, R A Padua
Journal: Blood Cancer Journal (2015)

Novel immunotherapeutic approaches have recently highlighted the benefit of adjuvant add-on immunotherapy approaches combined with chemotherapy or targeted therapies.To validate this approach, we took advantage of a mouse transplantable acute promyelocytic leukemia (APL) model 1 that has proven to be a very robust and reproducible in vivo pre-clinical model of all the current and prospective therapeutic approaches of this leukemia as a proof-on concept for other malignancies. 2Of relevance to this study, this model was used to demonstrate a synergy of all-trans D7 D27 D47 D6 ATO (28 days) +ATRA (21 days) MyD88 D60 CFU Anti-RARA IFNγ memT MRD DNA Booster (IM) D0 10 APL cells Days Survival (%) 100 200 300 0 Placebo (n=48) Vehicle+ATO + ATRA (n=12) pVAX14 + ATO + ATRA (n=26) 0 20 40 60 80 100 (n=17) (n=17) (n=3) Placebo Vehicle pVAX14 1000
Microbiota depletion promotes browning of white adipose tissue and reduces obesity
Authors: Nicolas Suárez-Zamorano, Salvatore Fabbiano, Claire Chevalier, Ozren Stojanović, Didier J Colin, Ana Stevanović, Christelle Veyrat-Durebex, Valentina Tarallo, Dorothée Rigo, Stéphane Germain, Miroslava Ilievska, Xavier Montet, Yann Seimbille, Siegfried Hapfelmeier, Mirko Trajkovski
Journal: Nature Medicine (2015)
Mental health problems contribute to a quarter of “later” maternal deaths after childbirth
Authors: Nigel Hawkes
Journal: BMJ (2015)

Maternal deaths in the United Kingdom have continued to fall, but more could be done to prevent suicides during pregnancy or in the first year after birth, the Confidential Enquiry into Maternal Deaths has found.1

While direct deaths—those caused by sepsis, eclampsia, thrombosis, or haemorrhage, for example—halved from 2003-05 to 2011-13, the number of indirect deaths showed little change. Women born outside the UK accounted for a quarter of the total deaths, but their risk of dying was not notably different in 2011-13 from those born in the UK.

Over this three year period the inquiry showed 69 direct deaths and a further 145 indirect deaths from causes such as cardiac disease, flu, or pneumonia. The corresponding figures from 2003-05 were 132 direct deaths and 163 indirect deaths. Total maternities rose from 2.11 million in 2003-05 …
Isolation of an NDM-5-producing ST16 Klebsiella pneumoniae from a Dutch patient without travel history abroad, August 2015
Authors: Erik Bathoorn, John W Rossen, Mariëtte Lokate, Alexander W Friedrich, Anette M Hammerum
Journal: Eurosurveillance (2015)

A New Delhi Metallo-beta-lactamase-5 (NDM-5)-producing ST16 Klebsiella pneumoniae strain was isolated from a Dutch patient in a long-term care facility without recent travel history abroad. Core genome multilocus sequence typing (cgMLST) revealed that the Dutch isolate was clonally related to isolates detected in four patients in Denmark in 2014. Public health experts and clinicians need to be informed; repetitive screening may be needed in patients without known risk factors for carbapenemases-producing Enterobacteriaceae who have undergone antibiotic treatment.
Prevalence of<i>MITF</i>p.E318K in Patients With Melanoma Independent of the Presence of<i>CDKN2A</i>Causative Mutations
Authors: Miriam Potrony, Joan Anton Puig-Butille, Paula Aguilera, Celia Badenas, Gemma Tell-Marti, Cristina Carrera, Luis Javier del Pozo, Julian Conejo-Mir, Josep Malvehy, Susana Puig
Journal: JAMA Dermatology (2015)

The main high-penetrance melanoma susceptibility gene is CDKN2A, encoding p16INK4A and p14ARF. The gene MITF variant p.E318K also predisposes to melanoma and renal cell carcinoma. To date, the prevalence of MITF p.E318K and its clinical and phenotypical implications has not been previously assessed in a single cohort of Spanish patients with melanoma or in p16INK4A mutation carriers.To evaluate the prevalence of MITF p.E318K in Spanish patients with melanoma and assess the association with clinical and phenotypic features.A hospital-based, case-control study was conducted at the Melanoma Unit of Hospital Clinic of Barcelona, with MITF p.E318K genotyped in all patients using TaqMan probes. We included 531 patients: 271 patients with multiple primary melanoma (MPM) without mutations affecting p16INK4A (wild-type p16INK4A); 191 probands from melanoma-prone families with a single melanoma diagnosis and without mutations affecting p16INK4A, and 69 probands from different families carrying CDKN2A mutations affecting p16INK4A. A population-based series of 499 age- and sex-matched cancer-free individuals from the Spanish National Bank of DNA were included as controls. Patients were recruited between January 1, 1992, and June 30, 2014; data analysis was conducted from September 1 to November 30, 2014.The genetic results of the MITF p.E318K variant were correlated with clinical and phenotypic features.Among the 531 patients, the prevalence of the MITF p.E318K variant was calculated among the different subsets of patients included and was 1.9% (9 of 462) in all melanoma patients with wild-type p16INK4A, 2.6% (7 of 271) in those with MPM, and 2.9% (2 of 69) in the probands of families with p16INK4A mutations. With results reported as odds ratio (95% CI), the MITF p.E318K was associated with an increased melanoma risk (3.3 [1.43-7.43]; P < .01), especially in MPM (4.5 [1.83-11.01]; P < .01) and high nevi count (>200 nevi) (8.4 [2.14-33.19]; P < .01). Two fast-growing melanomas were detected among 2 MITF p.E318K carriers during dermatologic digital follow-up.In addition to melanoma risk, MITF p.E318K is associated with a high nevi count and could play a role in fast-growing melanomas. Testing for MITF p.E318K should not exclude patients with known mutations in p16INK4A. Strict dermatologic surveillance, periodic self-examination, and renal cell carcinoma surveillance should be encouraged in this context.
Randomized Trial of Low-Dose Morphine Versus Weak Opioids in Moderate Cancer Pain
Authors: Elena Bandieri, Marilena Romero, Carla Ida Ripamonti, Fabrizio Artioli, Daniela Sichetti, Caterina Fanizza, Daniele Santini, Luigi Cavanna, Barbara Melotti, Pier Franco Conte, Fausto Roila, Stefano Cascinu, Eduardo Bruera, Gianni Tognoni, Mario Luppi
Journal: Journal of Clinical Oncology (2015)

The WHO guidelines on cancer pain management recommend a sequential three-step analgesic ladder. However, conclusive data are lacking as to whether moderate pain should be treated with either step II weak opioids or low-dose step III strong opioids.In a multicenter, 28-day, open-label randomized controlled study, adults with moderate cancer pain were assigned to receive either a weak opioid or low-dose morphine. The primary outcome was the number of responder patients, defined as patients with a 20% reduction in pain intensity on the numerical rating scale.A total of 240 patients with cancer (118 in the low-dose morphine and 122 in the weak-opioid group) were included in the study. The primary outcome occurred in 88.2% of the low-dose morphine and in 57.7% of the weak-opioid group (odds risk, 6.18; 95% CI, 3.12 to 12.24; P < .001). The percentage of responder patients was higher in the low-dose morphine group, as early as at 1 week. Clinically meaningful (≥ 30%) and highly meaningful (≥ 50%) pain reduction from baseline was significantly higher in the low-dose morphine group (P < .001). A change in the assigned treatment occurred more frequently in the weak-opioid group, because of inadequate analgesia. The general condition of patients, which was based on the Edmonton Symptom Assessment System overall symptom score, was better in the morphine group. Adverse effects were similar in both groups.In patients with cancer and moderate pain, low-dose morphine reduced pain intensity significantly compared with weak opioids, with a similarly good tolerability and an earlier effect.
Abstract 16863: Alirocumab Effect on Glycemic Measures in Patients Without Diabetes at Baseline
Authors: Helen M Colhoun, Henry N Ginsberg, Jennifer G Robinson, Lawrence A Leiter, Dirk Müller-Wieland, Robert R Henry, Bertrand Cariou, Marie T Baccara-Dinet, Robert Pordy, Laurence Merlet, Robert H Eckel
Journal: Circulation (2015)

Background: Statin use has been reported to have modest adverse effects on glycemia and incidence of diabetes mellitus (DM). We assessed effects of alirocumab (ALI), a PCSK9 inhibitor with substantial effect on LDL-C, on development of incident DM or impaired glucose control (IGC) in patients without diabetes at baseline in 10 trials in the ODYSSEY Phase 3 program. Methods: Five trials were controlled with placebo (N=2318 ALI vs 1174 placebo), and 5 with ezetimibe (N=864 ALI vs 618 ezetimibe), ranging in length from 24 to 104 wks. Most patients were receiving background statin. Different ways of assessing ALI effect on glycemic measures were used, including occurrence of treatment-emergent adverse events (TEAEs) related to DM, and fasting plasma glucose (FPG) and HbA1c measured at baseline and every 12-24 wks thereafter. Additional analysis using all 3 parameters was conducted (see Table footnote). Results: Duration of exposure is shown in the Table. At baseline, 32.8% of patients had DM, 93% based on medical history. Another 37.4% had IGC at baseline, based on laboratory data (93.6%) or medical history (6.4%). In patients without DM at baseline, there was no difference between ALI and control groups in occurrence of TEAEs related to DM with HR (95% CI) = 0.79 (0.44-1.43) in the placebo-controlled pool and 0.55 (0.22-1.41) in the ezetimibe-controlled pool. Mean change in FPG and HbA1c over time showed no meaningful differences between treatment groups by baseline glycemic status. In the additional analysis shown in the Table, there was no notable difference between ALI and control groups in % of patients with baseline normoglycemia developing DM or IGC, or those with baseline IGC developing DM. Conclusions: In 10 studies involving 4974 patients comparing ALI to either placebo or ezetimibe (median exposure 66 or 27 wks, respectively), data show no significant effect of ALI on transition to IGC or DM. Longer follow up with larger numbers is needed to conclusively rule out an effect.
Do severe asthma patients have altered sensitivity to carbon dioxide levels in the control of breathing when compared to healthy individuals
Authors: Wai Lo
Journal: European Respiratory Journal (2013)

Background : An existing theory suggests asthma patients are more sensitive to carbon dioxide (CO 2 ) and that small changes in CO 2  levels could induce hyperventilation. To date, little is known about the sensitivity of CO 2  in the control of breathing in severe asthma (SA) patients.   Aim : To investigate the relationships between changes in end tidal carbon dioxide levels (ETCO 2 ) and changes in breathing pattern parameters (BPP) in SA patients and healthy individuals.   Method : Ten SA patients and ten healthy individuals were recruited. BBP were monitored over 30 minutes of rest by respiratory inductive plethysmography. Changes in ETCO 2  and BPP were assessed by variability. Recorded parameters were: 1. Variability in tidal volume (VVt); 2. Variability in expiration time (VTe); 3. Variability in inspiratory time (VTi); 4. Variability in ETCO 2  levels (V-ETCO 2 ). Variability was assessed by coefficient of variation. Relationship between V-ETCO2 and BPP were analysed by Pearson correlation coefficient. Symptom of hyperventilation (SH) was measured by Nijmegen questionnaire (NQ).   Results : The SA group was positive for SH (NQ >23) whereas the healthy group was negative (NQ  2  and VVt, V-ETCO 2 and VTe, and ETCO 2  and VTi. Statistical significant levels were reached in the healthy group but not in the SA group.   Conclusion : The results suggest changes in BPP in SA group are less sensitive to changes in ETCO 2  levels than healthy individuals. This contradicts to existing theories and may impact on the design of breathing pattern interventions.
Evolution of<i>Prdm</i>Genes in Animals: Insights from Comparative Genomics
Authors: Michel Vervoort, David Meulemeester, Julien Béhague, Pierre Kerner
Journal: Molecular Biology and Evolution (2015)

Prdm genes encode transcription factors with a subtype of SET domain known as the PRDF1-RIZ (PR) homology domain and a variable number of zinc finger motifs. These genes are involved in a wide variety of functions during animal development. As most Prdm genes have been studied in vertebrates, especially in mice, little is known about the evolution of this gene family. We searched for Prdm genes in the fully sequenced genomes of 93 different species representative of all the main metazoan lineages. A total of 976 Prdm genes were identified in these species. The number of Prdm genes per species ranges from 2 to 19. To better understand how the Prdm gene family has evolved in metazoans, we performed phylogenetic analyses using this large set of identified Prdm genes. These analyses allowed us to define 14 different subfamilies of Prdm genes and to establish, through ancestral state reconstruction, that 11 of them are ancestral to bilaterian animals. Three additional subfamilies were acquired during early vertebrate evolution (Prdm5, Prdm11, and Prdm17). Several gene duplication and gene loss events were identified and mapped onto the metazoan phylogenetic tree. By studying a large number of nonmetazoan genomes, we confirmed that Prdm genes likely constitute a metazoan-specific gene family. Our data also suggest that Prdm genes originated before the diversification of animals through the association of a single ancestral SET domain encoding gene with one or several zinc finger encoding genes.
Identical non-identical twins and non-identical identical twins
Authors: Nirmal Vadgama, Niranjanan Nirmalananthan, Mustafa Sadiq, John Hardy, Jamal Nasir
Journal: BMJ (2015)

In recruiting monozygotic (MZ) twins for our ongoing research into de novo mutations in phenotypically discordant MZ twins, we have come across an increasing number of participants who have been told they are dizygotic (DZ) but have almost identical traits and physical features, or MZ but present more like fraternal siblings. Current practice guidelines for classifying twins as either MZ or DZ, which are still largely based on chorionicity (the notion of whether or not the twins …
SWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2
Authors: Kimberly H Kim, Woojin Kim, Thomas P Howard, Francisca Vazquez, Aviad Tsherniak, Jennifer N Wu, Weishan Wang, Jeffrey R Haswell, Loren D Walensky, William C Hahn, Stuart H Orkin, Charles W M Roberts
Journal: Nature Medicine (2015)
Race, Socioeconomic Status, and Life Expectancy After Acute Myocardial Infarction
Authors: Emily M. Bucholz, Shuangge Ma, Sharon-Lise T. Normand, Harlan M. Krumholz
Journal: Circulation (2015)

Previous studies have been unable to disentangle the negative associations of black race and low socioeconomic status (SES) with long-term outcomes of patients after acute myocardial infarction (AMI). Such information could assist in efforts to address both racial and socioeconomic disparities.
An Update on Overall Survival (Os) and Follow-On Therapies in Break-3, a Phase Iii, Randomized Trial: Dabrafenib (D) Vs. Dacarbazine (Dtic) in Patients (Pts) with Braf V600E Mutation-Positive Metastatic Melanoma (Mm)
Authors: A. Hauschild, J. Grobb, L. Demidov, T. Jouary, R. Gutzmer, M. Millward, P. Rutkowski, C. Blank, W. Miller, S. Martin-Algarra, B. Karaszewska, C. Mauch, V. Chiarion Sileni, G. Aktan, P. Haney, F. Jin, J. Legos, S. Swann, P. Chapman
Journal: Annals of Oncology (2014)
Distinct Chemokine Receptor Profile In Chronic Lymphocytic Leukaemia and Richter Transformed Diffuse Large B Cell Lymphomas Compared To Germinal Center B Cells and De Novo Diffuse Large B Cell Lymphomas
Authors: Kerstin Wenzl, Katharina Troppan, Alexander JA Deutsch, Werner Linkesch, Peter Neumeister, Christine Beham-Schmid
Journal: Blood (2013)
Antiaging Gene Klotho Regulates Adrenal CYP11B2 Expression and Aldosterone Synthesis
Authors: Xiaoli Zhou, Kai Chen, Yongjun Wang, Mariano Schuman, Han Lei, Zhongjie Sun
Journal: Journal of the American Society of Nephrology (2015)

Deficiency of the antiaging gene Klotho (KL) induces renal damage and hypertension through unknown mechanisms. In this study, we assessed whether KL regulates expression of CYP11B2, a key rate-limiting enzyme in aldosterone synthesis, in adrenal glands. We found that haplodeficiency of KL(+/-) in mice increased the plasma level of aldosterone by 16 weeks of age, which coincided with spontaneous and persistent elevation of BP. Blockade of aldosterone actions by eplerenone reversed KL deficiency-induced hypertension and attenuated the kidney damage. Protein expression of CYP11B2 was upregulated in adrenal cortex of KL(+/-) mice. KL and CYP11B2 proteins colocalized in adrenal zona glomerulosa cells. Silencing of KL upregulated and overexpression of KL downregulated CYP11B2 expression in human adrenocortical cells. Notably, silencing of KL decreased expression of SF-1, a negative transcription factor of CYP11B2, but increased phosphorylation of ATF2, a positive transcription factor of CYP11B2, which may contribute to upregulation of CYP11B2 expression. Therefore, these results show that KL regulates adrenal CYP11B2 expression. KL deficiency-induced spontaneous hypertension and kidney damage may be partially attributed to the upregulation of CYP11B2 expression and aldosterone synthesis.
Anti-Inflammatory Role of MicroRNA-146a in the Pathogenesis of Diabetic Nephropathy
Authors: Kirti Bhatt, Linda L. Lanting, Ye Jia, Sailee Yadav, Marpadga A. Reddy, Nathaniel Magilnick, Mark Boldin, Rama Natarajan
Journal: Journal of the American Society of Nephrology (2015)

Inflammation has a critical role in the pathogenesis of diabetic complications, including diabetic nephropathy (DN). MicroRNAs have recently emerged as important regulators of DN. However, the role of microRNAs in the regulation of inflammation during DN is poorly understood. Here, we examined the in vivo role of microRNA-146a (miR-146a), a known anti-inflammatory microRNA, in the pathogenesis of DN. In a model of streptozotocin-induced diabetes, miR-146a −/− mice showed significantly exacerbated proteinuria, renal macrophage infiltration, glomerular hypertrophy, and fibrosis relative to the respective levels in control wild-type mice. Diabetes-induced upregulation of proinflammatory and profibrotic genes was significantly greater in the kidneys of miR-146a −/− than in the kidneys of wild-type mice. Notably, miR-146a expression increased in both peritoneal and intrarenal macrophages in diabetic wild-type mice. Mechanistically, miR-146a deficiency during diabetes led to increased expression of M1 activation markers and suppression of M2 markers in macrophages. Concomitant with increased expression of proinflammatory cytokines, such as IL-1 β and IL-18, markers of inflammasome activation also increased in the macrophages of diabetic miR-146a −/− mice. These studies suggest that in early DN, miR-146a upregulation exerts a protective effect by downregulating target inflammation-related genes, resulting in suppression of proinflammatory and inflammasome gene activation. Loss of this protective mechanism in miR-146a −/− mice leads to accelerated DN. Taken together, these results identify miR-146a as a novel anti-inflammatory noncoding RNA modulator of DN.
A SPRINT to the Finish
Authors: Jeffrey M. Drazen, Stephen Morrissey, Edward W. Campion, John A. Jarcho
Journal: New England Journal of Medicine (2015)

When investigators enroll patients in a clinical study, they make an implicit contract with each participant. Through the data and safety monitoring board (DSMB) mechanism, they fulfill the first part of the contract — protecting the participant from avoidable harm that might result from participation in the trial. They fulfill the second part of the contract — the commitment to honor the time at risk that the participant spent in the trial — by deriving the clearest and most clinically directive information possible from the data gathered during the trial. This task takes tremendous time and energy.The SPRINT (Systolic . . .