tbuckley/cabot-search huggingface dataset:
RECENT PROGRESS AND PRESENT STATUS OF EXPERIMENAL RESEARCH IN CANCER
Authors: LEO LOEB
Journal: JAMA (1910)

Not uncommonly the criticism is heard that no progress has been made in our knowledge of cancer. I do not believe this statement to be correct and I fear that it may have a paralyzing effect on those who devote all or part of their efforts to this branch of pathology. I attribute this and similar other criticisms, in part at least, to a lack of contact between the theoretical and practical worker in the field of medicine, and I believe it to be due to a lack of knowledge of what has been accomplished in this field, and also to an underestimation of purely theoretical work on the part of the practical worker in medicine. In medicine not less than in physics and chemistry the most far-reaching advances in diagnosis and treatment follow as a natural result, in a certain sense as a by-product, of new theoretical knowledge and
MULTIPLE TUBERCULOUS BONE LESIONS COMPLICATING CHRONIC PULMONARY TUBERCULOSIS
Authors: JOSEPH ROSENBLATT
Journal: JAMA (1923)

My object in this paper is to place on record a rather unusual case of chronic pulmonary tuberculosis in an adult, with metastatic involvement of most of the ribs, the left clavicle, the frontal bone and the thyroid cartilage. While tuberculous involvement of the bones and joints as a complication of pulmonary tuberculosis is not so uncommon as some writers assert, it is extremely unusual to find such widespread involvement of the bones, especially in an adult. A search of the recent literature available did not disclose any record of a similar case. <h3>REPORT OF CASE</h3><h3>History.</h3> —J. H. C., a man, aged 28, a jeweler, admitted to the Rhode Island State Sanatorium, July 28, 1922, complained of slight cough and expectoration, moderate loss of weight and strength, and three painful swellings, one on the forehead, one in the lower part of the right midaxillary region, and one in the
Fat Cells and Insulin Resistance
Authors: Joan Stephenson
Journal: JAMA (2006)

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
Postinfarction Ventricular Septal Defect
Authors: PIETER M. BARNARD, JOHN H. KENNEDY
Journal: Circulation (1965)

A series of four patients who died following rupture of the ventricular septum due to myocardial infarction has been reported. One of these died of hemorrhage due to a defective clotting mechanism 8 hours after successful surgical repair. The 13 cases of surgical repair of postinfarction ventricular septal defect reported by other authors are reviewed. The time interval is important and preferably 3 to 6 months should elapse following myocardial infarction before surgery is undertaken. Surgery should be considered in every patient diagnosed as having an acute septal rupture following myocardial infarction who fails to respond to vigorous medical treatment.
Vaccinations against influenza and pneumococcus in children with diabetes: telephone questionnaire survey
Authors: P. Davies
Journal: BMJ (2004)

Since 1992, the Department of Health has encouraged people in certain at risk groups to have vaccinations against influenza and pneumococcus. 1 The vaccinations are recommended for patients with diabetes, heart disease, or chronic respiratory disease (including asthma), and all people older than 65.The campaign has no lower age limit; children are included by default.We investigated uptake of pneumococcus and influenza vaccine in all children with diabetes in our area.We also audited advice given about vaccination by consultants and paediatric diabetic nurse specialists in the hospitals in the region of the Eastern Deanery of the United Kingdom.
Hepatitis B virus S mutants in liver transplant recipients who were reinfected despite hepatitis B immune globulin prophylaxis
Authors: Marc G. Ghany, Brick Ayola, Federico G. Villamil, Robert G. Gish, Sergio Rojter, John M. Vierling, Anna S. Lok
Journal: Hepatology (1998)

Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. The aim of this study was to determine the prevalence of HBV S gene mutations in liver transplant recipients who developed recurrent hepatitis B despite HBIG prophylaxis, and to determine if these mutations can revert after withdrawal of HBIG. The entire S gene sequences in pre- and posttransplant sera from 20 patients who developed recurrent hepatitis B despite HBIG prophylaxis were compared. Ten (50%) patients had 18 amino acid substitutions involving the 'a' determinant in the posttransplant samples. These mutations were absent in 93% of the pretransplantation clones analyzed. There was a significant correlation between the development of mutations in the 'a' determinant region and the duration of HBIG therapy. Most of the mutations result in changes in predicted antigenicity of the S protein. During follow-up, mutations in 14 (78%) of 18 affected codons in the 'a' determinant region reverted back to the pretransplantation sequences; only 1 codon had a de novo change after the withdrawal of HBIG. Two control patients who did not receive HBIG had no change in the 'a' determinant in their posttransplantation samples. These data support the hypothesis that mutations in the S gene were induced or selected by immune pressure exerted by HBIG. HBV S mutants may play a role in HBV reinfection in liver transplant recipients who received HBIG prophylaxis.
F-18 Fluorodeoxyglucose Positron Emission Tomography-Positive Benign Adrenal Cortical Adenoma: Imaging Features and Pathologic Correlation
Authors: Sameet K Rao, Vicente J Caride, Ronald Ponn, Esthia Giakovis, Sin Hang Lee
Journal: Clinical Nuclear Medicine (2004)

Accurate characterization of adrenal lesions in lung cancer is essential in the staging of the disease. Computed tomography and magnetic resonance imaging as well as fluorodeoxyglucose–positron emission tomography (FDG-PET) imaging are used to differentiate adrenal metastases from benign adenomas. Although FDG-PET is highly accurate in this regard, benign adrenal cortical adenomas have been shown to accumulate FDG, although to a lesser degree. We present a patient with a history of lung cancer and FDG accumulation in a benign adenoma, probably reflecting areas of chronic inflammation also seen within the gland at pathology.
Abstract 5245: Regional analysis of DCE MR images to unravel tumor growth and response heterogeneity in SW-620 human colon adenocarcinoma xenografts
Authors: Vinod Kaimal, MaryAnne Meade, Michael Woolliscroft, Patrick McConville
Journal: Cancer Research (2010)

Abstract Introduction: Dynamic Contrast-Enhanced (DCE) MRI, a clinically relevant technique used to assess response to anti-angiogenic therapies, relies on imaging of a T1 modifying contrast agent to characterize vascular response by the dynamics of tracer exchange between the vessels and the interstitial space. The parameter Ktrans is a measure of the tumor vascular permeability, vascular surface area and blood flow, and is normally assessed as mean over the entire tumor volume. Generally, decreasing tumor mean Ktrans occurs after effective vascular targeting. However, localized tumor growth based necrosis/under-perfusion can also lower Ktrans, leading to uncoupling of the endpoint from the effect. Techniques that can overcome confounding effects of heterogeneity may improve Ktrans sensitivity and correlation with outcome. We applied a thresholding technique to Ktrans data to analyze regional Ktrans variations in subcutaneous SW-620 tumors treated with the vascular targeted agent, bevacizumab or vehicle. Materials and Methods: Female nu/nu mice were implanted with SW-620 tumor fragments on Day 0. On Day 14, mice were distributed into groups with matching tumor burden. DCE-MRI images were acquired 24 hours before treatment (vehicle or bevacizumab; IP; 5mg/kg; Q3Dx4), and one week after treatment. The data were fitted to a Tofts-Kermode kinetic model to generate Ktrans over the entire tumor volume. Thresholds we determined by pooling all the Ktransvalues from the pre-treatment DCE MRI scans. The Ktrans values for each image were distributed into low, mid and high Ktrans fractions and the percentage of voxels in each fraction was calculated. Results: Bevacusimab resulted in moderate tumor growth inhibition (T/C = 43% on Day 22). Tumor mean Ktrans one week post-treatment start did not correlate with this effect, with Ktrans (T/C) = 131%. Analysis of location of voxels in the low, mid and high Ktrans fractions in the pre-treatment images showed that lower Ktrans values were generally confined to the tumor core, while higher Ktrans values were generally confined to the tumor periphery. These regions presumably related to under-perfused (core) and well perfused (periphery) tissue. A comparison of the high Ktrans volume fractions one week post-treatment (treated vs control) showed a correlation with the growth based treatment effect (high Ktrans volume fraction (T/C) = 44%). Ktrans thresholding may therefore provide a means to increasing sensitivity to treatment-based vascular inhibition. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5245.
THE LOCALIZATION OF STREPTOCOCCUS VIRIDANS
Authors: H. K. Detweiler, H. B. Maitland
Journal: The Journal of Experimental Medicine (1918)

The results of our experiments do not substantiate in full the theory of the power of selective action of Streptococcus viridans. A few strains showed a remarkable constancy in location and type of lesion, but these strains were greatly in the minority. The location of the lesions in animals seemed to bear no relation to the origin of the organism or to the lesions produced by it in the patient from which the strain was obtained. Streptococcus viridans, regardless of site of origin in the patient, produced most lesions in the heart and joints.
Increased Red Blood Cell Distribution Width Is Associated With Greater Risk of All-Cause, Cardiovascular and Non-Cardiovascular Mortality in a Large Community-Based Cohort
Authors: Todd Perlstein
Journal: Circulation (2008)

Abstract 1253 Todd S Perlstein, Brigham and Women’s Hosp, Boston, MA; Jennifer Weuve, Harvard Sch of Public Health, Boston, MA; Marc A Pfeffer, Joshua A Beckman, Brigham and Women’s Hosp, Boston, MA Todd Perlstein, 2008 Finalist and Presenting Author
Website of the week: Childhood obesity
Authors: K. Abbasi
Journal: BMJ (2001)

One of the urban myths of parenting is that chubby children bloom into dumpy adults. There is evidence that childhood obesity is rising, perhaps dramatically. But Charlotte Wright and colleagues (pp 1280-4) infer from their cohort study that there is “no excess adult health risk [of disease] from childhood or teenage overweight.” Moreover, thin children are just as likely to be fat adults, with the thinnest having “the highest adult risk at every level of adult obesity.” This is welcome news for children fed up with hearing lectures about their eating habits and lack of exercise; less so for parents who like to set firm boundaries.

There is also ongoing debate about web pages coming with a health warning, but as a first step they could come with a date warning. Even the most accomplished search engines throw up stagnant or outdated links at the top of the list. KidSource Online is a “group of parents who want to make a positive and lasting difference in the lives of parents and children.” They warn that childhood obesity will persist throughout the life span (www.kidsource.com/kidsource/content2/obesity.html) and the best way to tackle it—and tackle it you must—is a programme of exercise, diet management, and behaviour modification. Shame that the page was last updated in April 2000 and the references date from the 1980s.

The pendulum swings the other way with the “intuitive eating” approach prescribed by Jane Hirschmann and Lela Zaphiropoulos (www.overcomingovereating.com/childhood.html). “Children must be in the driver's seat when it comes to their bodies and to their eating,” they argue. This involves “reconnecting” with feelings of hunger and eating that dominated the first months of life.

But don't despair, http://athealth.com, which aims to provide information and services for mental health practitioners and those they serve, links you to evidence from leading US medical publications (www.athealth.com/Consumer/newsletter/FPN_4_16.html#2). The United States department of agriculture offers similar avenues for educators and researchers (www.nal.usda.gov/fnic/pubs/bibs/topics/weight/childhoodobesity.html). Even so, neither site appears to have been updated since June 2000. The web might be alive, but much of it is already dead.
Effect ofLactobacillus supplementation with and without arginine on liver damage and bacterial translocation in an acute liver injury model in the rat
Authors: D Adawi, F B Kasravi, G Molin, B Jeppsson
Journal: Hepatology (1997)

In acute liver failure following hepatitis, toxic insults, or after major liver surgery, there is an increased bacterial translocation from the gut. This may explain some of the infectious complications seen in these conditions. To elucidate mechanisms and find possible preventive measures, we investigated the effect of rectal administration of arginine and probiotic bacteria (Lactobacillus spp.) on bacterial translocation and the extent of liver failure. Sprague–Dawley rats were used and five different Lactobacillus strains (Lb.) reuteri R2LC, Lb. rhamnosus DSM 6594 (= strain 271), Lb. plantarum DSM 9843 (= strain 299v), Lb. fermentum 8704:3 (= strain 245), and Lb. reuteri (= strain 108) were administered rectally once daily for 8 days with and without 2% arginine. Acute liver injury (ALI) was induced on the eighth day by intraperitoneal injection of D–galactosamine (1.1 g/kg body weight), and samples were collected after 24 and 48 hours. Bacterial translocation was evaluated by bacterial culture from portal and arterial blood, mesenteric lymph nodes, and liver tissue. Liver enzymes and bilirubin were evaluated in the serum. The bacterial load in the cecum and colon was determined and the liver histopathological changes were studied. There was no mortality at any time. The liver enzymes and bilirubin decreased in some of the groups supplemented with lactobacilli with and without arginine compared with the ALI control group. The incidence of bacterial translocation and the number of the translocated bacteria decreased significantly in some of the supplemented groups. Lb. plantarum + arginine administration significantly reduced the level of the released liver enzymes, hepatocellular necrosis and inflammatory cell infiltration, bacterial translocation, and the number of Enterobacteriaceae in the cecum and colon. Rectal administration of different Lactobacillus strains with and without arginine in an ALI model significantly modulates the extent of the liver failure and reduces bacterial translocation. Lb. plantarum DSM 9843 (= strain 299v) with or without arginine seemed superior to the other Lactobacillus strains. The beneficial effect of arginine administration alone indicates a possible role of nitric oxide and polyamines in this process, and the lactobacilli may execute their action via the same mechanisms or via bacterial antagonism and/or enhancement of systemic and intestinal mucosal immunity.
Antibodies to Neuronal Structures
Authors: Aaron I. Vinik, Dharshan Anandacoomaraswamy, Jagdeesh Ullal
Journal: Diabetes Care (2005)

Diabetic neuropathies are a group of clinical syndromes that affect distinct regions of the nervous system, singly or combined, and markedly affect quality of life (1) and activities of daily living and increase morbidity and mortality (2). Therapy directed at the basic pathogenesis is sorely needed. Neurologic complications occur equally in type 1 and type 2 diabetes and additionally in various forms of acquired diabetes (3). Diabetic neuropathies may be diffuse somatic and involve proximal or distal nerves, occur as focal mononeuritides, and involve the autonomic nervous system (4,5).

The pathogenesis of diabetic neuropathies is multifactorial. Hyperglycemia causes nerve damage by inducing the activation of the polyol, protein kinase C, and hexosamine pathways and the accumulation of advanced glycation end products. Hyperglycemia also induces oxidative stress by enhancement of mitochondrial respiration, redox alteration, and uncoupling proteins, which leads to elevated superoxide anions (6,7). Oxidative stress depletes nitric oxide within the peripheral nerves and endothelium of the microvasculature by reducing endothelial nitric oxide synthase, altering nerve perfusion (8). In addition, there is deficiency of or a poor response to neurotrophic factors (9). However, there is now increasing evidence to suggest that autoimmunity has a role to play in the development and progression of diabetic neuropathies.

Fifty years ago, Waksman and Adams (10) suggested an autoimmune etiology of peripheral neuropathy when they injected rabbits with neuronal components to produce what they called “allergic neuritis. ” To be able to implicate autoimmunity as a causative factor of neuropathy, there would have to be a clear association between the antibody and the disease; neuropathy would have to be induced by introduction or development of antibodies, and there would have to be reversal of the disease with removal or neutralization of the antibodies. Peripheral nerves are normally protected against the …
Long-Term Evaluation of Tetralogy Patients with Pulmonary Valvular Insufficiency Resulting from Outflow-Patch Correction Across the Pulmonic Annulus
Authors: ELLIS L. JONES, C. RICHARD CONTI, CATHERINE A. NEILL, VINCENT L. GOTT, ROBERT K. BRAWLEY, J. ALEX HALLER
Journal: Circulation (1973)

In the operative correction of tetralogy of Fallot with a severely narrowed right ventricular outflow tract, widening of the pulmonic annulus is frequently necessary to prevent a high residual pressure gradient and to reduce right ventricular pressure overload. This can be accomplished by incising the pulmonic annulus and inserting a patch graft across the valve, but this usually results in pulmonary valvular insufficiency. Of 426 patients who underwent total correction of Fallot's tetralogy between 1959 and 1970, 63 required a patch across the pulmonic annulus. The mortality rate for this group was 30.1%, compared with a total mortality among the 426 patients of 18%. The high mortality rate is influenced by the fact that the majority were corrected in the early years of the series. Fifteen patients were restudied by cardiac catheterization and cineangiography an average of 9.1 years after total correction. Twelve patients were asymptomatic and three patients had only mild symptoms on exertion in spite of angiographically significant pulmonic regurgitation. The average right ventricular systolic pressure was 40 mm Hg; right ventricular end-diastolic pressure was 7 mm Hg; and the right ventricular/pulmonary arterial peak systolic pressure gradient was 14.9 mm Hg. This experience suggests that after a more difficult immediate postoperative period, patients who have right ventricular outflow reconstruction with patches across the pulmonic ic annulus tolerate their chronic pulmonic regurgitation very well.
Abstract 2202: HMG box-containing protein 1 (HBP1) is a direct target of transcription factor FOXO1 in invasive oral cancer
Authors: I-Tai Chou, Chien-Yi Chan, Ming-Fen Lee, Chun-Yin Huang
Journal: Cancer Research (2012)

Abstract Constitutively activated PI3K/Akt signaling with deregulated activity of FOXO factors is often associated with tumorigenesis. Reduced HBP1 expression and/or loss-of-function HBP1 mutants have been observed in several types of cancer. FOXO1 and HBP1 seem to share common biological roles such as cell growth inhibition. We have previously demonstrated that, in oral cancer, reduced HBP1 expression expedited cell proliferation, growth, and migration, while the role of FOXO1 remains unclear. Hence, the objective of the current study is to investigate the reciprocal roles of FOXO1 and HBP1 in oral cancer. In a subset of oral tumor specimen, we found that both FOXO1 and HBP1 expression levels were significantly lower than those of the control tissues. In addition, FOXO1 expression was positively correlated with that of HBP1, and the status of low FOXO1 and HBP1 was associated with invasiveness of oral tumor, indicating a coordinated down-regulation of FOXO1 and HBP1 in invasive oral cancer. To further examine if HBP1 is a transcriptional target of FOXO1, we searched for putative binding sites within a 2-kb HBP1 promoter region, and identified two FOXO1 consensus sites, located −177 to −184 bp and −388 to −395 bp, from the transcription start site. As shown by reporter analysis and in vivo chromatin IP assay, these cis-acting elements and trans-acting FOXO1 factors, with functional DNA-binding domains, were necessary for complete activation. Furthermore, suppression of FOXO1 led to a reduction of HBP1 expression. In a reciprocal manner, FOXO1-mediated inhibition of colony formation, cell growth, and invasion was disrupted upon HBP1 knockdown in invasive oral cancer cells. Taken together, our data provide the significant findings that HBP1 is a novel downstream target of FOXO1 and that the FOXO1-HBP1 pathway might be a prospective means of intervention in invasive oral cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2202. doi:1538-7445.AM2012-2202
Unusual Appearance of Hyperintense Hemangiomata on Tc-99m Colloid SPECT/CT
Authors: Rajan Rakheja, Stephan Probst, Robert Lisbona
Journal: Clinical Nuclear Medicine (2010)

A 44-year-old woman was investigated for hepatic steatosis, and underwent Xe-133 and Tc-99m colloid SPECT/CT. The colloid scan demonstrated 2 unexpected foci of hyperaccumulation corresponding to 2 CT-diagnosed hemangiomata. Further evaluation with Tc-99m RBC blood pool SPECT/CT confirmed these 2 lesions as intensely increased on delayed images, confirming hemangiomata. Hemangiomata are the most common benign mesenchymal hepatic tumors, and almost invariably present as defects on nuclear colloidal imaging.1–3,8 This case serves to illustrate that hemangiomata can rarely be hyperintense on colloid imaging.7 It is possible that the Xe-133 confirmed hepatic steatosis was a confounding factor in this patient.