tbuckley/cabot-search huggingface dataset:
Dependence of forced vital capacity manoeuvre on time course of preceding inspiration in patients with restrictive lung disease
Authors: NG Koulouris, P Rapakoulias, A Rassidakis, J Dimitroulis, M Gaga, J Milic-Emili, J Jordanoglou
Journal: European Respiratory Journal (1997)

In normal subjects and patients with airway obstruction, flows during a forced vital capacity (FVC) manoeuvre are higher after a fast inspiration without an end-inspiratory pause (manoeuvre 1) as compared to a slow inspiration with an end-expiratory pause of approximately 5 s (manoeuvre 2). In this study, we investigated the influence of these manoeuvres on maximal expiratory volume-time and flow-volume curves in patients with restrictive lung disease. Eleven patients with restrictive lung disease were studied. Their average (+/-SD) lung function test results were: FVC=55+/-12% predicted value, forced expiratory volume in one second (FEV1) 52+/-20% pred, FEV1/FVC 85+/-6%, total lung capacity 55+/-8% pred, and carbon monoxide transfer factor 47+/-18% pred. The patients performed the two FVC manoeuvres in random order. We compared the ensuing spirograms and maximal expiratory flow-volume curves from which peak expiratory flow, FEV1, FEV1/FVC, maximal mid-expiratory flow, and maximal flows were computed. All spirometric indices were significantly higher with manoeuvre 1 than 2. Maximal expiratory flows at the same lung volume were also significantly higher with manoeuvre 1 than 2, in all patients. Routine spirometric indices, obtained during a forced vital capacity manoeuvre depend on the time course of the preceding inspiration in patients with restrictive lung disease. Therefore, the forced vital capacity manoeuvre should be standardized if used in clinical, epidemiological and research studies.
Behcet's disease in Iraqi patients.
Authors: Z S Al-Rawi, K E Sharquie, S J Khalifa, F M Al-Hadithi, J J Munir
Journal: Annals of the Rheumatic Diseases (1986)

The clinical features of 60 patients (45 male, 15 female) with Behçet9s disease (BD) are reported in this prospective study. Ninety seven per cent had mouth ulceration, 83% genital ulceration, 75% skin lesions, 48% ocular involvement, 48% synovitis, 17% thrombophlebitis, and 22% of the male patients had epidiymitis, while constitutional symptoms were reported by 63%. The arthritis was intermittent, self limiting, and non-destructive, involving large joints, mainly the knees and ankles. The pathergy test was positive in 37 of 52 patients with BD, and negative in all 120 healthy controls and in 20 healthy volunteers who possessed the HLA-B51 antigen. HLA-B51 was present in 32 of 52 (62%) patients with BD compared with 51 of 175 (29%) unrelated normal controls. Both the pathergy and HLA-B51 tests were negative in four of 52 patients with BD. Behçet9s disease is not uncommon in Iraq. Practising physicians, dermatologists, and ophthalmologists must be more aware of its existence.
Cutaneous granulocytic sarcoma (chloroma) presenting as the first sign of relapse following autologous bone marrow transplantation for acute myeloid leukaemia
Authors: D.W.S. HARRIS, L.S. OSTLERE, M.H.A. RUSTIN
Journal: British Journal of Dermatology (1992)

A 25-year-old man suffering from acute myeloid leukaemia developed a solitary lesion on the upper abdominal wall 6 months after receiving an autologous bone marrow transplant. The lesion was a chloroma and proved to be the only evidence of clinical relapse. This is the first reported case of this rare condition occurring following bone marrow transplantation.
Lung immunopathology in cases of sudden asthma death
Authors: JL Faul, VJ Tormey, C Leonard, CM Burke, J Farmer, SJ Horne, LW Poulter
Journal: European Respiratory Journal (1997)

The histopathology of airway inflammation in rare cases of sudden asphyxic asthma death (SAAD) is unclear. This study examines, for the first time, the relative disposition of lymphocyte and macrophage subsets and eosinophils in proximal and distal tissues of such cases. Multiple resection specimens from five cases of SAAD were studied. Tissue blocks were obtained at necroscopy and immediately frozen in liquid nitrogen within 18 hours of death (death occurring within 1 h of the onset of an unprovoked asphyxic asthma attack). After immunohistological staining, frozen sections underwent semi-quantitative analysis (cell counts per unit area) for T-cells, macrophages and eosinophils using computerized imaging systems. Subsets of T-cells and macrophages were estimated using double immunofluorescence techniques. Variability within samples, between samples and between cases was compared. These cases of fatal asthma showed infiltrates of T-cells, macrophages and eosinophils within peribronchial tissues. Distinct from stable asthma, a CD8+ T-cell dominance was found. A high proportion of eosinophils were activated (EG2+), whereas the relative proportion of antigen-presenting cells (RFD1+) did not seem to be abnormal, although numbers of these cells were high. These features were seen both in proximal and distal tissues. The variability of these parameters within an individual was 9.4-15.2%, however, the variability between individual cases was greater. Sudden asphyxic asthma is associated with inflammatory infiltrates both of proximal and distal lung tissues. In contrast to stable asthma, this infiltrate contains large numbers of CD8+ T-cells, suggesting distinct qualitative as well as quantitative characteristics in the immunopathology of sudden asthma death.
P494Ox-HDL Modulates the expression of lectin-like oxidized low density lipoprotein receptor 1 (LOX-1) expression and proinflammatory cytokines in human differentiated monocytes in atherosclerosis.
Authors: N Kaur
Journal: Cardiovascular Research (2014)

Introduction: Lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) is the main scavanger receptor for oxidized low density lipoprotein (OxLDL) and highly expressed in endothelial cells of atherosclerotic lesions, Its expression has also been found to be unregulated by the several inflammatory cytokines (such as TNF-α, IL-8) under oxidative stress and various pathological conditions, such as hyperlowdensity lipoproteinemia, dyslipidemia, hypertension, and diabetes. Methods: Isolated fractions of HDL were modified and expression profiling of LOX-1 and associated different inflammatory genes were studied both at mRNA and protein levels in PMA differentiated monocytes in presence and absence of both nHDL and Ox-HDL. The expression of NF-kappa B protein was studied by electrophoretic mobility shift assay under same conditions, futher the expression of cIAPs proteins was also studied in differentiated monocyte to develop the cross talk if any between expression of LOX-1 and inflammation during progression of atherosclerosis Results and conclusion: High density lipoprotein (HDL) possess anti-oxidative and anti-inflammatory characteristics , however under stressed pathological conditions HDL undergoes modification and become associated with inflammation and oxidative stress, HDL become dysfunctional and exhibit pro-inflammatory properties. In vitro, HDL can be modified by oxidation of lipid and protein moiety under the atherosclerotic conditions. Here we reported that, after modification due to oxidation , HDL lose their ability to inhibit the expression of LOX-1 expression which is induced by pro-inflammatory cytokines under pathological conditions in differentiated monocytes in addition, oxidatively modified HDL induce the higher expression of LOX-1 both at mRNA and protein levels. These studies were further confirmed by studying the expression of NF-kappa B transcription factor which modulates the function of various pro inflammatory genes including TNF-α and IL-8. Altogether these findings confirmed that oxidatively modified HDL possess a pro-atherogenic role and leads to the progression of atherosclerosis.
A STUDY OF THE OPERATIVE TREATMENT FOR LOSS OF NERVE SUBSTANCE IN PERIPHERAL NERVES.
Authors: G. Carl Huber
Journal: JAMA (1896)

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
Modulation of promiscuous T cell receptor recognition by mutagenesis of CDR2 residues.
Authors: J V Brawley, P Concannon
Journal: The Journal of Experimental Medicine (1996)

The T cell receptor (TCR) recognizes a ligand composed of a major histocompatibility complex (MHC) molecule and a peptide antigen. Prior studies of murine T cell clones have demonstrated that residues in the CDR3 region of TCR interact with amino acids in the peptide during MHC-restricted antigen recognition. However, the questions of whether direct TCR MHC contacts are made and where such contact sites might map in the TCR have not been resolved. In this study, we have taken advantage of the promiscuous recognition of a peptide from influenza virus (HA 307-319) by human T cell clones to map sites in the TCR that mediate differences in human leukocyte antigen-D related (HLA-DR) restriction in the presence of a common peptide antigen. Site-specific mutagenesis of cloned TCR genes and transfection into Jurkat cells were used to demonstrate that single amino acid substitutions in CDR2 of the TCR-alpha chain controlled whether a T cell was restricted by the product of a single DR allele (DR7) or would respond to the HA 307-319 peptide when presented by the products of one of several different DR alleles (DR1, DR4, DR5, or DR7). Because the relevant DR alleles are defined by polymorphism in the DR-beta chain, these results also suggest a rotational orientation for recognition in which TCR-alpha interacts with DR beta.
Targeting β-Cell Mass in Type 2 Diabetes: Promise and Limitations of New Drugs Based on Incretins
Authors: Marzieh Salehi, Benedikt A. Aulinger, David A. D'Alessio
Journal: Endocrine Reviews (2008)

Abstract Progressive insulin secretory defects, due to either functional abnormalities of the pancreatic β-cells or a reduction in β-cell mass, are the cornerstone of type 2 diabetes. Incretin-based drugs hold the potential to improve glucose tolerance by immediate favorable effect on β-cell physiology as well as by expanding or at least maintaining β-cell mass, which may delay the progression of the disease. Long-term studies in humans are needed to elaborate on these effects.
The liver X receptor agonist <scp>AZ876</scp> protects against pathological cardiac hypertrophy and fibrosis without lipogenic side effects
Authors: Megan V. Cannon, Hongjuan Yu, Wellington M. Candido, Martin M. Dokter, Eva‐Lotte Lindstedt, Herman H.W. Silljé, Wiek H. van Gilst, Rudolf A. de Boer
Journal: European Journal of Heart Failure (2015)
Specific glycosylation of alpha1-acid glycoprotein characterises patients with familial Mediterranean fever and obligatory carriers of MEFV
Authors: D C W Poland
Journal: Annals of the Rheumatic Diseases (2001)

<h3>BACKGROUND</h3> Familial Mediterranean fever (FMF) is a periodic febrile disorder, characterised by fever and serositis. The acute phase response during attacks of FMF results from the release of cytokines, which in turn induce increased expression and changed glycosylation of acute phase proteins. A recent study indicated that attacks in FMF are accompanied by a rise of plasma concentrations of serum amyloid A (SAA) and C reactive protein (CRP), which remain significantly raised during remission relative to healthy controls. Another study suggested that obligatory heterozygotes also display an inflammatory acute phase response. <h3>OBJECTIVE</h3> To determine the state of inflammation in homozygotic and heterozygotic MEFV genotypes. <h3>METHODS</h3> CRP and SAA were studied by enzyme linked immunosorbent assay (ELISA). The glycosylation of the acute phase protein, α<sub>1</sub>-acid glycoprotein (AGP), was visualised with crossed affinoimmunoelectrophoresis with concanavalin A as diantennary glycan-specific component and Aleuria aurantia lectin as fucose-specific affinity component. <h3>RESULTS</h3> FMF attacks were associated with an increase (p&lt;0.05) in the serum inflammation parameters CRP, SAA, and AGP. The glycosylation of AGP showed an increase (p&lt;0.05) in fucosylated AGP glycoforms, whereas the branching of the glycans remained unaffected. The glycosylation of AGP in the MEFV carrier group, compared with that in a healthy control group, was characterised by a significant increase (p&lt;0.05) in branching of the glycans, whereas the fucosylation remained unaffected. <h3>CONCLUSION</h3> The findings suggest an FMF-specific release of cytokines, resulting in a different glycosylation of AGP between a homozygotic and heterozygotic MEFV genotype.
Peter Kenneth Barnes
Authors: F. B. M. Barnes
Journal: BMJ (2013)

Shortly after starting anaesthesia training at Charing Cross Hospital, Peter Kenneth Barnes took a short service commission in the Royal Air Force, which included two years in Singapore. A research post at the Westminster Hospital followed until, in 1976, he became an assistant professor of anaesthesia at the University of California, San Francisco.

On his return he was appointed as a senior registrar to the Westminster Hospital but was rapidly promoted to senior lecturer to the Westminster Medical School in April 1978. He …
Acceptance of the different denominations for reflex sympathetic dystrophy
Authors: B Alvarez-Lario
Journal: Annals of the Rheumatic Diseases (2001)

<h3>OBJECTIVE</h3> To elucidate the real impact in the medical literature of the different denominations for reflex sympathetic dystrophy (RSD). <h3>METHODS</h3> A search was performed through the Medline database (WinSPIRS, SilverPlatter International, NS), from 1995 to 1999, including the following descriptors: RSD, complex regional pain syndrome (CRPS), CRPS type I, algodystrophy, Sudeck, shoulder-hand syndrome, transient osteoporosis, causalgia, and CRPS type II. <h3>RESULTS</h3> The descriptor RSD was detected in 576 references, algodystrophy in 54, transient osteoporosis in 42, CRPS type I in 24, Sudeck in 16, and shoulder-hand syndrome in 11. One hundred records were obtained for the descriptor causalgia and five for CRPS type II. The descriptor RSD was detected in the title of 262 references, algodystrophy in 29, transient osteoporosis in 29, CRPS type I in 15, Sudeck in 3, shoulder-hand syndrome in 5, causalgia in 17, and CRPS type II in 3 references. <h3>CONCLUSIONS</h3> The new CRPS terminology has not effectively replaced the old one. RSD and causalgia are the most used denominations.
Mandatory Reporting of Human Immunodeficiency Virus Testing Would Deter Blacks and Hispanics From Being Tested
Authors: E. James Fordyce
Journal: JAMA (1989)

To the Editor.—  In a recent letter by Kegeles et al, 1 the authors reported that people at risk (homosexuals) for acquired immunodeficiency syndrome would decline to take the antibody test if their identity was disclosed to public health officials. This reluctance to be tested because of fear of disclosure is not only true for men who have sex with men, but for other groups as well. A study of the knowledge, attitudes, and behaviors pertaining to acquired immunodeficiency syndrome of a predominantly black and Hispanic population attending inner-city sexually transmitted disease clinics in New York City was conducted in 1988. One of the questions asked was the respondent's likelihood of taking the human immunodeficiency virus—antibody test if the respondent's test results and name had to be reported to a public health official. Among 1047 black and Hispanic respondents, 22% (Table) responded that they would not elect to take the
All-trans retinoic acid modulates the retinoic acid receptor-alpha in promyelocytic cells.
Authors: C Chomienne, N Balitrand, P Ballerini, S Castaigne, H de Thé, L Degos
Journal: Journal of Clinical Investigation (1991)

We have recently demonstrated that all-trans retinoic acid (RA), the active metabolite of vitamin A, is an efficient alternative to chemotherapy in the treatment of acute promyelocytic leukemia (AML3). We have further shown that, in these AML3 cells, the gene of the retinoic acid receptor-alpha (RAR alpha) is translocated from chromosome 17 to chromosome 15, and fused to a new gene, PLM. This results in the expression of both normal and chimeric RAR alpha transcripts in AML3 cells. The PLM-RAR alpha protein may account for the impairment of differentiation and thus leukemogenesis, but not for the paradoxical efficacy of RA in these cells. In an attempt to elucidate RA's differentiative effect in AML3 patients, the present work examined the in vitro and in vivo modulation of the normal RAR alpha transcripts by all-trans RA in seven cases of AML3. In all samples, Northern blot analysis revealed a low expression of the two normal RAR alpha transcripts compared with other human myeloid leukemic cells. No modulation was observed after 4-8 d of in vivo therapy with all-trans RA 45 mg/m2 per d. In vitro incubation with all-trans RA, however, increased the level of expression of the normal RAR alpha transcripts in AML3 cells but not in other AML leukemic subtypes. This modulation of the two normal RAR alpha transcripts appeared to be an early and primary event of RA's differentiating effect. We therefore suggest that up-regulation of the normal RAR alpha gene expression by pharmacological concentrations of all-trans RA may restore the normal differentiation pathway in these cells.
Activation of glomerular mitogen-activated protein kinases in angiotensin II-mediated hypertension.
Authors: A Hamaguchi, S Kim, M Yano, S Yamanaka, H Iwao
Journal: Journal of the American Society of Nephrology (1998)

The in vivo signal transduction pathway, responsible for hypertension-induced glomerular injury, remains to be clarified. In this study, the effect of angiotensin II (Ang II)-induced hypertension was examined on glomerular mitogen activated protein kinases (MAPK), including extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK), and on glomerular transcription factors activator protein-1 (AP-1) and Sp 1. MAPK activities were determined by in-gel kinase assay. DNA binding activity of AP-1 and Sp 1 was determined by gel mobility shift assay. Continuous infusion of Ang II (1000 ng/kg per min, intravenously) to conscious rats rapidly increased BP, followed by the rapid and transient activation of glomerular p42 and p44 ERK and p46 and p55 JNK with the peak at 15 to 180 min. Glomerular AP-1 binding activity was increased 2.6-fold (P < 0.01) at 24 h after the start of Ang II infusion. Supershift analysis showed that the activated AP-1 complexes contained c-Fos and c-Jun proteins. On the other hand, glomerular Sp 1 DNA binding activity was not changed throughout 7 d of Ang II infusion. These results provided the first in vivo evidence that Ang II-induced hypertension causes the activation of glomerular ERK and JNK, leading to the activation of AP-1. Thus, ERK and JNK signaling cascades, via the activation of AP-1, may be implicated in the development of hypertension-induced glomerular injury.
The Interpretation of Skiagraphs
Authors: E. M. Little
Journal: BMJ (1899)

L Z109Names for these various devices seem for purposes of refer- ence necessary, and I would propose calling the following two postures aphelic (a&rb ci'Axi) positions.The first is to be done, according to severity and bodily vigour, once, twice, or even three times a-day, of course not nude, but divested of any even slightly stiff corset.The annexed photograph from the patipnt, depicted in Fir. 4 of
Pulmonary embolism risk stratification: where are we heading?
Authors: Luis Paiva, Sérgio Barra, Rui Providência
Journal: European Respiratory Journal (2013)

To the Editor :

We read with great interest the paper by Sanchez et al. [1], in which the authors suggested that biomarkers and echocardiography findings would provide additional prognostic information to traditional risk models, such as the pulmonary embolism severity index (PESI), in normotensive acute pulmonary embolism (PE) patients. Patients were assigned to low- (PESI I–II), intermediate- (PESI III–IV) and high-risk classes (PESI V) and further stratified according to right ventricle dysfunction markers (right ventricle/left ventricle ratio, and troponin and brain natriuretic peptide (BNP) levels). The authors reported that low-risk PESI patients without any right ventricle dysfunction markers had a significantly lower risk for adverse events than low-risk patients with abnormal right ventricle/left ventricle ratio, troponin and/or BNP levels. However, the same results were not found for the remaining PESI classes (intermediate and high risk).

Reliable risk stratification represents the cornerstone of PE management, which should be capable of recognising patients at high risk of death, who could receive specific therapeutic interventions, and those suitable for outpatient management, with important savings in healthcare costs. Although the PESI score has a proven high discriminative performance in the identification of low-risk patients, outperforming other validated PE risk models [2, 3], some authors have recently demonstrated that the 48-h recalculation of PESI can more accurately identify those eligible for outpatient management …
Impact of bacterial signaling molecules on the expression of Th2 and Th17 cells
Authors: Raphaël Prungnaud, Marc Kästle, Oliver Eickelberg, Tobias Stöger, Susanne Krauss-Etschmann
Journal: European Respiratory Journal (2014)

Introduction   Bacterial quorum sensing molecules (e.g. N-Acyl Homoserine Lactones (AHLs)) have been shown to influence the host9s adaptive immune response. Understanding the cross talk of AHLs with barrier organs and the immune system could e.g. enable strategies to reduce exacerbations in asthma. Since T helper cells (Th) 2 and 17 essentially participate in the etiology of atopic and non-atopic forms of asthma, we asked if AHLs affect Th cell function or activation which might improve the host9s health.   Methods   Naive CD4 +  T cells from spleens of Balb/c mice were differentiated to Th2 cells using IL-2/-4 or Th17 cells using IL-6/-23 and TGF β1, in a media containing anti-CD3/CD28/IFNγ antibodies. Differentiation was confirmed via qPCR for Gata3 and Rorc. Th2/17 cells were then cultivated for 72/96h with  P. aeruginosa9s  active AHLs (3-OC 12 -HSL, 3-OC 4 -HSL) or controls (C 12 -HSL, DMSO) at concentrations up to 100 µM. PMA/Ionomycin cell activation was used prior to flow cytometric analysis of intracellular IL-4/-17 expression.   Results   Our differentiation protocol yielded 10% Th2 and 15% Th17 cells respectively. No effect of AHLs on IL-4/-17 production was observed at any time point or concentration.   Conclusion   The lack of impact of AHLs on T cell cytokine production suggests a more complex model involving other immune response cells mediating the interaction. In fact, airborne bacteria encounter first alveolar macrophages (AM) and epithelial cells in the lungs. This may subsequently modulate T cell recruitment or function. Thus, in current experiments we focus on the effects of AHLs on AM polarization, and epithelial barrier function, including assays for transepithelial resistance and wound healing.