tbuckley/cabot-search huggingface dataset:
The Relationship of Serum Hexosamine, Globulins, and Antibodies to Experimental Amyloidosis1
Authors: Robert B. Giles, Evan Calkins
Journal: Journal of Clinical Investigation (1958)

Amyloid as a disease in human beings occurs not only de novo, but also secondary to a variety of chronic infectious diseases, to rheumatoid ar- thritis, and to multiple myeloma.These appar- ently unrelated diseases may, therefore, have some characteristics in common, as evidenced by their ability to produce amyloid.Knowledge of the specific biological alterations that are responsible for secondary amyloidosis may highlight certain factors common to these diverse primary diseases as well as aid in elucidating the basic physiological alterations responsible for the disease process of rheumatoid arthritis, which is complicated by a high incidence of amyloidosis.Secondary amyloidosis has been produced in experimental animals by numerous workers (1- 11).Whether the amyloid produced in experi- mental animals is identical in chemical structure and pathogenesis to the primary and secondary amyloid found in human beings has not been established.Though several workers have pointed out the frequency with which hyperglobulinemia occurs (2, 3, 7, 12, 13), others have demonstrated that alterations in blood lipoproteins (7) and ele- vation of the serum hexosamine (14) occur.On the basis of these observations it has been sug- gested that amyloid may be the product of an anti- gen-antibody precipitate (13, 15, 16) or the indi- rect result of other immunological reactions.
Gut Hormones and Related Concepts
Authors: Zachary T. Bloomgarden
Journal: Diabetes Care (2006)

This is the first in a series of articles on presentations at the American Diabetes Association’s 66th Scientific Sessions, Washington, D.C., 9–13 June 2006.

At a symposium at the 2006 American Diabetes Association (ADA) Scientific Sessions on the implications of taste perception, Robert F. Margolskee (New York, NY) discussed the molecular biology of taste. Multiple taste buds are contained within papillae of the tongue. Taste receptors are present in cells of the front, side, and posterior portion of the tongue, with different taste responses in different areas. The innervation of the taste buds involves the facial nerves and vagus. Each taste bud contains 50–100 taste receptor cells, specialized epithelial cells with neuron-like properties making contact with taste stimuli in the oral cavity, leading to activation of an intracellular cascade with subsequent neurotransmitter release. Two taste qualities, salty and sour, are mediated by microvilli in the superior portions of the taste receptor cells, with salty taste involving sodium-specific channels and sour taste involving a number of different mechanisms (either receptors or via blockade of apical potassium entry). The three other tastes are bitter, sweet, and umami (Japanese for “delicious,” the taste of monosodium glutamate), all mediated by G-protein receptors. Bitter taste receptors have 25–30 different structures coupled to a specific G-protein, while umami and sweet depend on a different family of taste receptors—T1R2 and T1R3 for sweet, and T1R1 and T1R3 (as well as other complex combinations) for the taste of glutamate. Both the sweet and umami receptors have large extracellular domains.

Sweet taste genetics have been studied in inbred mice strains to determine the saccharine taste locus, with some strains tasting and others not tasting this. In humans, similar studies allowed identification of loci on chromosome 1p38.33 with a candidate gene identified for T1R3, which was previously thought to be …
BRAIN DRAIN: EVALUATING THE IMPACT OF INCREASED COGNITIVE LOAD DURING SELF-PACED RUNNING PERFORMANCE
Authors: J McCarron, TL Hodgson, MF Smith
Journal: British Journal of Sports Medicine (2013)

The brain plays a central role in the control of a pacing strategy, yet the brain has a limited information processing capacity and energy supply (Harris et al . Neuron 2012;75:762–77). This study is the first to evaluate the impact of increasing the already required cognitive demands of self-pacing (Suzuki et al . NeuroImage 2004;23:1020–26) on 5 km running performance. Eleven participants (24±4 y; 178±6 cm; 75.0±7.2 kg; 53.1±2.7 ml·kg·min −1 ) ran, in a randomised order and on separate days, three 5 km trials on a self-paced treadmill. This included i) a baseline trial (CON), ii) a trial during a continuous Wisconsin Card Sorting Task (WCST 5 km ) and iii), a trial during a continuous Simplified Go/No-Go Task (SGNG 5 km ). Electromyographic measures (EMG) of the Vastus Lateralis, task effort awareness (TEA), physical-ratings of perceived exertion (P-RPE) and feeling scale (FS) were obtained every 0.5 km. Finishing times from CON (1706±273 s) to SGNG 5 km (1750±282 s) were not significantly increased (p=0.18), yet an increase was found from CON to WCST 5 km (1783±293 s; p&lt;0.01). EMG was reduced from CON to SGNG 5 km (p&lt;0.01) and from CON to WCST 5 km (p&lt;0.01). P-RPE was reduced from CON to WCST 5 km (p=0.049) and from SGNG 5 km to WCST 5 km (p&lt;0.01). TEA was reduced from CON to SGNG 5 km (p=0.03) and WCST 5 km (p&lt;0.01). FS during WCST 5 km was increased against CON (p&lt;0.01) and SGNG 5 km (p=0.04). Percentage correct responses were not significantly reduced during SGNG 5 km against a baseline SGNG (p=0.06), yet a reduction was found during WCST 5 km against a baseline WCST (p&lt;0.01). Increased cognitive load negatively affects pacing of a 5 km run suggesting a ‘draining’ effect occurs during the task. Brain areas associated with the WCST (prefrontal regions) may have a role in the implementation of pace regulation during self-paced running. This study provides a novel approach for future research investigating the role of the brain during endurance exercise performance.
Anoxia Is Necessary for Tumor Cell Toxicity Caused by a Low-Oxygen Environment
Authors: Ioanna Papandreou, Chaya Krishna, Fiona Kaper, Deli Cai, Amato J. Giaccia, Nicholas C. Denko
Journal: Cancer Research (2005)

Abstract Cells exposed to oxygen deprivation in vitro have been shown to reduce proliferation and/or engage in programmed cell death. There is considerable controversy in the literature as to the role of hypoxia-inducible factor-1 (HIF-1) and HIF-1 target genes in initiating these responses. We therefore examined the oxygen dependence and the role of the hypoxia-responsive transcription factor HIF-1 in making the cellular death decision. Oxygen concentrations as low as 0.5% did not alter the growth of HIF-1–proficient or HIF-1–deficient murine fibroblasts, or human tumor cells, despite the appropriate induction of HIF-1 target genes. Severe hypoxia (&amp;lt;0.01% oxygen) did induced apoptosis, resulting in decreased colony formation, chromatin condensation, DNA fragmentation, and caspase activation but also independent of HIF1α status. Transcriptional induction of HIF-1–dependent genes putatively involved in cell death like BNip3 and BNip3L was therefore disassociated from hypoxia-dependent toxicity. Likewise, forced overexpression of a nondegradable form of HIF-1α in several human tumor cell lines was not sufficient to induce apoptosis under normoxic conditions. Taken together, these findings indicate that additional molecular events are triggered by anoxia in a HIF-1–independent manner, and these changes are necessary for cell death observed in low-oxygen environments.
Maternal exposure to angiotensin converting enzyme inhibitors in the first trimester and risk of malformations in offspring: a retrospective cohort study
Authors: D.-K. Li, C. Yang, S. Andrade, V. Tavares, J. R. Ferber
Journal: BMJ (2011)

<b>Objective</b> To examine a reported association between use of angiotensin converting enzyme (ACE) inhibitors during the first trimester and risk of malformations in offspring. <b>Design</b> A population based, retrospective cohort study linking automated clinical and pharmacy databases including comprehensive electronic medical records. <b>Participants</b> Pregnant women and their live born offspring (465 754 mother-infant pairs) in the Kaiser Permanente Northern California region from 1995 to 2008. <b>Main outcome measure</b> Congenital malformation in live births. <b>Results</b> The prevalence of ACE inhibitor use in the first trimester only was 0.9/1000, and the use of other antihypertensive medications was 2.4/1000. After adjustment for maternal age, ethnicity, parity, and obesity, use of ACE inhibitors during the first trimester only seemed to be associated with increased risk of congenital heart defects in offspring compared with normal controls (those with neither hypertension nor use of any antihypertensives during pregnancy) (15/381 (3.9%) <i>v</i> 6232/400&nbsp;021 (1.6%) cases, odds ratio 1.54 (95% confidence interval 0.90 to 2.62)). A similar association was observed for use of other antihypertensives (28/1090 (2.6%) cases of congenital heart defects, odds ratio 1.52 (1.04 to 2.21)). However, compared with hypertension controls (those with a diagnosis of hypertension but without use of antihypertensives) (708/29 735 (2.4%) cases of congenital heart defects), neither use of ACE inhibitors or of other antihypertensives in the first trimester was associated with increased congenital heart defects risk (odds ratios 1.14 (0.65 to 1.98) and1.12 (0.76 to 1.64) respectively). <b>Conclusions</b> Maternal use of ACE inhibitors in the first trimester has a risk profile similar to the use of other antihypertensives regarding malformations in live born offspring. The apparent increased risk of malformations associated with use of ACE inhibitors (and other antihypertensives) in the first trimester is likely due to the underlying hypertension rather than the medications.
Bronchiolitis obliterans organizing pneumonia and rheumatoid arthritis
Authors: R J van Thiel, S van der Burg, A D Groote, G D Nossent, S H Wills
Journal: European Respiratory Journal (1991)

Bronchiolitis obliterans, with or without organizing pneumonia, can be a serious and life-threatening complication of rheumatoid arthritis. We describe a case of bronchiolitis obliterans organizing pneumonia in a patient who recently developed rheumatoid arthritis, presenting as a severe respiratory insufficiency. Diagnosis was made by means of open lung biopsy. Treatment with corticosteroids induced a quick response and substantial improvement of the respiratory symptoms. A simultaneous strong rise in titres of serological tests suggests a relationship between the bronchiolitis obliterans organizing pneumonia and the rheumatoid arthritis.
THE CONTROL OF INFECTIOUS DISEASES IN RAPIDLY MOBILIZED TROOPS
Authors: A. P. Hitchens
Journal: Annals of Internal Medicine (1941)

Article1 August 1941THE CONTROL OF INFECTIOUS DISEASES IN RAPIDLY MOBILIZED TROOPSA. P. HITCHENSA. P. HITCHENSSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-15-2-172 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAssembling men from widely different environments, into the close contacts of military mobilizations favors the accelerated spread of infectious diseases and the development of explosive outbreaks. This means that carefully planned procedures for blocking their spread must be weighed against the exigencies of the military emergency. Whenever it is possible, and to the greatest extent possible, we want to counteract the passage of infection from the carrier to the susceptible recruit.Zinsser1and others have suggested a scheme of "gradual mobilization" which would consist of regional aggregations of recruits in small groups of several hundred men in separate local camps...Bibliography1. ZINSSER H: On the medical control of mobilization, Mil. Surgeon, 1940, lxxxvii, 214-221. Google Scholar2. JORDANHALPERIN EPG: Tetanus toxoid for prophylaxis, War Medicine, 1941, i, 227-246. Google Scholar3. SIMMONS J: Immunization against infectious diseases in the United States Army, South. Med. Jr., 1941, xxxiv, 62-67. CrossrefGoogle Scholar4. Circular Letter No. 9, Office of the Surgeon General, War Department, February 12, 1941. Google Scholar5. Circular Letter No. 334.7-1, Office of the Surgeon General, War Department, January 27, 1941. Google Scholar6. WILDER RM: Nutrition planning for the national defense, War Medicine, 1941, i, 143-157. Google Scholar7. FLÜGGE C: Ueber Luft Infektion, Ztschr. f. Hyg. u. Infektionskr., 1897, xxv, 179. Google Scholar8. WELLSWELLS WFMW: Air-borne infections, Jr. Am. Med. Assoc., 1936, cvii, 1698-1703, 1805-1809. CrossrefGoogle Scholar9. Circular Letter, No. 334.7-1, Office of the Surgeon General, War Department, December 27, 1940. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Read at the Boston meeting of the American College of Physicians, April 24, 1941. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byImpact of infectious diseases on war 1 August 1941Volume 15, Issue 2Page: 172-177KeywordsArmed forcesCyclic adenosine monophosphateInfectious diseases ePublished: 1 December 2008 Issue Published: 1 August 1941 PDF downloadLoading ...
Early Parenteral Nutrition in Critical Illness
Authors: L. John Hoffer
Journal: JAMA (2013)

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
Supravalvar aortic stenosis syndrome with stenosis of all aortic arch branches.
Authors: I J Copperman, S Low
Journal: Thorax (1975)

A 9-year-old girl with the supravalvar aortic stenosis syndrome is presented. In addition to the classical features of the syndrome, namely supravalvar aortic stenosis, peripheral pulmonary stenosis, typical facies, and mental retardation, she was also found to have stenosis at the origin of all aortic arch main branches, a hitherto undescribed feature.
The role of the KCa3.1 channel in the regulation of airway mucus hypersecretion in asthma
Authors: Greer Arthur, Erol Gaillard, Peter Bradding
Journal: European Respiratory Journal (2014)

The Ca 2+ -activated potassium channel, K Ca 3.1, is implicated in the process of exocytic release of intracellular granules from secretory cells such as human lung mast cells (HLMCs). MUC5AC is a human mucin that is upregulated in asthmatic human airways, and is hypothesised to be released from secretory human bronchial epithelial cells (HBECs) via exocytosis of intracellular granules. The aim was to investigate whether K Ca 3.1 plays a role in MUC5AC synthesis and secretion from HBECs. Expression of MUC5AC and K Ca 3.1 was investigated in primary HBEC cultures using quantitative RT-PCR and western blotting, and in bronchial biopsies using immunohistochemistry. K Ca 3.1 activity was examined using patch clamp electrophysiology. K Ca 3.1 mRNA expression was similar in submerged asthmatic and healthy HBECs, and protein expression was evident in western blots. MUC5AC and K Ca 3.1 immunoreactivity were demonstrated in the bronchial epithelium in severe, moderate and mild asthmatics, and in healthy controls. MUC5AC and K Ca 3.1 immunostaining co-localised in approximately 50% of cells. Severe asthmatic bronchial epithelium displayed higher levels of K Ca 3.1 (P = 0.001) and MUC5AC (P = 0.018) immunostaining. Asthmatic HBECs exhibited larger K Ca 3.1 currents than healthy HBECs (P = 0.023). Co-localisation of MUC5AC with K Ca 3.1 immunostaining suggests that mucus-secreting airway epithelial cells express K Ca 3.1. These results demonstrate the potential for K Ca 3.1 to contribute to pathological mucus secretion in asthma.
S120 Hyperpolarised 3HE diffusion MRI and multiple breath inert gas washout in patients with asthma: Abstract S120 Table 1.
Authors: S Gonem, S Hardy, N Buhl, M Soares, R Costanza, P Gustafsson, CE Brightling, J Owers-Bradley, S Siddiqui
Journal: Thorax (2013)

<h3>Background</h3> Multiple breath inert gas washout (MBW) is a technique for detecting abnormal ventilation distribution in patients with asthma and other airway diseases. S<sub>cond</sub> and S<sub>acin</sub> are measures of convective-dependent inhomogeneity (CDI) and diffusion-convection-dependent inhomogeneity (DCDI) respectively. Hyperpolarised <sup>3</sup>He diffusion magnetic resonance imaging (<sup>3</sup>He-MRI) may be used to probe lung microstructure at a variety of length scales, with short timescale (14 ms) apparent diffusion coefficient (ADC) corresponding to diffusion within an alveolus or a single acinar airway, and long timescale (1.5s–6s) ADC corresponding to diffusion path lengths of up to 8mm. We aimed to determine the microstructural correlates of S<sub>cond</sub> and S<sub>acin</sub> in patients with asthma, using <sup>3</sup>He-MRI. <h3>Methods</h3> Twenty-nine patients with asthma underwent MBW using sulphur hexafluoride as the inert tracer gas, and the parameters S<sub>cond</sub> and S<sub>acin</sub> were calculated. <sup>3</sup>He-MRI was performed and the ADC was calculated at both short (14ms) and long (1.5s, 3s and 6s) timescales. <sup>3</sup>He-MRI data was also fitted to a previously reported geometrical model of the acinus (Yablonskiy DA <i><i>et al</i></i>, <i>J Appl Physiol</i>. 2009;107(4):1258–65), and estimates of the alveolar duct outer radius (R) and alveolar sleeve width (h) were derived. <h3>Results</h3> Correlations between MBW and <sup>3</sup>He-MRI parameters are shown in Table 1. The approximate length scales probed by short and long timescale ADC are also indicated for reference. Significant positive correlations were observed between S<sub>acin</sub> and ADC at 14ms, 1.5s and 3s, but not 6s. In a stepwise linear regression model, ADC at 1.5s was the only significant determinant of S<sub>acin</sub>, with a model R<sup>2</sup> of 0.334. S<sub>cond</sub> did not correlate significantly with any of the MRI parameters. Yablonskiy model estimates of alveolar sleeve width and alveolar duct outer radius did not correlate significantly with either S<sub>cond</sub> or S<sub>acin</sub>. <h3>Conclusion</h3> S<sub>acin</sub> in patients with asthma is associated with an elevated ADC at 1.5s, corresponding to length scales of the order of 4mm. This suggests that DCDI in asthma is associated with structural asymmetries at the level of the distal acinar airways and/or collateral ventilation between parallel intra-acinar airways.
Epigenetic Histone Modification and Cardiovascular Lineage Programming in Mouse Embryonic Stem Cells Exposed to Laminar Shear Stress
Authors: Barbara Illi, Alessandro Scopece, Simona Nanni, Antonella Farsetti, Liliana Morgante, Paolo Biglioli, Maurizio C. Capogrossi, Carlo Gaetano
Journal: Circulation Research (2005)

Experimental evidence indicates that shear stress (SS) exerts a morphogenetic function during cardiac development of mouse and zebrafish embryos. However, the molecular basis for this effect is still elusive. Our previous work described that in adult endothelial cells, SS regulates gene expression by inducing epigenetic modification of histones and activation of transcription complexes bearing acetyltransferase activity. In this study, we evaluated whether SS treatment could epigenetically modify histones and influence cell differentiation in mouse embryonic stem (ES) cells. Cells were exposed to a laminar SS of 10 dyne per cm 2 /s −1 , or kept in static conditions in the presence or absence of the histone deacetylase inhibitor trichostatin A (TSA). These experiments revealed that SS enhanced lysine acetylation of histone H3 at position 14 (K14), as well as serine phosphorylation at position 10 (S10) and lysine methylation at position 79 (K79), and cooperated with TSA, inducing acetylation of histone H4 and phosphoacetylation of S10 and K14 of histone H3. In addition, ES cells exposed to SS strongly activated transcription from the vascular endothelial growth factor (VEGF) receptor 2 promoter. This effect was paralleled by an early induction of cardiovascular markers, including smooth muscle actin, smooth muscle protein 22-α, platelet-endothelial cell adhesion molecule-1, VEGF receptor 2, myocyte enhancer factor-2C (MEF2C), and α-sarcomeric actin. In this condition, transcription factors MEF2C and Sma/MAD homolog protein 4 could be isolated from SS-treated ES cells complexed with the cAMP response element-binding protein acetyltransferase. These results provide molecular basis for the SS-dependent cardiovascular commitment of mouse ES cells and suggest that laminar flow may be successfully applied for the in vitro production of cardiovascular precursors.
Users of oestrogen replacement therapy have more knee cartilage than non-users
Authors: A E Wluka
Journal: Annals of the Rheumatic Diseases (2001)

<h3>BACKGROUND</h3> Osteoarthritis (OA) is increasingly prevalent in the years after menopause. Epidemiological data suggest that the use of oestrogen replacement therapy (ERT) may protect against knee OA. <h3>AIM</h3> To test the hypothesis that long term ERT (longer than five years) is associated with increased knee cartilage in postmenopausal women. <h3>METHODS</h3> The study involved 81 women (42 current users (⩾ five years) of ERT and 39 who had never used it). Articular cartilage volumes were determined by processing images acquired in the sagittal plane using a T1 weighted fat suppressed magnetic resonance sequence on an independent work station. <h3>RESULTS</h3> After bone size had been accounted for, ERT users had higher tibial cartilage volume than non-users. Total tibial cartilage volume was 7.7% (0.23 ml) greater in the group of ERT users (2.98 (0.47) ml; mean (SD)) than in the untreated group (2.75 (0.50) ml). The difference, after adjustment for the significant explanatory factors (years since menopause, body mass index, age at menopause, and smoking), between the ERT users and non-users increased from 0.23 ml to 0.30 ml (95% confidence interval 0.08 to 0.52, p=0.008). These differences persisted after exclusion of women with OA. <h3>CONCLUSIONS</h3> After adjustment for multiple confounders, women using long term ERT have more knee cartilage than controls. This may indicate that ERT prevents loss of knee articular cartilage.