tbuckley/cabot-search huggingface dataset:
Use of capillary blood for the evaluation of iron status
Authors: Yuying Lu, Sean R. Lynch, James D. Cook, Nishi Madan, William L. Bayer
Journal: American Journal of Hematology (1987)

Abstract The accuracy and precision of measurements of iron status made on the capillary blood from a single 75 × 1‐mm microhematocrit tube were evaluated in 301 normal volunteers. After recording the hematocrit value, a hematofluorometer was used to assay erythrocyte protoporphyrin directly on the packed red cell fraction. Values in the low normal range were 50‐100% higher than assays by an extraction technique in simultaneously collected venous blood. However, measurements in the iron deficient range were only 12 % greater. Plasma ferritin concentration was determined by using an enzyme‐linked immunoassay on 10‐μl plasma retrieved after measuring the hematocrit. Capillary values were approximately 7% higher than venous concentrations, the proportional difference being consistent throughout the measured range. When the individual measurements were combined to calculate the iron storage status of each individual, the frequency distribution of iron stores in 141 female volunteers between 18 and 36 years of age was approximately Gaussian and paralleled that calculated for women aged 18‐44 years in NHANES II. These studies demonstrate that iron status can be r'etermined accurately from the measurement of hematocrit, erythrocyte protoporphyrin, and ferritin on a single microhematocrit tube of capillary blood.
Sphingosine 1-Phosphate Transactivates the Platelet-Derived Growth Factor β Receptor and Epidermal Growth Factor Receptor in Vascular Smooth Muscle Cells
Authors: Tatsuo Tanimoto, Andreea O. Lungu, Bradford C. Berk
Journal: Circulation Research (2004)

Sphingosine 1-phosphate (S1P) is a bioactive lipid generated during vascular injury that regulates cell growth, differentiation, survival, and motility via endothelial differentiation gene (EDG) family G protein-coupled receptors. Although several G protein-coupled receptor ligands transactivate receptor tyrosine kinases, such as the epidermal growth factor receptor (EGFR), S1P-stimulated receptor tyrosine kinase transactivation has not been well studied. We show that platelet-derived growth factor beta receptor (PDGFbetaR) and EGFR are tyrosine phosphorylated in response to S1P in rat aortic vascular smooth muscle cells (VSMCs). S1P-stimulated transactivation of PDGFbetaR and EGFR was mediated via Gi-coupled EDG receptors. S1P-stimulated transactivation of EGFR and PDGFbetaR was dependent on Src, reactive oxygen species, and cholesterol-rich membranes. A phosphoinositide 3-kinase-Akt pathway was activated by S1P and blocked by AG1296 and AG1478. Activation of extracellular signal-regulated kinase (ERK) 1 and ERK2 pathway by S1P was blocked only by AG1478. In Chinese hamster ovary cells that expressed exogenous EDG-1, activation of Akt and ERK1/2 in response to S1P was observed and was enhanced by coexpression of PDGFbetaR or EGFR. S1P-mediated VSMC proliferation was shown to be secondary to transactivation, because it was suppressed by AG1296 and AG1478. These data establish S1P as an important stimulus for EGFR and PDGFbetaR activation in VSMCs that may have important implications for the vessel response to injury.
Anti-Interferon Auto-Antibodies in Autoimmune Polyendocrinopathy Syndrome Type 1
Authors: Michael Levin
Journal: PLoS Medicine (2006)

Autoimmunity is a common mechanism underlying many common human diseases. Although the mechanisms are not well understood, autoimmunity is thought to arise from a failure in self-tolerance, resulting in a sustained immunological attack by specific antibody, T cells, or both, directed against antigens within the target tissues or organs [ 1]. Many autoimmune disorders appear to have a genetic basis, but attempts to identify the human genes involved have had only limited success, probably because of the polygenic nature of most common autoimmune disorders, and because of the complexity of the immunological pathways involved [ 2]. 

Many of the most important clues as to the working of the human immune system have come from the study of patients with rare single gene defects. Autoimmune Polyendocrinopathy Syndrome Type 1 (APS-1) is a rare, recessively inherited disorder, which is more common in the Finnish, Sardinian, and Iranian Jewish populations than in the general population[ 3]. The disorder usually presents in early childhood, with chronic mucocutaneous candidiasis, and adrenal or para-thyroid failure. The clinical manifestations of the disorder are extremely variable and include diabetes, keratitis, chronic diarrhoea, alopecia, hepatitis, pernicious anaemia, and primary hypogonadism [ 4]. 

Immunologically, the disease is characterised by lymphocytic infiltration of the target organs and by the presence of auto-antibodies against a wide range of tissue-specific antigens [ 5, 6]. Mucocutaneous candidiasis occurs in all patients with APS-1, but the immunological basis of the failure to eliminate candida is not understood. In general, the defect in elimination of candida is not associated with defective handling of other pathogens, suggesting a candida-specific immune defect [ 7].
Abstract 3143: PKD as a downstream target for K-ras in pancreatic cancer
Authors: Peter Storz
Journal: Cancer Research (2010)

Abstract Growth factor and K-ras-induced generation of reactive oxygen species have important roles in mediating pancreatic ductal adenocarcinoma. Pancreatic cancer cells also express high levels of active transcription factor Nuclear Factor-κB (NF-κB), which is responsible for cell survival and resistance to chemotherapeutics. The serine/threonine kinase Protein Kinase D1 (PKD1) is a sensor for oxidative stress and protects cancer cells by inducing anti-apoptotic and anti-oxidant genes. Here we provide evidence that PKD1 is the means of how high NF-κB activity levels are achieved in pancreatic cancer cells. We also show the contribution of K-ras, which is upregulated in its activity in over 90% of PDAC (pancreatic ductal adenocarcinoma). We found that K-ras in pancreatic ductal HPDE cells increases PKD1 activity and that the depletion of the pancreatic ductal adenocarcinoma cell line Panc-1 from K-ras leads to decreased PKD1 activity and NF-κB activation. As a mechanism we found that K-ras mediates activation of PKD1 via Src and that these signaling events relay to high NF-κB levels. Our data reveal K-ras as an activator of PKD1 and show that both oncogenes, Src and K-ras cooperate to activate NF-κB in PDAC through PKD1. This suggests the K-ras/Src/PKD1/NF-κB pathway as a new potential drug target for pancreatic cancer. 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 3143.
Portrait of a Young Woman
Authors: M. Therese Southgate
Journal: JAMA (2007)

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 Journals 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 2024 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
Antihypertensive Medications and the Risk of Incident Type 2 Diabetes
Authors: Eric N. Taylor, Gary C. Curhan
Journal: Diabetes Care (2006)

We thank Gosmanov et al. (1) for their comments. As stated in our article (2) and the accompanying editorial (3), data on the specific use of ACE inhibitors were obtained only in the Nurses’ Health Study (NHS) I and data …
THE HISTOLOGICAL CHANGES IN NERVE CELLS DUE TO TOTAL TEMPORARY ANÆMIA OF THE CENTRAL NERVOUS SYSTEM
Authors: Liborio Gomez, F. H. Pike
Journal: The Journal of Experimental Medicine (1909)

With the return of the circulation, dilation of the pericellular lymph space and slight swelling of the cell body occurs, disappearing as recovery progresses. Chromatolysis, as evidenced by poor affinity for stains, clumping, diffuse staining, and breaking into dust-like particles, induced by anaemia, is not necessarily fatal. Death of the cell is not shown histologically when tissue is removed and fixed immediately after the experiment. Some time must elapse for the detection of the vacuolation, displacement of the nucleus and solution of the chromatic substance, indicative of profound changes. Neurones from different regions as well as neurones of the same region differ in degree of resistance to anaemia. The small pyramidal cells are the most susceptible, and then come the Purkinje cells, cells of the medulla oblongata, retina, cervical cord, lumbar cord, spinal ganglia and, most resistant of all, the sympathetic ganglion cells. Failure to resuscitate animals after anaemia of the central nervous system is probably due to the destruction of many of the cells of the vital centers (vaso-motor and respiratory) which do not have histological peculiarities by which they may be defined. Death, however, of a few cells of any center does not necessarily mean the total loss of function of that center, since the remaining cells may be sufficient to discharge the function of the center.
Missed GP appointments cost NHS money
Authors: L. Beecham
Journal: BMJ (1999)

An estimated £150m ($240m) worth of appointment time is lost each year because of the patients in the United Kingdom who fail to keep appointments with their GPs, according to a survey by the Doctor Patient Partnership (DPP).

The DPP, which was set up to encourage better communication between patients and healthcare professionals and promote the responsible use of NHS services, has launched its latest campaign, “Keep it or cancel it.” …
Variability of gluten intolerance in treated childhood coeliac disease.
Authors: B McNicholl, B Egan-Mitchell, P F Fottrell
Journal: Gut (1979)

Fifty children consecutively attending a clinic for coeliac disease co-operated in a trial; 10 found to have flat mucosa were excluded. Forty children of mean age 9.8 years, whose duodenal or jejunal mucosa had returned to normal or near normal appearance after a mean of 5.8 years on gluten-free diets, were put back on normal diets. In 37, mucosal occurred in a mean of 16.9 months (four to 74 months). Four of the 37 had serial biopsies, in which mucosal enzymes (particularly lactase) fell and interepithelial lymphocyte counts rose before the mucosal morphology was regarded as definitely 9coeliac9. Three children had normal mucosal appearance after 58 to 73 months on normal diets, one of whom showed temporary mucosal abnormalities, another having occasionally low enzymes, in both suggesting underlying gluten sensitivity. Lactase suppression and raised IEL counts appear to be sensitive indicators of gluten intolerance. In our experience, a diagnosis of coeliac disease based on severe mucosal damage and a satisfactory response to a gluten-free but milk-containing diet implies a very strong likelihood of permanent or prolonged gluten intolerance, but with a striking variability in its expression.
Help from unexpected sources
Authors: V. Shenolikar
Journal: BMJ (1997)

A year and a half ago my previously happy world came to an end. After finding out that my polycystric kidneys were failing, my surgeon husband walked out on me and our three sons. I was left alone, unemployed—I had given up my senior house officer post to look after my family—penniless, and absolutely terrified.

There seemed no future for me. Suicide was a definite option. I planned it in detail. A cocktail of opiate, intravenous induction agent, and muscle relaxant. Easy to get hold of as an anaesthetist. It was a comfortable way to leave it all behind me.

Help came from unexpected sources. Firstly, from my children. With their father effectively gone, I was all they had left. They were desperately worried about me, but showed tremendous courage during my many hospital visits. The nagging question of who would look after my boys in the event of my death kept me fighting on.

Secondly, I had help from the local hospital where we had both worked and where …
Abstract 1401: Transcription of angiogenin and ribonuclease 4 is regulated by RNA polymerase III elements and a CTCF-dependent intragenic chromatin loop
Authors: Jinghao Sheng, Chi Luo, Yuxiang Jiang, Philip W. Hinds, Zhengping Xu, Guo-fu Hu
Journal: Cancer Research (2014)

Abstract Angiogenin (ANG) and ribonuclease 4 (RNASE4), two members of the secreted and vertebrate-specific ribonuclease superfamily, play important roles in cancers and neurodegenerative diseases. The ANG and RNASE4 genes share the same promoters but their structure and regulation are unknown. We have characterized the promoters, defined the transcription start site, and identified a mechanism of transcription regulation that involves both RNA polymerase III (Pol III) elements and CCCTC-binding factor (CTCF) sites. We found that two Pol III elements within the promoter regulate ANG and RNASE4 expression in a position- and orientation-dependent manner. We also provide evidence for the presence of an intragenic chromatin loop between the two CTCF binding sites located in two introns flanking the ANG coding exon. We found that formation of this intragenic loop preferentially enhances ANG transcription. These results suggest a multilayer transcriptional regulation of ANG and RNASE4 gene locus. These data also add more direct evidence to the notion that Pol III elements are able to directly regulate Pol II gene transcription. Furthermore, our data indicate that a CTCF-dependent chromatin loop is able to differentially regulate transcription of genes that share the same promoters. Citation Format: Jinghao Sheng, Chi Luo, Yuxiang Jiang, Philip W. Hinds, Zhengping Xu, Guo-fu Hu. Transcription of angiogenin and ribonuclease 4 is regulated by RNA polymerase III elements and a CTCF-dependent intragenic chromatin loop. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1401. doi:10.1158/1538-7445.AM2014-1401
Sarcoidosis in an adult with cystic fibrosis.
Authors: S D Rettinger, E P Trulock, B Mackay, H S Auerbach
Journal: Thorax (1989)

Sarcoidosis in an adult patient with cystic fibrosis lung disease was diagnosed on the basis of pulmonary function and radiographic data. It should be considered in the differential diagnosis of new diffuse interstitial infiltrates or hilar adenopathy in a patient with cystic fibrosis; biopsy of lung, lymph node, or skin lesions and interleukin-2 receptor levels may help to obtain a diagnosis.
Atherosclerosis; mechanisms as a guide to prevention
Authors: Nancy E. Warner
Journal: JAMA (1963)

This excellent monograph is a concise and thorough review of the factors concerned in the genesis of atherosclerosis. In the introduction the author discusses his philosophy concerning the question of prevention of human atherosclerosis. Here he also states his purpose in surveying the current concepts of pathogenesis, namely, to afford his readers a better understanding of methods aimed at control of factors which accelerate the disease and at the prevention of its complications. In successive chapters the author deals with geographic distribution, pathogenesis, localization of atherosclerotic lesions, cholesterol metabolism and lipoproteins, biosynthesis of steroid hormones from cholesterol, and the role of hormones in lipid metabolism. Subsequently the identification of individuals susceptible to the disease, the role of heredity, smoking, exercise, and emotional stress in atherosclerosis, the hypocholesterolemic drugs, and finally diet are taken up in turn. The list of references appended to each chapter is extensive, enhancing the value of
EXPERIMENTS IN THE USE OF ALUMINIUM FOR ARTIFICIAL VITREOUS.
Authors: D. C. BRYANT
Journal: JAMA (1898)

Some two years ago, after experimenting with several other kinds of material for an artificial vitreous, I commenced the use of aluminium for this purpose, and so far have met with nothing but very satisfactory results in its use. In the beginning of my experiments a complete hollow ball was used, and the results were about the same as are secured by the use of the glass ball, that is, good results in a majority of cases, with an occasional case in which, sooner or later, the ball was extruded. The fact that this unfortunate result would occasionally occur, led me to try the experiment of using a frame instead of a complete ball, allowing the cavity to fill up with granulation tissue. These experiments were carried on with dogs, and proved fairly satisfactory, the failures, when they did occur, being due to infection, which is very difficult to avoid
Abstract 3230: Fenofibrate-mediated energy crisis and apoptotic cell death of glioblastoma
Authors: Anna M. Wilk, Katarzyna Urbanska, David Impastato, Krzysztof Reiss
Journal: Cancer Research (2012)

Abstract Glioblastomas are one of the most aggressive brain tumors which are characterized by rapid cell growth, infiltration of the Central Nervous System (CNS), and resistance to all known anticancer regiments. Therefore, the development of new more effective therapies against Glioblastoma is the major challenge for modern medicine. Fenofibrate, a drug widely utilized to lower lipid concentration in the blood, is one of the very promising anti-cancer treatments with low systemic toxicity. This potent agonist of PPARδ is thought to shift energy metabolism from glycolysis to fatty acid α-oxidation and, therefore, it may be toxic to glycolysis -dependent brain tumor cells (Warburg effect). While the toxicity to cancer cells appears to be clear, the precise mechanism/s of fenofibrate action against brain tumors seems to be much more complex and remains to be elucidated. To understand metabolic basis of the anti-cancer action of fenofibrate, we have analyzed extracellular acidification (ECAR) and oxygen consumption (OCR) using XF 24 Extracellular Flux Analyzer (Seahorse Bioscience), mitochondrial membrane potential as well as ATP level in different glioblastoma cell lines (LN229, U87MG, T98G). Surprisingly, we found that basal oxygen consumption (OCR) decreased significantly in Glioblastoma cells pretreated with fenofibrate, and the addition of metabolic toxins did not change their metabolic profile. Decreased oxygen consumption was due to the direct interaction of fenofibrate with complex I, a protein involved in the mitochondrial electron transport chain. We additionally found that, in parallel to the metabolic changes, fenofibrate triggers cell cycle arrest followed by apoptosis. The mechanisms involve a PPARδ-mediated effect, which leads to the energy crisis and apoptosis, as well as a PPARδ-independent pathway which results in FOXO3a nuclear translocation and activation of the proapoptotic protein Bim. Overall our data strongly support an anticancer action of fenofibrate by shifting the glycolitic-dependent cell metabolism to fatty acids α-oxidation with subsequent energy crisis and apoptotic cell death. 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 3230. doi:1538-7445.AM2012-3230
M12 EBUS- are two needles better than one?: Abstract M12 Table 1.
Authors: WA Khan, S Bailey, M Najib
Journal: Thorax (2013)

<h3>Introduction</h3> The introduction of endobronchial ultrasound has allowed visual sampling of nodes compared to the previous blind TBNA techniques. It was widely been used for patients with suspected lung. The purpose of our current study was to evaluate the usefulness of using a 2 needle technique compared to a single needle method in ebus sampling. The primary endpoint was to see the effect on the total number of biopsy passes, time between needle exchange and also total time taken to complete an ebus procedure. <h3>Method</h3> 20 patients with mediastinal and hilar lymphadenopathy or suspected lung cancer in our institution were included in this prospective study. EBUS-TBNA was performed in all cases. 10 procedures were used using a 2 needle technique and 10 procedures were performed with single needle. Two trained bronchoscopists with 2 trained nurses performing the needle exchange and on site cytopathologist were present at the bronchoscopy giving an instant preliminary diagnosis. Equal numbers of procedures were performed by each of the operators. <h3>Results</h3> EBUS-TBNA was successfully performed in all 20 patients recruited. In the single needle technique the average number biopsy passes performed was 3.8 per ebus with an average needle changeover delay of 2 minutes 21 seconds and an average ebus time of 27 minutes. The two needle technique showed a greater number biopsy passes of 4.4 per ebus with a significantly reduced changeover needle time delay of 18 seconds per changeover and a reduction in overall ebus time to 21 minutes per procedure. All the procedures were uneventful without complications. All sample were labelled adequate by the histocytopathologist. <h3>Conclusions</h3> Although the numbers performed in the study are small, there is enough evidence from our data to show a significant benefit in a 2 needle technique with a greater number of biopsy passes performed, reduced delay in needle changeover time and reduction in ebus procedure time. This is both beneficial to the patient with a reduced procedure time but also with a potential cost benefit if more procedures can be performed safely in a shorter time period.