tbuckley/cabot-search huggingface dataset:
Evaluation of Control Measures Implemented in the Severe Acute Respiratory Syndrome Outbreak in Beijing, 2003
Authors: Xinghuo Pang, Zonghan Zhu, Fujie Xu, Jiyong Guo, Xiaohong Gong, Donglei Liu, Zejun Liu, Daniel P Chin, Daniel R Feikin
Journal: JAMA (2003)

Beijing, China, experienced the world's largest outbreak of severe acute respiratory syndrome (SARS) beginning in March 2003, with the outbreak resolving rapidly, within 6 weeks of its peak in late April. Little is known about the control measures implemented during this outbreak.To describe and evaluate the measures undertaken to control the SARS outbreak.Data were reviewed from standardized surveillance forms from SARS cases (2521 probable cases) and their close contacts observed in Beijing between March 5, 2003, and May 29, 2003. Procedures implemented by health authorities were investigated through review of official documents and discussions with public health officials.Timeline of major control measures; number of cases and quarantined close contacts and attack rates, with changes in infection control measures, management, and triage of suspected cases; and time lag between illness onset and hospitalization with information dissemination.Health care worker training in use of personal protective equipment and management of patients with SARS and establishing fever clinics and designated SARS wards in hospitals predated the steepest decline in cases. During the outbreak, 30 178 persons were quarantined. Among 2195 quarantined close contacts in 5 districts, the attack rate was 6.3% (95% confidence interval [CI], 5.3%-7.3%), with a range of 15.4% (95% CI, 11.5%-19.2%) among spouses to 0.36% (95% CI, 0%-0.77%) among work and school contacts. The attack rate among quarantined household members increased with age from 5.0% (95% CI, 0%-10.5%) in children younger than 10 years to 27.6% (95% CI, 18.2%-37.0%) in adults aged 60 to 69 years. Among almost 14 million people screened for fever at the airport, train stations, and roadside checkpoints, only 12 were found to have probable SARS. The national and municipal governments held 13 press conferences about SARS. The time lag between illness onset and hospitalization decreased from a median of 5 to 6 days on or before April 20, 2003, the day the outbreak was announced to the public, to 2 days after April 20 (P<.001).The rapid resolution of the SARS outbreak was multifactorial, involving improvements in management and triage in hospitals and communities of patients with suspected SARS and the dissemination of information to health care workers and the public.
Staging of breast cancer: What standards should be used in research and clinical practice?
Authors: A Ravaioli, D Tassinari, G Pasini, A Polselli, M Papi, P P Fattori, E Pasquini, A Masi, F Alessandrini, D Canuti, I Panzini, G Drudi
Journal: Annals of Oncology (1998)
CIRRHOSIS OF THE LIVER CAUSED BY EXCESS DIETARY CYSTINE
Authors: David P. Earle, Joseph Victor
Journal: The Journal of Experimental Medicine (1941)

1. Cystine fed to young albino rats as 10 per cent of the diet resulted in: (a) Portal hemorrhagic necrosis, resembling eclampsia, within 3 or 4 days. (b) A high mortality rate. (c) Fatty infiltration of hepatic cells in all rats surviving the initial acute lesion. (d) Cirrhosis of the liver in rats surviving more than 2 weeks. 2. 5 per cent dietary cystine produced marked fatty infiltration of the liver, followed by portal hemorrhagic necrosis. Cirrhosis was present in one of the two rats on the diet for 6 weeks. 3. The livers of rats fed 5 or 10 per cent cystine diets followed by the McCollum stock diet, showed evidence of residual cellular damage, and of regeneration as shown by mitotic figures. 4. In this series of 30 rats on excess dietary cystine, a renal lesion was found in only one case.
Characterization of somatically mutated S107 VH11-encoded anti-DNA autoantibodies derived from autoimmune (NZB x NZW)F1 mice.
Authors: S M Behar, D L Lustgarten, S Corbet, M D Scharff
Journal: The Journal of Experimental Medicine (1991)

We have studied 19 S107 heavy chain variable region gene (VH11)-encoded monoclonal antibodies from NZBWF1 mice. These studies show that a single VH gene can encode both antibodies to foreign antigens (anti-phosphorylcholine) and to self antigens (anti-double-stranded DNA) in the same animal. All of the anti-DNA antibodies contain many somatic mutations compared with the relevant germline genes. Since the anti-DNA antibodies were extensively somatically mutated and had undergone isotype switching, the response seems to be T cell dependent. While some of the antibodies appear to be the products of an antigen-driven and antigen-selected response, a number of characteristics of the antibodies suggest that forces other than antigen are contributing to the stimulation and selection of this response.
Occult HBV infection and YMDD variants in hemodialysis patients with chronic HCV infection
Authors: Fatih Besisik, Çetin Karaca, Filiz Akyüz, Sibel Horosanlı, Derya Önel, Selim Badur, Mehmet Şükrü Sever, Ahmet Danalıoǧlu, Kadir Demir, Sabahattin Kaymakoǧlu, Yılmaz Çakaloǧlu, Atilla Ökten
Journal: Journal of Hepatology (2003)
National and regional estimates of term and preterm babies born small for gestational age in 138 low-income and middle-income countries in 2010
Authors: Anne CC Lee, Joanne Katz, Hannah Blencowe, Simon Cousens, Naoko Kozuki, Joshua P Vogel, Linda Adair, Abdullah H Baqui, Zulfiqar A Bhutta, Laura E Caulfield, Parul Christian, Siân E Clarke, Majid Ezzati, Wafaie Fawzi, Rogelio Gonzalez, Lieven Huybregts, Simon Kariuki, Patrick Kolsteren, John Lusingu, Tanya Marchant, Mario Merialdi, Aroonsri Mongkolchati, Luke C Mullany, James Ndirangu, Marie-Louise Newell, Jyh Kae Nien, David Osrin, Dominique Roberfroid, Heather E Rosen, Ayesha Sania, Mariangela F Silveira, James Tielsch, Anjana Vaidya, Barbara A Willey, Joy E Lawn, Robert E Black
Journal: The Lancet Global Health (2013)

National estimates for the numbers of babies born small for gestational age and the comorbidity with preterm birth are unavailable. We aimed to estimate the prevalence of term and preterm babies born small for gestational age (term-SGA and preterm-SGA), and the relation to low birthweight (<2500 g), in 138 countries of low and middle income in 2010.Small for gestational age was defined as lower than the 10th centile for fetal growth from the 1991 US national reference population. Data from 22 birth cohort studies (14 low-income and middle-income countries) and from the WHO Global Survey on Maternal and Perinatal Health (23 countries) were used to model the prevalence of term-SGA births. Prevalence of preterm-SGA infants was calculated from meta-analyses.In 2010, an estimated 32·4 million infants were born small for gestational age in low-income and middle-income countries (27% of livebirths), of whom 10·6 million infants were born at term and low birthweight. The prevalence of term-SGA babies ranged from 5·3% of livebirths in east Asia to 41·5% in south Asia, and the prevalence of preterm-SGA infants ranged from 1·2% in north Africa to 3·0% in southeast Asia. Of 18 million low-birthweight babies, 59% were term-SGA and 41% were preterm-SGA. Two-thirds of small-for-gestational-age infants were born in Asia (17·4 million in south Asia). Preterm-SGA babies totalled 2·8 million births in low-income and middle-income countries. Most small-for-gestational-age infants were born in India, Pakistan, Nigeria, and Bangladesh.The burden of small-for-gestational-age births is very high in countries of low and middle income and is concentrated in south Asia. Implementation of effective interventions for babies born too small or too soon is an urgent priority to increase survival and reduce disability, stunting, and non-communicable diseases.Bill & Melinda Gates Foundation by a grant to the US Fund for UNICEF to support the activities of the Child Health Epidemiology Reference Group (CHERG).
Prognosis of Transient Neurological Attacks
Authors: Mitchell S. V. Elkind
Journal: JAMA (2008)

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
Prognostic Value of CT Angiography in Patients With Inconclusive Functional Stress Tests
Authors: Clerio F. de Azevedo, Marcelo S. Hadlich, Sabrina G. Bezerra, João L. Petriz, Rogério R. Alves, Olga de Souza, Miguel Rati, Denilson C. Albuquerque, Jorge Moll
Journal: JACC. Cardiovascular imaging (2011)
Inhibition of Heat Shock Protein 90 Function by 17-Allylamino-17-Demethoxy-Geldanamycin in Hodgkin's Lymphoma Cells Down-Regulates Akt Kinase, Dephosphorylates Extracellular Signal–Regulated Kinase, and Induces Cell Cycle Arrest and Cell Death
Authors: Georgios V. Georgakis, Yang Li, Georgios Z. Rassidakis, Hector Martinez-Valdez, L. Jeffrey Medeiros, Anas Younes
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Heat shock protein 90 (HSP90) is a chaperone for several client proteins involved in transcriptional regulation, signal transduction, and cell cycle control. HSP90 is abundantly expressed by a variety of tumor types and has been recently targeted for cancer therapy. The objective of this study was to determine the role of HSP90 in promoting growth and survival of Hodgkin's lymphoma and to determine the molecular consequences of inhibiting HSP90 function by the small-molecule 17-allylamino-17-demethoxy-geldanamycin (17-AAG) in Hodgkin's lymphoma. Experimental Design: HSP90 expression in Hodgkin's lymphoma cell lines was determined by Western blot and in primary lymph node sections from patients with Hodgkin's lymphoma by immunohistochemistry. Cell viability was determined by the 3-(4,5-dimethyl-thiazol-2yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. Apoptosis and cell cycle fractions were determined by flow cytometry. Expression of intracellular proteins was determined by Western blot. Results: HSP90 is overexpressed in primary and cultured Hodgkin's lymphoma cells. Inhibition of HSP90 function by 17-AAG showed a time- and dose-dependent growth inhibition of Hodgkin's lymphoma cell lines. 17-AAG induced cell cycle arrest and apoptosis, which were associated with a decrease in cyclin-dependent kinase (CDK) 4, CDK 6, and polo-like kinase 1 (PLK1), and induced apoptosis by caspase-dependent and caspase-independent mechanisms. Furthermore, 17-AAG depleted cellular contents of Akt, decreased extracellular signal–regulated kinase (ERK) phosphorylation, and reduced cellular FLICE-like inhibitory protein levels (FLIP), and thus enhanced the cytotoxic effect of doxorubicin and agonistic anti–tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) death receptor antibodies. Conclusion: Inhibition of HSP90 function induces cell death and enhances the activity of chemotherapy and anti–tumor necrosis factor–related apoptosis-inducing ligand death receptor antibodies, suggesting that targeting HSP90 function might be of therapeutic value in Hodgkin's lymphoma.
Bortezomib plus melphalan and prednisone in elderly untreated patients with multiple myeloma: results of a multicenter phase 1/2 study
Authors: María-Victoria Mateos, José-M. Hernández, Miguel-T. Hernández, Norma-C. Gutiérrez, Luis Palomera, Marta Fuertes, Joaquín Díaz-Mediavilla, Juan-J. Lahuerta, Javier de la Rubia, María-José Terol, Ana Sureda, Joan Bargay, Paz Ribas, Felipe de Arriba, Adrian Alegre, Albert Oriol, Dolores Carrera, José García-Laraña, Ramón García-Sanz, Joan Bladé, Felipe Prósper, Gemma Mateo, Dixie-Lee Esseltine, Helgi van de Velde, Jesús-F. San Miguel
Journal: Blood (2006)
Is the “3+3” Dose-Escalation Phase I Clinical Trial Design Suitable for Therapeutic Cancer Vaccine Development? A Recommendation for Alternative Design
Authors: Osama E. Rahma, Emily Gammoh, Richard M. Simon, Samir N. Khleif
Journal: Clinical Cancer Research (2014)

Abstract Purpose: Phase I clinical trials are generally conducted to identify the maximum tolerated dose (MTD) or the biologically active dose (BAD) using a traditional dose-escalation design. This design may not be applied to cancer vaccines, given their unique mechanism of action. The FDA recently published “Guidance for Industry: Clinical Considerations for Therapeutic Cancer Vaccines.” However, many questions about the design of cancer vaccine studies remain unanswered. Experimental Design: We analyzed the toxicity profile in 239 phase I therapeutic cancer vaccine trials. We addressed the ability of dose escalation to determine the MTD or the BAD in trials that used a dose-escalation design. Results: The rate of grade 3/4 vaccine-related systemic toxicities was 1.25 adverse events per 100 patients and 2 per 1,000 vaccines. Only two of the 127 dose-escalation trials reported vaccine-related dose limiting toxicities, both of which used bacterial vector vaccines. Out of the 116 trials analyzed for the dose–immune response relationship, we found a statistically significant dose–immune response correlation only when the immune response was measured by antibodies (P &amp;lt; 0.001) or delayed type hypersensitivity (P &amp;lt; 0.05). However, the increase in cellular immune response did not appear further sustainable with the continued increase in dose. Conclusions: Our analysis suggests that the risks of serious toxicities with therapeutic cancer vaccines are extremely low and that toxicities do not correlate with dose levels. Accordingly, the conventional dose-escalation design is not suitable for cancer vaccines with few exceptions. Here, we propose an alternative design for therapeutic cancer vaccine development. Clin Cancer Res; 20(18); 4758–67. ©2014 AACR.
Observational Study of Inhaled Corticosteroids on Outcomes for COPD Patients with Pneumonia
Authors: Dennis Chen, Marcos I. Restrepo, Michael J. Fine, Mary Jo V. Pugh, Antonio Anzueto, Mark L. Metersky, Brandy Nakashima, Chester Good, Eric M. Mortensen
Journal: American Journal of Respiratory and Critical Care Medicine (2011)

Rationale: Treatment with inhaled corticosteroids (ICS) for those with chronic obstructive pulmonary disease (COPD) has been shown to be associated with an increased incidence of pneumonia. However, it is unclear if this is associated with increased mortality.Objectives: The aim of this study was to examine the effects of prior use of ICS on clinical outcomes for patients with COPD hospitalized with pneumonia.Methods: We conducted a retrospective cohort study using the national administrative databases of the Department of Veterans Affairs. Eligible patients had a preexisting diagnosis of COPD, had a discharge diagnosis of pneumonia, and received treatment with one or more appropriate pulmonary medications before hospitalization. Outcomes included mortality, use of invasive mechanical ventilation, and vasopressor use.Measurements and Main Results: There were 15,768 patients (8,271 with use of ICS and 7,497 with no use of ICS) with COPD who were hospitalized for pneumonia. There was also a significant difference for 90-day mortality (ICS 17.3% vs. no ICS 22.8%; P < 0.001). Multilevel regression analyses demonstrated that prior receipt of ICS was associated with decreased mortality at 30 days (odds ratio [OR] 0.80; 95% confidence interval [CI], 0.72–0.89) and 90 days (OR 0.78; 95% CI, 0.72–0.85), and decreased use of mechanical ventilation (OR 0.83; 95% CI, 0.72–0.94). There was no significant association between receipt of ICS and vasopressor use (OR 0.88; 95% CI, 0.74–1.04).Conclusions: For patients with COPD, prior use of ICS is independently associated with decreased risk of short-term mortality and use of mechanical ventilation after hospitalization for pneumonia.
Tbx2 Is Overexpressed and Plays an Important Role in Maintaining Proliferation and Suppression of Senescence in Melanomas
Authors: Keith W. Vance, Suzanne Carreira, Gerald Brosch, Colin R. Goding
Journal: Cancer Research (2005)

Abstract The INK4a and ARF genes found at the CDKN2A locus are key effectors of cellular senescence that is believed to act as a powerful anticancer mechanism. Accordingly, mutations in these genes are present in a wide variety of spontaneous human cancers and CDKN2A germ line mutations are found in familial melanoma. The TBX2 gene encoding a key developmental transcription factor is amplified in pancreatic cancer cell lines and preferentially amplified and overexpressed in BRCA1 and BRCA2 mutated breast tumors. Overexpression of Tbx2 and the related factor Tbx3, which is also overexpressed in breast cancer and melanomas, can suppress senescence in defined experimental systems through repression of ARF expression. However, it is not known how Tbx2 mediates its repressive effect nor whether endogenous Tbx2 or Tbx3 perform a similar antisenescence function in transformed cells. This is a particularly important question because the loss of CDKN2A in many human cancers would, in principle, bypass the requirement for Tbx2/3-mediated repression of ARF in suppressing senescence. We show here that Tbx2 is overexpressed in melanoma cell lines and that Tbx2 targets histone deacetylase 1 to the p21Cip1 (CDKN1A) initiator. Strikingly, expression of an inducible dominant-negative Tbx2 (dnTbx2) leads to displacement of histone deacetylase 1, up-regulation of p21Cip1 expression, and the induction of replicative senescence in CDKN2A-null B16 melanoma cells. In human melanoma cells, expression of dnTbx2 leads to severely reduced growth and induction of senescence-associated heterochromatin foci. The results suggest that the activity of endogenous Tbx2 is critically required to maintain proliferation and suppress senescence in melanomas.
Microbubble Persistence in the Microcirculation During Ischemia/Reperfusion and Inflammation Is Caused by Integrin- and Complement-Mediated Adherence to Activated Leukocytes
Authors: Jonathan R. Lindner, Matthew P. Coggins, Sanjiv Kaul, Alexander L. Klibanov, Gary H. Brandenburger, Klaus Ley
Journal: Circulation (2000)

Background —Albumin microbubbles that are used for contrast echocardiography persist within the myocardial microcirculation after ischemia/reperfusion (I-R). The mechanism responsible for this phenomenon is unknown. Methods and Results —Intravital microscopy of the microcirculation of exteriorized cremaster muscle was performed in 12 wild-type mice during intravenous injections of fluorescein-labeled microbubbles composed of albumin, anionic lipids, or cationic lipids. Injections were performed at baseline and after 30 to 90 minutes of I-R in 8 mice and 2 hours after intrascrotal tumor necrosis factor-α (TNF-α) in 4 mice. Microbubble adherence at baseline was uncommon (&lt;2/50 high-power fields). After I-R, adherence increased ( P &lt;0.05) to 9±5 and 5±4 per 50 high-power fields for albumin and anionic lipid microbubbles, respectively, due to their attachment to leukocytes adherent to the venular endothelium. TNF-α produced even greater microbubble binding, regardless of the microbubble shell composition. The degree of microbubble attachment correlated ( r =0.84 to 0.91) with the number of adhered leukocytes. Flow cytometry revealed that microbubbles preferentially attached to activated leukocytes. Albumin microbubble attachment was inhibited by blocking the leukocyte β 2 -integrin Mac-1, whereas lipid microbubble binding was inhibited when incubations were performed in complement-depleted or heat-inactivated serum rather than control serum. Conclusions —Microvascular attachment of albumin and lipid microbubbles in the setting of I-R and TNF-α–induced inflammation is due to their β 2 -integrin– and complement-mediated binding to activated leukocytes adherent to the venular wall. Thus, microbubble persistence on contrast ultrasonography may be useful for the detection and monitoring of leukocyte adhesion in inflammatory diseases.
Drug-induced lung disease: 1990 review
Authors: D Israel-Biet, S Labrune, GJ Huchon
Journal: European Respiratory Journal (1991)

Numerous drug-induced pulmonary manifestations have been reported but studies of their pathogenic mechanisms are still rare. These mechanisms should, however, be precisely determined in order to identify subjects at risk and to prevent some of these complications by the proper use of certain drugs in more appropriate conditions. The possibility of an iatrogenic manifestation should always be considered in patients developing pulmonary symptoms. Data from biological investigations, although not specific, contribute to the understanding of lung injury mechanisms.
Action and Toxicity of Cyclosporine
Authors: W M Bennett, D J Norman
Journal: Annual Review of Medicine (1986)

Cyclosporine is a potent new immunosuppressive agent that has proven particularly useful in organ transplantation. The unique action of the drug on T-cell immunity without myelosuppression is summarized. Cyclosporine pharmacology and adverse reactions, particularly nephrotoxicity, are reviewed in this paper.
Arterial wall and smooth muscle cell development in young Wistar rats and the effects of surgical denervation.
Authors: M E Todd, B Gowen
Journal: Circulation Research (1991)

Development of the muscular saphenous artery and the effect of surgical denervation on normal development was investigated in young rats at 3 and 6 weeks of age. During this interval, the weight and blood pressures (systolic, diastolic, and mean) of the animals increased significantly. The tunica media of the artery and the lumen increased significantly with age, but the proportion of smooth muscle cell to paracellular matrix did not alter. Computer-assisted three-dimensional reconstructions were used to investigate the smooth muscle cells. They increased significantly in length, volume, and angle of orientation within the vessel wall with age but maintained an approximate surface area-to-volume ratio. The cells in any one vessel tended to be oriented in either a clockwise or counterclockwise direction. The size of the nucleus also increased significantly in length and volume with age, but an approximate surface area-to-volume ratio and a constant nucleocytoplasmic ratio were maintained. The nuclei tended to be eccentrically located, with less than half of all nuclei wholly within the middle third of the cell. Surgical denervation at 10 days of age resulted in abnormalities of growth in vessel dimensions, thinner tunica media at 3 weeks (denervated 11 days previously), and smaller lumen at 6 weeks (denervated 32 days previously). Elevated amounts of paracellular matrix occurred in both age groups, but denervation did not alter smooth muscle cell size. In the 3-week-old animals, denervation resulted in smooth muscle cells with hypertrophied nuclei. This may account for the increase in growth of the tunica media between 3 and 6 weeks of age in the denervated artery.(ABSTRACT TRUNCATED AT 250 WORDS)