tbuckley/cabot-search huggingface dataset:
The Effect of Pantothenic Acid on Growth and Maintenance of Life in Mice of the C3H Strain
Authors: Harold P. Morris, Stuart W. Lippincott
Journal: JNCI Journal of the National Cancer Institute (1941)

Journal Article The Effect of Pantothenic Acid on Growth and Maintenance of Life in Mice of the C3H Strain Get access Harold P. Morris, Harold P. Morris senior nutrition chemist Search for other works by this author on: Oxford Academic PubMed Google Scholar Stuart W. Lippincott Stuart W. Lippincott research fellow National Cancer Institute, National Institute of Health, United States Public Health Service1 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 2, Issue 1, August 1941, Pages 29–38, https://doi.org/10.1093/jnci/2.1.29 Published: 01 August 1941
Dynamic Single-Cell Network Profiles in Acute Myelogenous Leukemia Are Associated with Patient Response to Standard Induction Therapy
Authors: Steven M. Kornblau, Mark D. Minden, David B. Rosen, Santosh Putta, Aileen Cohen, Todd Covey, David C. Spellmeyer, Wendy J. Fantl, Urte Gayko, Alessandra Cesano
Journal: Clinical Cancer Research (2010)

Abstract Purpose: Complete response to induction chemotherapy is observed in ∼60% of patients with newly diagnosed non-M3 acute myelogenous leukemia (AML). However, no methods exist to predict with high accuracy at the individual patient level the response to standard AML induction therapy. Experimental Design: We applied single-cell network profiling (SCNP) using flow cytometry, a tool that allows a comprehensive functional assessment of intracellular signaling pathways in heterogeneous tissues, to two training cohorts of AML samples (n = 34 and 88) to predict the likelihood of response to induction chemotherapy. Results: In the first study, univariate analysis identified multiple signaling “nodes” (readouts of modulated intracellular signaling proteins) that correlated with response (i.e., AUCROC ≥ 0.66; P ≤ 0.05) at a level greater than age. After accounting for age, similar findings were observed in the second study. For patients &amp;lt;60 years old, complete response was associated with the presence of intact apoptotic pathways. In patients ≥60 years old, nonresponse was associated with FLT3 ligand–mediated increase in phosphorylated Akt and phosphorylated extracellular signal-regulated kinase. Results were independent of cytogenetics, FLT3 mutational status, and diagnosis of secondary AML. Conclusions: These data emphasize the value of performing quantitative SCNP under modulated conditions as a basis for the development of tests highly predictive for response to induction chemotherapy. SCNP provides information distinct from other known prognostic factors such as age, secondary AML, cytogenetics, and molecular alterations and is potentially combinable with the latter to improve clinical decision making. Independent validation studies are warranted. Clin Cancer Res; 16(14); 3721–33. ©2010 AACR.
Eosinophilic fasciitis and myositis: use of imaging modalities for diagnosis and monitoring: Figure 1
Authors: F Dybowski, E Neuen-Jacob, J Braun
Journal: Annals of the Rheumatic Diseases (2008)

The basolateral amygdala (BLA) is obligatory for fear learning. This learning is linked to BLA excitatory projection neurons whose activity is regulated by complex networks of inhibitory interneurons, dominated by parvalbumin (PV)-expressing GABAergic neurons. The roles of these GABAergic interneurons in learning to fear and learning not to fear, activity profiles of these interneurons across the course of fear learning, and whether or how these change across the course of learning all remain poorly understood. Here, we used PV cell-type-specific recording and manipulation approaches in male transgenic PV-Cre rats during pavlovian fear conditioning to address these issues. We show that activity of BLA PV neurons during the moments of aversive reinforcement controls fear learning about aversive events, but activity during moments of nonreinforcement does not control fear extinction learning. Furthermore, we show expectation-modulation of BLA PV neurons during fear learning, with greater activity to an unexpected than expected aversive unconditioned stimulus (US). This expectation-modulation was specifically because of BLA PV neuron sensitivity to aversive prediction error. Finally, we show that BLA PV neuron function in fear learning is conserved across these variations in prediction error. We suggest that aversive prediction-error modulation of PV neurons could enable BLA fear-learning circuits to retain selectivity for specific sensory features of aversive USs despite variations in the strength of US inputs, thereby permitting the rapid updating of fear associations when these sensory features change. <b>SIGNIFICANCE STATEMENT</b> The capacity to learn about sources of danger in the environment is essential for survival. This learning depends on complex microcircuitries of inhibitory interneurons in the basolateral amygdala. Here, we show that parvalbumin-positive GABAergic interneurons in the rat basolateral amygdala are important for fear learning during moments of danger, but not for extinction learning during moments of safety, and that the activity of these neurons is modulated by expectation of danger. This may enable fear-learning circuits to retain selectivity for specific aversive events across variations in expectation, permitting the rapid updating of learning when aversive events change.
Clinical applicability of the EULAR Sjögren's syndrome disease activity index: a cumulative ESSDAI score adds in describing disease severity
Authors: Anna P Risselada, Aike A Kruize, Johannes W J Bijlsma
Journal: Annals of the Rheumatic Diseases (2012)

The European League Against Rheumatism (EULAR) Sjogren's task force proposed the EULAR Sjogren's syndrome disease activity index (ESSDAI) in 2010.1 This index scores the activity of primary Sjogren's syndrome (pSS) within 12 organ domains, intended for both clinical trials and daily practice. For the construction of the index, patients and vignettes with (highly) active systemic disease were used. No reports applying ESSDAI on a clinical cohort have been published yet. Our aim is to determine the applicability of ESSDAI as an activity index in clinical practice and we propose a cumulative ESSDAI score for describing disease severity.

We retrospectively analysed the medical charts of all patients with pSS according to the …
Complicated Grief, Depression, and Anxiety as Distinct Postloss Syndromes: A Confirmatory Factor Analysis Study
Authors: Paul A. Boelen, Jan van den Bout
Journal: American Journal of Psychiatry (2005)

OBJECTIVE: The authors used confirmatory factor analysis to replicate earlier findings that complicated grief, depression, and anxiety are distinct syndromes. METHOD: Data were derived from 1,321 bereaved individuals. Complicated grief was measured with the Inventory of Traumatic Grief. Depression and anxiety were measured with the SCL-90. RESULTS: A model in which symptoms of complicated grief, depression, and anxiety loaded on separate factors was superior to a one-factor model, revealed good model fit, and was invariant across subgroups. CONCLUSIONS: Previous findings of a distinction among complicated grief, depression, and anxiety were confirmed.
Factors Associated with Tuberculin Conversion in Canadian Microbiology and Pathology Workers
Authors: Dick Menzies, Anne Fanning, Lillian Yuan, J. Mark FitzGerald
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

The risk of occupational tuberculosis (TB) infection and associated factors was estimated among all microbiology and pathology technicians and compared with a sample of nonclinical personnel in 17 Canadian acute care hospitals. Participants underwent tuberculin skin testing and completed questionnaires. Prior skin tests and vaccinations and all patients with TB hospitalized in the preceding 3 years were reviewed. Of the work areas where direction of air flow and air changes per hour were measured, only 51% were adequately ventilated. Among participating lab workers the average annual risk of tuberculin conversion was 1.0%. This was associated with lower hourly air exchange rates (16.7 versus 32.5 in workers with no conversion, p < 0.001) work in pathology (adjusted odds ratio [OR]: 5.4; [95% confidence interval: 1.3, 22], higher proportion of patients with missed diagnosis in the first 24 hours (per 20% increase-OR: 2.0; [1.3, 3.2], treatment delayed 1 week or more (per 20% increase-OR: 2.0; [3.2, 3.2]), and higher mortality (per 20% increase-OR: 2.5; [1.1, 5.6]). We conclude that laboratory workers, with no direct patient contact, have increased risk of tuberculin conversion in hospitals where a greater proportion of patients with TB die, or have delayed, or missed diagnosis, although this may be modified by workplace ventilation.
Sodium channel β1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans
Authors: Hiroshi Watanabe, Tamara T. Koopmann, Solena Le Scouarnec, Tao Yang, Christiana R. Ingram, Jean-Jacques Schott, Sophie Demolombe, Vincent Probst, Frédéric Anselme, Denis Escande, Ans C.P. Wiesfeld, Arne Pfeufer, Stefan Kääb, H.-Erich Wichmann, Can Hasdemir, Yoshifusa Aizawa, Arthur A.M. Wilde, Dan M. Roden, Connie R. Bezzina
Journal: Journal of Clinical Investigation (2008)

Brugada syndrome is a genetic disease associated with sudden cardiac death that is characterized by ventricular fibrillation and right precordial ST segment elevation on ECG. Loss-of-function mutations in SCN5A, which encodes the predominant cardiac sodium channel alpha subunit NaV1.5, can cause Brugada syndrome and cardiac conduction disease. However, SCN5A mutations are not detected in the majority of patients with these syndromes, suggesting that other genes can cause or modify presentation of these disorders. Here, we investigated SCN1B, which encodes the function-modifying sodium channel beta1 subunit, in 282 probands with Brugada syndrome and in 44 patients with conduction disease, none of whom had SCN5A mutations. We identified 3 mutations segregating with arrhythmia in 3 kindreds. Two of these mutations were located in a newly described alternately processed transcript, beta1B. Both the canonical and alternately processed transcripts were expressed in the human heart and were expressed to a greater degree in Purkinje fibers than in heart muscle, consistent with the clinical presentation of conduction disease. Sodium current was lower when NaV1.5 was coexpressed with mutant beta1 or beta1B subunits than when it was coexpressed with WT subunits. These findings implicate SCN1B as a disease gene for human arrhythmia susceptibility.
Policy Options to Improve Discharge Planning and Reduce Rehospitalization
Authors: Vincent Mor
Journal: JAMA (2011)

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
A decision tree for genetic diagnosis of hereditary periodic fever in unselected patients
Authors: L Federici, C Rittore-Domingo, I Kone-Paut, C Jorgensen, M Rodiere, A Le Quellec, I Touitou
Journal: Annals of the Rheumatic Diseases (2006)

<b>Background:</b> The diagnostic value of molecular analysis of the familial Mediterranean fever (FMF) gene (Mediterranean fever (<i>MEFV</i>)) has been well established only in patients selected on the basis of ethnic background or clinical criteria. Genetic diagnosis for other hereditary periodic fever syndromes has been poorly evaluated. <b>Objective:</b> To determine the diagnostic contribution of genetic tests for hereditary periodic syndromes in a large, unselected series of patients. <b>Methods:</b> A retrospective study was conducted on 1941 patients referred to us for FMF genetic tests between 1997 and 2005. <i>MEFV</i> genotypes were compared with clinical data to appraise criteria for FMF diagnosis. Genetic tests for tumour necrosis factor receptor-associated periodic syndrome (TRAPS), hyperimmunoglobulinaemia D syndrome (HIDS) and cryopyrin-associated periodic syndromes (CAPS) were also reviewed. <b>Results:</b> 71% of the 1574 patients with enough data had a clinical diagnosis of FMF according to the widely used Israeli criteria. Two MEFV mutations were found in only 409 patients of this subgroup (sensitivity = 37%) and in 15 (3.3%) of the patients with an improbable clinical diagnosis of FMF (specificity = 97%). Molecular diagnosis for alternate hereditary periodic syndromes was carried out in 456 of the patients having a non-conclusive FMF genetic test. A positive diagnosis was obtained in 31 of these patients (TRAPS (n = 19), HIDS (n = 4) and CAPS (n = 8)). <b>Conclusions:</b> First-line MEFV mutation screening in patients with clinically typical FMF may be appropriate only in particular areas. To optimise genetic diagnosis, we propose a decision tree, which, with the advice of an expert practitioner, could help redirect test indications towards non-FMF hereditary periodic syndromes.
A novel compound heterozygous mutation in Werner syndrome results in WRN transcript decay
Authors: F.B. Muller, A. Tsianakas, C. Kuwert, B.P. Korge, N. Hunzelmann
Journal: British Journal of Dermatology (2005)

Background Werner syndrome (WS) is a rare autosomal recessive progeroid disorder caused by mutations of the WRN gene encoding a protein of the RecQ-type family of DNA helicases. Objectives To develop a rapid and simple reverse transcription-polymerase chain reaction (RT-PCR) strategy for mutation analysis of the WRN gene, to identify pathogenic mutations in a German patient with WS and to determine the effects of the pathogenic mutations on WRN mRNA stability. Methods Allele-specific RT-PCR, semiquantitative RT-PCR, DNA sequencing. Results We describe a novel and rapid RT-PCR-based method for mutation analysis in WS and report a German patient with WS carrying a previously reported (1396delA) as well as a novel nonsense mutation (2334delAC) of the WRN gene. By semiquantitative RT-PCR analysis we demonstrate that this compound heterozygous genotype leads to WRN transcript decay. Conclusions In previous studies WS was primarily attributed to a loss of function of stable truncated WRN gene products. Our findings indicate that mutations can also lead to markedly decreased WRN transcript stability.
Upper Airway Anesthesia Reduces Phasic Genioglossus Activity During Sleep Apnea
Authors: RICHARD B. BERRY, MICHAEL I. McNELLIS, KERRI KOUCHI, RICHARD W. LIGHT
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

We hypothesize that stimulation of upper-airway mechanoreceptors during obstructive apnea augments upper airway muscle activity. If so, upper-airway anesthesia (UAA) should reduce mechanoreceptor output and therefore upper-airway muscle activity. To test this hypothesis, we studied the effect of UAA on the relationship between the phasic activity of the moving-time average (MTA) of the genioglossus electromyogram (EMG-GG) and the esophageal pressure deflection (DP) during obstructive apneas in non-rapid-eye-movement (NREM) sleep in a group of six men with severe sleep apnea. Before UAA, the phasic EMG-GG was linearly related to the deflections in esophageal pressure (DP) during the last three occluded breaths (both progressively increased). After UAA, the mean ratio of EMG-GG to DP decreased to 23% of the control value, from 0.17 +/- 0.04 to 0.04 +/- 0.01 (mean +/- SEM) arbitrary units/cm H2O (p < 0.05). The mean slope of the EMG-GG-versus-DP regression lines also decreased to 23% of the control value, from 0.22 +/- 0.03 to 0.05 +/- 0.01 arbitrary units/ cm H2O (p < 0.01). These findings suggest that stimulation of upper-airway mechanoreceptors during obstructive apnea in NREM sleep augments phasic genioglossus activity.
Diabetic Cardiomyopathy
Authors: Indu G. Poornima, Pratik Parikh, Richard P. Shannon
Journal: Circulation Research (2006)

Although diabetes is recognized as a potent and prevalent risk factor for ischemic heart disease, less is known as to whether diabetes causes an altered cardiac phenotype independent of coronary atherosclerosis. Left ventricular systolic and diastolic dysfunction, left ventricular hypertrophy, and alterations in the coronary microcirculation have all been observed, although not consistently, in diabetic cardiomyopathy and are not fully explained by the cellular effects of hyperglycemia alone. The recent recognition that diabetes involves more than abnormal glucose homeostasis provides important new opportunities to examine and understand the impact of complex metabolic disturbances on cardiac structure and function.
Right Ventricular Involvement in Diabetic Cardiomyopathy
Authors: Ralph L. Widya, Rutger W. van der Meer, Johannes W.A. Smit, Luuk J. Rijzewijk, Michaela Diamant, Jeroen J. Bax, Albert de Roos, Hildo J. Lamb
Journal: Diabetes Care (2012)

To compare magnetic resonance imaging-derived right ventricular (RV) dimensions and function between men with type 2 diabetes and healthy subjects, and to relate these parameters to left ventricular (LV) dimensions and function.RV and LV volumes and functions were assessed in 78 men with uncomplicated type 2 diabetes and 28 healthy men within the same range of age using magnetic resonance imaging. Steady-state free precession sequences were used to assess ventricular dimensions. Flow velocity mapping across the pulmonary valve and tricuspid valve was used to assess RV outflow and diastolic filling patterns, respectively. Univariate general linear models were used for statistical analyses.RV end-diastolic volume was significantly decreased in patients compared with healthy subjects after adjustment for BMI and pulse pressure (177 ± 28 mL vs. 197 ± 47 mL, P < 0.01). RV systolic function was impaired: peak ejection rate across the pulmonary valve was decreased (433 ± 54 mL/s vs. 463 ± 71 mL/s, P < 0.01) and pulmonary flow acceleration time was longer (124 ± 17 ms vs. 115 ± 25 ms, P < 0.05). Indexes of RV diastolic function were impaired: peak filling rate and peak deceleration gradient of the early filling phase were 315 ± 63 mL/s vs. 356 ± 90 mL/s (P < 0.01) and 2.3 ± 0.8 mL/s(2) × 10(-3) vs. 2.8 ± 0.8 mL/s(2) × 10(-3) (P < 0.01), respectively. All RV parameters were strongly associated with its corresponding LV parameter (P < 0.001).Diabetic cardiomyopathy affects the right ventricle, as demonstrated by RV remodeling and impaired systolic and diastolic functions in men with type 2 diabetes, in a similar manner as changes in LV dimensions and functions. These observations suggest that RV impairment might be a component of the diabetic cardiomyopathy phenotype.
Leser-Trélat syndrome in patients affected by six multiple metachronous primitive cancers
Authors: Giovanni Ponti, Gabriele Luppi, Lorena Losi, Alberto Giannetti, Stefania Seidenari
Journal: Journal of Hematology & Oncology (2010)

Leser-Trélat syndrome is characterized by the eruptive appearance of multiple seborrheic keratoses in association with underlying malignant disease. Usually, the sign of Leser-Trélat is associated with adenocarcinoma, most frequently of the colon, breast, or stomach, but also of the lung, kidney, liver, and pancreas. Herein, we present a case that we believe is the first report of the sign of Leser-Trélat in association with occult gastric adenocarcinoma and the anamnestic oncologic history of five other multiple primitive cancers. Epidermal growth factor receptor (EGFR) immunohistochemical expression analysis of multiple seborrheic keratoses revealed an intense membranous staining in the basal keratinocytes and in all the upper epidermal layers. Patients with the sign of Leser-Trélat should undergo a diagnostic screening programme for malignant disease along with patients with known Leser-Trélat syndrome who present with a recent acute and florid eruption of their seborrheic keratoses. We propose the importance of combining the molecular features of multiple seborrheic keratoses with EGFR immunohistochemistry analyses to determine the likelihood of Leser-Trélat syndrome and the consequent high risk of underlying multiple visceral malignancies.
Temporal Changes in mRNA Expression for Bikunin in the Kidneys of Rats during Calcium Oxalate Nephrolithiasis
Authors: SHIZUKA IIDA, AMMON B. PECK, JOANNE JOHNSON-TARDIEU, MANABU MORIYAMA, PATRICIA A. GLENTON, KAREN J. BYER, SAEED R. KHAN
Journal: Journal of the American Society of Nephrology (1999)

Abstract. Inter-α-inhibitor and other bikunin-containing proteins are synthesized in relatively large quantities by the liver. These proteins function as Kunitz-type serine protease inhibitors and appear capable of inhibiting calcium oxalate (CaOx) crystallization in vitro . Preliminary studies have shown that renal tubular epithelial cells synthesize bikunin in response to CaOx challenge. To examine this response in vivo , a sensitive reverse transcription-quantitative competitive template-PCR was developed to detect and quantify poly(A) + -tailed bikunin mRNA expression in kidney tissue from normal rats and rats developing CaOx nephrolithiasis after challenge with ethylene glycol. Bikunin mRNA expression in rat liver tissue was assessed as a positive control. The expression of bikunin mRNA in liver did not differ significantly between normal control rats and experimental rats with induced hyperoxaluria and renal CaOx crystallization. In contrast, there were significant temporal increases in the levels of bikunin mRNA expression in rat kidneys during CaOx nephrolithiasis after challenge with ethylene glycol. Urinary excretion of bikunin-containing proteins seemed to increase concomitantly. These findings indicate an association between the induction of hyperoxaluria/CaOx nephrolithiasis and the expression of the bikunin gene in rat kidneys.