tbuckley/cabot-search huggingface dataset:
Postponing or preventing death? Trends in infant survival
Authors: B. Dujardin
Journal: JAMA (1986)

<h3>To the Editor.—</h3> In a recent article, "Postponing or Preventing Death," Buehler et al<sup>1</sup>examined trends in infant survival by birth-weight groups and studied the perinatal-related postneonatal deaths. They concluded that "advances in perinatal care have led to postponement rather than prevention of a few infant deaths, although overall many more deaths were prevented." In a correspondence about this article, Sepkowitz<sup>2</sup>discusses the idea that recent declines in neonatal mortality in the United States could be largely attributed to a greater utilization of neonatal intensive care units among low-birth-weight infants. To explain his statement, Sepkowitz invokes different biases such as selection biases as possible factors leading to a distortion of neonatal mortality rates reported from neonatal intensive care units. However, we think that other biases could also explain an underestimation of the number of perinatal-related postneonatal deaths in Buehler's study. The problem concerns the cause of death ascertainment.
Leads from the MMWR. Lung cancer and breast cancer among women--Texas
Journal: JAMA (1984)

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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Peripartum cardiomyopathy
Authors: Michael C Honigberg, Michael M Givertz
Journal: BMJ (2019)

Abstract Peripartum cardiomyopathy (PPCM) is a rare, often dilated, cardiomyopathy with systolic dysfunction that presents in late pregnancy or, more commonly, the early postpartum period. Although the condition is prevalent worldwide, women with black ancestry seem to be at greatest risk, and the condition has a particularly high incidence in Nigeria and Haiti. Other risk factors include pre-eclampsia, advanced maternal age, and multiple gestation pregnancy. Although the complete pathophysiology of peripartum cardiomyopathy remains unclear, research over the past decade suggests the importance of vasculo-hormonal pathways in women with underlying susceptibility. At least some women with the condition harbor an underlying sarcomere gene mutation. More than half of affected women recover systolic function, although some are left with a chronic cardiomyopathy, and a minority requires mechanical support or cardiac transplantation (or both). Other potential complications include thromboembolism and arrhythmia. Currently, management entails standard treatments for heart failure with reduced ejection fraction, with attention to minimizing potential adverse effects on the fetus in women who are still pregnant. Bromocriptine is one potential disease specific treatment under investigation. In this review, we summarize the current literature on peripartum cardiomyopathy, as well as gaps in the understanding of this condition and future research directions.
Clinical metagenomics
Authors: Charles Y. Chiu, Steven A. Miller
Journal: Nature Reviews Genetics (2019)

Clinical metagenomic next-generation sequencing (mNGS), the comprehensive analysis of microbial and host genetic material (DNA and RNA) in samples from patients, is rapidly moving from research to clinical laboratories. This emerging approach is changing how physicians diagnose and treat infectious disease, with applications spanning a wide range of areas, including antimicrobial resistance, the microbiome, human host gene expression (transcriptomics) and oncology. Here, we focus on the challenges of implementing mNGS in the clinical laboratory and address potential solutions for maximizing its impact on patient care and public health. Clinical metagenomic next-generation sequencing (mNGS) is rapidly moving from bench to bedside. This Review discusses the clinical applications of mNGS, including infectious disease diagnostics, microbiome analyses, host response analyses and oncology applications. Moreover, the authors review the challenges that need to be overcome for mNGS to be successfully implemented in the clinical laboratory and propose solutions to maximize the benefits of clinical mNGS for patients.
The costs and benefits of senotherapeutics for human health
Authors: Marco Raffaele, Manlio Vinciguerra
Journal: The Lancet Healthy Longevity (2022)

Cellular senescence is a major contributor to age-related diseases in humans; however, it also has a beneficial role in physiological and pathological processes, including wound healing, host immunity, and tumour suppression. Reducing the burden of cell senescence in animal models of cardiometabolic disorders, inflammatory conditions, neurodegenerative diseases, and cancer using pharmaceutical approaches that selectively target senescent cells (ie, senolytics) or that suppress senescence-associated secretory phenotype (ie, senomorphics) holds great promise for the management of chronic age-associated conditions. Although studies have provided evidence that senolytics or senomorphics are effective at decreasing the number of senescent cells in humans, the short-term and long-term side-effects of these therapies are largely unknown. In this Review, we systematically discuss the senolytics and senomorphics that have been investigated in clinical trials or have been used off-label, presenting their various adverse effects. Despite the potential of senotherapeutics to transform anti-ageing medicine, a cautionary approach regarding unwanted dose-dependent side-effects should be adopted.
Liver metastases
Authors: Diamantis I. Tsilimigras, Pnina Brodt, Pierre-Alain Clavien, Ruth J. Muschel, Michael I. D’Angelica, Itaru Endo, Rowan W. Parks, Majella Doyle, Eduardo de Santibañes, Timothy M. Pawlik
Journal: Nature Reviews Disease Primers (2021)
International Comments
Journal: JAMA (1970)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Interphase Cytogenetics of Workers Exposed to Benzene
Authors: Luoping Zhang, Nathaniel Rothman, Yunxia Wang, Richard B. Hayes, William Bechtold, Pravina Venkatesh, Songnian Yin, Yaozhu Wang, Mustafa Dosemeci, Guilan Li, Wei Lu, Martyn T. Smith
Journal: Environmental Health Perspectives (1996)

Fluorescence in situ hybridization (FISH) is a powerful new technique that allows numerical chromosome aberrations (aneuploidy) to be detected in interphase cells.In previous studies, FISH has been used to demonstrate that the benzene metabolites hydroquinone and 1,2,4-benzenetriol induce aneuploidy of chromosomes 7 and 9 in cultures of human cells.In the present study, we used an interphase FISH procedure to perform cytogenetic analyses on the blood cells of 43 workers exposed to benzene (median=31 ppm, 8-hr time-weighted average) and 44 matched controls from Shanghai, China.High benzene exposure (>31 ppm, n=22) increased the hyperdiploid frequency of chromosome 9 (p<0.01),but lower exposure (<31 ppm, n=21) did not.Trisomy 9 was the major form of benzene-induced hyperdiploidy.The level of hyperdiploidy in exposed workers correlated with their urinary phenol level (r=0.58,p<0.0001), a measure of internal benzene dose.A significant correlation was also found between hyperdiploidy and decreased absolute lymphocyte count, an indicator of benzene hematotoxicity, in the exposed group (r=-0.44,p=0.003) but not in controls (r=-0.09,p=0.58).These results show that high benzene exposure induces aneuploidy of chromosome 9 in nondiseased individuals, with trisomy being the most prevalent form.They further highlight the usefulness of interphase cytogenetics and FISH for the rapid and sensitive detection of aneuploidy in exposed human populations.
Soft tissue and visceral sarcomas: ESMO–EURACAN–GENTURIS Clinical Practice Guidelines for diagnosis, treatment and follow-up☆
Authors: A. Gronchi, A.B. Miah, A.P. Dei Tos, N. Abecassis, J. Bajpai, S. Bauer, R. Biagini, S. Bielack, J.Y. Blay, S. Bolle, S. Bonvalot, I. Boukovinas, J.V.M.G. Bovee, K. Boye, B. Brennan, T. Brodowicz, A. Buonadonna, E. De Álava, X.G. Del Muro, A. Dufresne, M. Eriksson, F. Fagioli, A. Fedenko, V. Ferraresi, A. Ferrari, A.M. Frezza, S. Gasperoni, H. Gelderblom, F. Gouin, G. Grignani, R. Haas, A.B. Hassan, S. Hecker-Nolting, N. Hindi, P. Hohenberger, H. Joensuu, R.L. Jones, C. Jungels, P. Jutte, L. Kager, B. Kasper, A. Kawai, K. Kopeckova, D.A. Krákorová, A. Le Cesne, F. Le Grange, E. Legius, A. Leithner, A. Lopez-Pousa, J. Martin-Broto, O. Merimsky, C. Messiou, O. Mir, M. Montemurro, B. Morland, C. Morosi, E. Palmerini, M.A. Pantaleo, R. Piana, S. Piperno-Neumann, P. Reichardt, P. Rutkowski, A.A. Safwat, C. Sangalli, M. Sbaraglia, S. Scheipl, P. Schöffski, S. Sleijfer, D. Strauss, S. Strauss, K. Sundby Hall, A. Trama, M. Unk, M.A.J. van de Sande, W.T.A. van der Graaf, W.J. van Houdt, T. Frebourg, P.G. Casali, S. Stacchiotti
Journal: Annals of Oncology (2021)
Errors in Figure Headings
Authors: Katherine Rediger, D Miles, Seth Berkowitz, Jean Terranova, John Hsu, Cecil Sheps
Journal: JAMA Internal Medicine (2019)

Dimitrios A. Koutoukidis, PhD; Nerys M. Astbury, PhD; Kate E. Tudor, PhD; Elizabeth Morris, BMBCh; John A. Henry, BA; Michaela Noreik, PhD; Susan A. Jebb, PhD; Paul Aveyard, PhD
Metabolic dysfunction and cancer in HCV: Shared pathways and mutual interactions
Authors: Jack Leslie, Daniel Geh, Ahmed M. Elsharkawy, Derek A. Mann, Michele Vacca
Journal: Journal of Hepatology (2022)

HCV hijacks many host metabolic processes in an effort to aid viral replication. The resulting hepatic metabolic dysfunction underpins many of the hepatic and extrahepatic manifestations of chronic hepatitis C (CHC). However, the natural history of CHC is also substantially influenced by the host metabolic status: obesity, insulin resistance and hepatic steatosis are major determinants of CHC progression toward hepatocellular carcinoma (HCC). Direct-acting antivirals (DAAs) have transformed the treatment and natural history of CHC. While DAA therapy effectively eradicates the virus, the long-lasting overlapping metabolic disease can persist, especially in the presence of obesity, increasing the risk of liver disease progression. This review covers the mechanisms by which HCV tunes hepatic and systemic metabolism, highlighting how systemic metabolic disturbance, lipotoxicity and chronic inflammation favour disease progression and a precancerous niche. We also highlight the therapeutic implications of sustained metabolic dysfunction following sustained virologic response as well as considerations for patients who develop HCC on the background of metabolic dysfunction.
Metabolic Codependencies in the Tumor Microenvironment
Authors: Prasenjit Dey, Alec C. Kimmelman, Ronald A. DePinho
Journal: Cancer Discovery (2021)

Metabolic reprogramming enables cancer cell growth, proliferation, and survival. This reprogramming is driven by the combined actions of oncogenic alterations in cancer cells and host cell factors acting on cancer cells in the tumor microenvironment. Cancer cell-intrinsic mechanisms activate signal transduction components that either directly enhance metabolic enzyme activity or upregulate transcription factors that in turn increase expression of metabolic regulators. Extrinsic signaling mechanisms involve host-derived factors that further promote and amplify metabolic reprogramming in cancer cells. This review describes intrinsic and extrinsic mechanisms driving cancer metabolism in the tumor microenvironment and how such mechanisms may be targeted therapeutically. SIGNIFICANCE: Cancer cell metabolic reprogramming is a consequence of the converging signals originating from both intrinsic and extrinsic factors. Intrinsic signaling maintains the baseline metabolic state, whereas extrinsic signals fine-tune the metabolic processes based on the availability of metabolites and the requirements of the cells. Therefore, successful targeting of metabolic pathways will require a nuanced approach based on the cancer's genotype, tumor microenvironment composition, and tissue location.
Erratum
Authors: S Aarons, J Allison, C Anderson, G Anderson, H Balfour, N Bardswell, W Begg, J Bell, H Benson, E Birrell, J Blackburn, G Blackmore, J Bowes, L Bowman, E Brierley, N Caine, H Cardale, S Carr, J Coates, W Chipman, W Coulthard, J Crawford, R Cross, R Cunningham, J M', E Dalziel, J Dawson, M Dee, T Dewar, A Easmon, W Eason, H Ewald, H Eyres, A Fenn, F Fitchett, A Fleming, J Forbes, J Forrest, J Fraser, W Garbutt, F Gardiner, W Gibb, T Gibson, J Gilchrist, S Gilfillan, M Gillies, J Gilruth, W Glegg, C Gorringe, D Graham, J Gray, E Greie, J Grieve, J Griffiths, H Halton, J Hay, R Haygarth, C Rector, R Heddle, G Henderson, J Henderson, I Howden, M Hughes, W Hunter, H Huntly, A Husband, D Hutton, G Jenkins, D Jones, J Kelly, L Ker, M Kirk, D Landsborough, J Landsborough, L Laurie, D Lawson, H Leebody, R M', W Leith, T Lewis, W Lillie, G Lundie, A Lupton, S Lusk, W Liittig, A Lyalj, R M'carthy- Morrogh, A M'camon, M Macdonald, F Macdonald, J M'donald, W Macdonald, W M'dowell, T Mac- Fie, D Mackay, C-M' Laurin, K M'lean, J Macmillan, N Macmillan, W Malcolm, W Mander, J Martin, F Mompid, R Moorhead, J Norwell, E Ormerod, R Owen, H Peach, A Pearson, G Peill, W Plante, B Potts, W Price, G Proctor, J Rait, D Rankine, M Ran, J Raymond, E Reid, H Richardson, W Richardson, R Risely, G Roberts, R Robson, T Roddis, V Ross, T Roycroft, R Sadler, F Samut, R Scott, H Selby, E Simson, E Skeete, J Snijman, F Somerville, W Stanwell, J Steele, A Stenhouse, W Stewart, J Stokes, T Stuart, D Stuart, W Sutton, F Taylor, J Thompson, J Thwaits, J Tough, A Veitch, G Wallace, D Wallace, J Watson, J Watt, A Wilson, W De, W Wishart, J Wood
Journal: BMJ (1895)

A LADY is sent by a physician, A., to a health resort, provided with a closed letter addressed to a local practitioner, C. Before making acquaintance with U;. she forms that of H. C
Corrigendum to ‘Genomic sequencing identifies WNK2 as a driver in hepatocellular carcinoma and a risk factor for early recurrence’ [J Hepatol 71 (2019) 1152-63]
Authors: Shao-Lai Zhou, Zheng-Jun Zhou, Zhi-Qiang Hu, Cheng-Li Song, Yi-Jie Luo, Chu-Bin Luo, Hao-Yang Xin, Xin-Rong Yang, Ying-Hong Shi, Zheng Wang, Xiao-Wu Huang, Ya Cao, Jia Fan, Jian Zhou
Journal: Journal of Hepatology (2022)
Treating COVID-19: Evolving approaches to evidence in a pandemic
Authors: Cheryl K. Lee, Louis T. Merriam, Jeffrey C. Pearson, Michael S. Lipnick, William McKleroy, Edy Y. Kim
Journal: Cell Reports Medicine (2022)

The rapid pace of the COVID-19 pandemic precluded traditional approaches to evaluating clinical research and guidelines. We highlight notable successes and pitfalls of clinicians' new approaches to managing evidence amidst an unprecedented crisis. In "Era 1" (early 2020), clinicians relied on anecdote and social media, which democratized conversations on guidelines, but also led clinicians astray. "Era 2" (approximately late 2020 to early 2021) saw preprints that accelerated new interventions but suffered from a surfeit of poor-quality data. In the current era, clinicians consolidate the evidentiary gains of Era 2 with living, online clinical guidelines, but the public suffers from misinformation. The COVID-19 pandemic is a laboratory on how clinicians adapt to an absence of clinical guidance amidst an informational and healthcare crisis. Challenges remain as we integrate new approaches to innovations made in the traditional guideline process to confront both the long tail of COVID-19 and future pandemics.
Acute exacerbation of idiopathic pulmonary fibrosis after SARS-CoV-2 vaccination
Authors: Tomohiro Bando, Reoto Takei, Yoshikazu Mutoh, Hajime Sasano, Yasuhiko Yamano, Toshiki Yokoyama, Toshiaki Matsuda, Kensuke Kataoka, Tomoki Kimura, Yasuhiro Kondoh
Journal: European Respiratory Journal (2022)

<b>Although the association between acute exacerbation of interstitial lung disease and vaccination is not yet clarified, this is the first case report describing the possibility that SARS-CoV-2 vaccination may trigger acute exacerbation</b> https://bit.ly/3tpu6Cz
Occupational cancer in central European countries
Authors: E Fabiánová, N Szeszenia-Dabrowska, K Kjaerheim, P Boffetta
Journal: Environmental Health Perspectives (1999)

Romania, and Bulgaria, suffer from environmental and occupational health problems created during the political system in place until the late 1980s.This situation is reflected by data on workplace exposure to hazardous agents.Such data have been systematically collected in Slovakia and the Czech Republic since 1977.The data presented describe mainly the situation in the early 1 990s.The number of workers exposed to risk factors at the workplace represent about 10% of the working population in Slovakia and 30% in Poland.In Slovakia in 1992 the percentage of persons exposed to chemical substances was 16.4%, to ionizing radiation 4.3%, and to carcinogens 3.3% of all workers exposed to risk factors.The total number of persons exposed to substances proven to be carcinogens in Poland was 1.3% of the employees; 2.2% were exposed to the suspected carcinogens.The incidence of all certified occupational diseases in the Slovak Republic was 53 per 100,000 insured employees in 1992.Cancers certified as occupational cancers are skin cancer caused by occupational exposure to carcinogens, lung cancer caused by ionizing radiation, and asbestosis together with lung cancer.Specific information on occupational cancers from Romania and Bulgaria was not available for this paper.It is difficult to predict a trend for future incidences of occupational cancer.Improved control technology, governmental regulatory activity to reduce exposure, surveillance of diseases and risk factors, and vigilant use of preventive measures should, however, ultimately reduce occupational
Novel Paradigms of Salt and Hypertension
Authors: Wenguang Feng, Louis J. Dell’Italia, Paul W. Sanders
Journal: Journal of the American Society of Nephrology (2017)

Salt resistance/sensitivity refers specifically to the effect of dietary sodium chloride (salt) intake on BP. Increased dietary salt intake promotes an early and uniform expansion of extracellular fluid volume and increased cardiac output. To compensate for these hemodynamic changes and maintain constant BP in salt resistance, renal and peripheral vascular resistance falls and is associated with an increase in production of nitric oxide. In contrast, the decline in peripheral vascular resistance and the increase in nitric oxide are impaired or absent in salt sensitivity, promoting an increase in BP in these individuals. Endothelial dysfunction may pose a particularly significant risk factor in the development of salt sensitivity and subsequent hypertension. Vulnerable salt-sensitive populations may have in common underlying endothelial dysfunction due to genetic or environmental influences. These individuals may be very sensitive to the hemodynamic stress of increased effective blood volume, setting in motion untoward molecular and biochemical events that lead to overproduction of TGF- β , oxidative stress, and limited bioavailable nitric oxide. Finally, chronic high-salt ingestion produces endothelial dysfunction, even in salt-resistant subjects. Thus, the complex syndrome of salt sensitivity may be a function of the endothelium, which is integrally involved in the vascular responses to high salt intake.
Final Analysis of Efficacy and Safety of Single-Dose Ad26.COV2.S
Authors: Jerald Sadoff, Glenda Gray, An Vandebosch, Vicky Cárdenas, Georgi Shukarev, Beatriz Grinsztejn, Paul A. Goepfert, Carla Truyers, Ilse Van Dromme, Bart Spiessens, Johan Vingerhoets, Jerome Custers, Gert Scheper, Merlin L. Robb, John Treanor, Martin F. Ryser, Dan H. Barouch, Edith Swann, Mary A. Marovich, Kathleen M. Neuzil, Lawrence Corey, Jeffrey Stoddard, Karin Hardt, Javier Ruiz-Guiñazú, Mathieu Le Gars, Hanneke Schuitemaker, Johan Van Hoof, Frank Struyf, Macaya Douoguih
Journal: New England Journal of Medicine (2022)

The Ad26.COV2.S vaccine was highly effective against severe–critical coronavirus disease 2019 (Covid-19), hospitalization, and death in the primary phase 3 efficacy analysis.
Diagnosis and management of iatrogenic endoscopic perforations: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement – Update 2020
Authors: Gregorios A. Paspatis, Marianna Arvanitakis, Jean-Marc Dumonceau, Marc Barthet, Brian Saunders, Stine Ydegaard Turino, Angad Dhillon, Maria Fragaki, Jean-Michel Gonzalez, Alessandro Repici, Roy L.J. van Wanrooij, Jeanin E. van Hooft
Journal: Endoscopy (2020)

Summary of Recommendations 1 ESGE recommends that each center implements a written policy regarding the management of iatrogenic perforations, including the definition of procedures that carry a higher risk of this complication. This policy should be shared with the radiologists and surgeons at each center. 2 ESGE recommends that in the case of an endoscopically identified perforation, the endoscopist reports its size and location, with an image, and statement of the endoscopic treatment that has been applied. 3 ESGE recommends that symptoms or signs suggestive of iatrogenic perforation after an endoscopic procedure should be rapidly and carefully evaluated and documented with a computed tomography (CT) scan. 4 ESGE recommends that endoscopic closure should be considered depending on the type of the iatrogenic perforation, its size, and the endoscopist expertise available at the center. Switch to carbon dioxide (CO2) endoscopic insufflation, diversion of digestive luminal content, and decompression of tension pneumoperitoneum or pneumothorax should also be performed. 5 ESGE recommends that after endoscopic closure of an iatrogenic perforation, further management should be based on the estimated success of the endoscopic closure and on the general clinical condition of the patient. In the case of no or failed endoscopic closure of an iatrogenic perforation, and in patients whose clinical condition is deteriorating, hospitalization and surgical consultation are recommended.