tbuckley/cabot-search huggingface dataset:
Coronary Artery Flow Velocity Is Related To Lumen Area and Regional Left Ventricular Mass
Authors: H. Vernon Anderson, Michael J. Stokes, Miltiadis Leon, Subhi A. Abu-Halawa, Yvonne Stuart, Richard L. Kirkeeide
Journal: Circulation (2000)

Coronary flow velocity varies widely between individuals, even at rest. Because of this variation, indices with less apparent deviation, such as the ratio of hyperemic to resting velocity (coronary flow reserve), have been more commonly studied. We tested the hypothesis that the flow continuity principle could be used to model resting coronary flow, and we examined the resulting velocity relationship.We studied coronary velocity in 59 patients using a Doppler wire to measure resting and hyperemic average peak velocities in the left anterior descending artery. Quantitative techniques were used to calculate lumen cross-sectional area and the lengths of all distal coronary branches. Branch lengths were used to estimate regional left ventricular mass. We then calculated the ratio of lumen area to regional mass (A/m). Regional perfusion was estimated from the double product of heart rate and systolic blood pressure. Resting velocity (V) varied inversely with A/m ratio [V=46.5/(A/m); r=0.68, P<0.001]. Disease in the left anterior descending artery was categorized as none or luminal irregularities only (n=22), mild (n=15), or moderate (n=22). The A/m ratio declined across these groups (8.7+/-4.0, 8.5+/-6.2, and 5. 6+/-3.0 mm(2)/100 g, respectively; P<0.04), and the resting average peak velocity increased (27+/-16, 33+/-11, and 37+/-20 cm/s, respectively; P=0.06).Resting coronary artery flow velocity is inversely related to the ratio of lumen area to regional left ventricular mass. Higher resting velocities are found when insufficient lumen size exists for the distal myocardial bed, as occurs with diffuse mild or moderate coronary atherosclerosis.
Expression of BLyS and its receptors in B-cell non-Hodgkin lymphoma: correlation with disease activity and patient outcome
Authors: Anne J. Novak, Deanna M. Grote, Mary Stenson, Steven C. Ziesmer, Thomas E. Witzig, Thomas M. Habermann, Brandon Harder, Kay M. Ristow, Richard J. Bram, Diane F. Jelinek, Jane A. Gross, Stephen M. Ansell
Journal: Blood (2004)
Role of Ia antigens in graft vs. host reactions. II. Molecular and functional analysis of T cell alloreactivity by the characterization of host Ia antigens on alloactivated donor T cells.
Authors: T L Delovitch, J F Harris, R Battistella, K Kaufman
Journal: The Journal of Experimental Medicine (1982)

Graft vs. host response (GVHR)-activated donor T cells bind to stimulatory host cell-derived Ia antigens. Radioimmune cell-binding assays demonstrate that activated donor T cells acquire both host I-A and I-E alloantigens on their surface. Approximately threefold to fivefold less I-E products than I-A products are transferred. Immunoprecipitation and one-dimensional and two-dimensional gel electrophoresis analyses show that radioiodinated alpha and beta polypeptide chains of both I-A and I-E-encoded host Ia molecules may be transferred in an apparently structurally unaltered form from host cells to donor cells. Biosynthetic studies indicate that [35S]methionine-labeled activated donor T cells do not synthesize Ia antigens of the donor haplotype. Functional analyses with fluorescence-activated cell sorter sorted donor T cell subpopulations show that donor T cells that bind host I-A antigens preferentially cooperate with nonimmune host B cells. Donor T cells that do not bind detectable amounts of host I-A antigens preferentially help nonimmune donor B cells. By contrast, donor T cells that either bind or do not bind host I-A antigens display no H-2-restricted interaction and help both donor and host immune B cells. These data reveal that the Ia antigen-binding specificity of distinct functional subpopulations of alloactivated donor T cells regulates their I-region-restricted (self or allo) helper activity for nonimmune B cells but not immune B cells. Furthermore, they suggest that T cell-macrophage and T cell-B cell collaboration is mediated by a complementary anti-Ia:Ia receptor:ligand type of interaction in which the receptor of a T cell binds to the ligand of an antigen-presenting macrophage and/or B cell.
Relation between dentition and dyspeptic disorders.
Authors: W Sircus, R J Prescott
Journal: BMJ (1985)

children raises the possibility of respiratory infection, as previously reported in man and birds.The oocvst is small enough to be carried by dust.Much of the inhaled dust (possibly in the form of dried poultry litter) is undoubtedly cleared from the tracheobronchial mucosa by the cilia.It is then swallowed and enters the gastrointestinal tract.Many families in Bangladesh keep their poultry and cattle within their premises.Cryptosporidium was recently detected in 140) of calves with diarrhoea and 1 " of calves without diarrhoea at a dairy farm in Bangladesh, as well as in 8-50() of their handlers with diarrhoea.Cryptosporidizum was not, however, found in healthy people.We are now carrying out more extensive studies.
A stratified model for health outcomes in ankylosing spondylitis
Authors: Pedro Machado, Robert Landewé, Jürgen Braun, Kay-Geert A Hermann, Xenofon Baraliakos, Daniel Baker, Ben Hsu, Désirée van der Heijde
Journal: Annals of the Rheumatic Diseases (2011)

Objective To investigate the relationships between several health outcomes in ankylosing spondylitis (AS). Methods Baseline pretreatment data from 214 patients with AS participating in the AS Study for the Evaluation of Recombinant Infliximab Therapy were analysed. Measures of health-related quality of life (HRQoL) and physical function were used as dependent variables in linear regression analysis. Associations between HRQoL (36-Item Short Form (SF-36)), physical function, clinical disease activity, spinal mobility, structural damage, MRI inflammation, disease duration, age, gender, body mass index and HLA-B27 were explored. Univariate associations were retested in multivariate models. The robustness of the models was evaluated by sensitivity analyses. Results The physical component of SF-36 was independently associated with measures of physical function and disease activity (adjusted R 2 (adjR 2 )=0.39–0.40). The mental component of SF-36 was independently associated with physical function (adjR 2 =0.07). Physical function was independently associated with measures of spinal mobility and disease activity (adjR 2 =0.39–0.45). Spinal mobility was hierarchically shown to be an intermediate variable between structural damage and physical function, while physical function was shown to be intermediate between spinal mobility and the physical component of SF-36. Conclusion According to the proposed stratified model for health outcomes in AS, HRQoL is determined by physical function and disease activity, physical function is determined by spinal mobility and disease activity, and spinal mobility is determined by structural damage and inflammation of the spine. As more is learnt about how to measure AS, knowledge about the disease improves and better decisions can be made on the assessment and treatment of this disease.
Response to Comment on: Kim et al. Prospective Study of Serum Adiponectin and Incident Metabolic Syndrome: The ARIRANG Study. Diabetes Care 2013;36:1547–1553
Authors: Jang-Young Kim, Song Vogue Ahn, Eliseo Guallar
Journal: Diabetes Care (2013)

We thank Dr. Kawada (1) for his comments in response to the ARIRANG study findings on the predictive ability of adiponectin for metabolic syndrome (2). Dr. Kawada raised concerns about the appropriateness of logistic regression because there was some variability in the follow-up times of study participants even though the follow-up period was relatively short (median 2.4 years, interquartile range 2.0–2.9 years). In response, we repeated the analyses using a Cox model with very similar results. The …
Letter by Shroff and Orlandi Regarding Article, “Randomized Trial of Atorvastatin for Reduction of Postoperative Atrial Fibrillation in Patients Undergoing Cardiac Surgery: Results of the ARMYDA-3 (Atorvastatin for Reduction of Myocardial Dysrhythmia After Cardiac Surgery) Study”
Authors: Gautam R. Shroff, Quirino G. Orlandi
Journal: Circulation (2007)
Phase III Randomized Trial Comparing Three Platinum-Based Doublets in Advanced Non–Small-Cell Lung Cancer
Authors: G.V. Scagliotti, F. De Marinis, M. Rinaldi, L. Crinò, C. Gridelli, S. Ricci, E. Matano, C. Boni, M. Marangolo, G. Failla, G. Altavilla, V. Adamo, A. Ceribelli, M. Clerici, F. Di Costanzo, L. Frontini, M. Tonato
Journal: Journal of Clinical Oncology (2002)

To evaluate whether two commonly used newer platinum-based regimens offer any advantage over vinorelbine-cisplatin (reference regimen) in response rate for patients with advanced non-small-cell lung cancer (NSCLC).Chemotherapy-naive patients were randomized to receive gemcitabine 1,250 mg/m(2) days 1 and 8 plus cisplatin 75 mg/m(2) day 2 every 21 days (GC arm), or paclitaxel 225 mg/m(2) (3-hour infusion) then carboplatin (area under the concentration-time curve of 6 mg/mL x min), both on day 1 every 21 days (PCb arm), or vinorelbine 25 mg/m(2)/wk for 12 weeks then every other week plus cisplatin 100 mg/m(2) day 1 every 28 days (VC arm).Six hundred twelve patients were randomized to treatment (205 GC, 204 PCb, and 203 VC). Overall response rates for the GC (30%) and PCb (32%) arms were not significantly different from that of the VC arm (30%). There were no differences in overall survival, time to disease progression, or time to treatment failure. Median survival for the GC, PCb, and VC groups was 9.8, 9.9, and 9.5 months, respectively. Neutropenia was significantly higher on the VC arm (GC 17% or PCb 35% v VC 43% of cycles, P <.001), as was thrombocytopenia on the GC arm (GC 16% v VC 0.1% of cycles, P <.001). Alopecia and peripheral neurotoxicity were most common on the PCb arm, as was nausea/vomiting on the VC arm (P <.05).Efficacy end points were not significantly different between experimental and reference arms, although toxicities showed differences. These findings suggest that chemotherapy in NSCLC has reached a therapeutic plateau.
VARIATIONS IN THE RESPONSES OF C57BL/10J AND A/J MICE TO SHEEP RED BLOOD CELLS
Authors: Donald M. Silver, Ian F. C. McKenzie, Henry J. Winn
Journal: The Journal of Experimental Medicine (1972)

In response to repeated injections of sheep red blood cells, C57BL/10J mice produce predominantly 19S antibody in increasingly higher amounts, while A/J mice initially produce 19S antibody and then switch to produce increasing 7S antibody titers. In an F(1) generation all mice responded like the C57BL/10J mice. Backcross data implied genetic control involving at least three loci.
Cetuximab administered once every second week to patients with metastatic colorectal cancer: a two-part pharmacokinetic/pharmacodynamic phase I dose-escalation study
Authors: J. Tabernero, F. Ciardiello, F. Rivera, E. Rodriguez-Braun, F.J. Ramos, E. Martinelli, M.E. Vega-Villegas, S. Roselló, S. Liebscher, O. Kisker, T. Macarulla, J. Baselga, A. Cervantes
Journal: Annals of Oncology (2009)
Association of &lt;emph type="ital"&gt;FKBP5&lt;/emph&gt; Polymorphisms and Childhood Abuse With Risk of Posttraumatic Stress Disorder Symptoms in Adults
Authors: Elisabeth B. Binder
Journal: JAMA (2008)

<h3>Context</h3>In addition to trauma exposure, other factors contribute to risk for development of posttraumatic stress disorder (PTSD) in adulthood. Both genetic and environmental factors are contributory, with child abuse providing significant risk liability.<h3>Objective</h3>To increase understanding of genetic and environmental risk factors as well as their interaction in the development of PTSD by gene × environment interactions of child abuse, level of non–child abuse trauma exposure, and genetic polymorphisms at the stress-related gene FKBP5.<h3>Design, Setting, and Participants</h3>A cross-sectional study examining genetic and psychological risk factors in 900 nonpsychiatric clinic patients (762 included for all genotype studies) with significant levels of childhood abuse as well as non–child abuse trauma using a verbally presented survey combined with single-nucleotide polymorphism (SNP) genotyping. Participants were primarily urban, low-income, black (&gt;95%) men and women seeking care in the general medical care and obstetrics-gynecology clinics of an urban public hospital in Atlanta, Georgia, between 2005 and 2007.<h3>Main Outcome Measures</h3>Severity of adult PTSD symptomatology, measured with the modified PTSD Symptom Scale, non–child abuse (primarily adult) trauma exposure and child abuse measured using the traumatic events inventory and 8 SNPs spanning the FKBP5 locus.<h3>Results</h3>Level of child abuse and non–child abuse trauma each separately predicted level of adult PTSD symptomatology (mean [SD], PTSD Symptom Scale for no child abuse, 8.03 [10.48] vs ≥2 types of abuse, 20.93 [14.32]; and for no non–child abuse trauma, 3.58 [6.27] vs ≥4 types, 16.74 [12.90]; P &lt; .001). Although FKBP5 SNPs did not directly predict PTSD symptom outcome or interact with level of non–child abuse trauma to predict PTSD symptom severity, 4 SNPs in the FKBP5 locus significantly interacted (rs9296158, rs3800373, rs1360780, and rs9470080; minimum P = .0004) with the severity of child abuse to predict level of adult PTSD symptoms after correcting for multiple testing. This gene × environment interaction remained significant when controlling for depression severity scores, age, sex, levels of non–child abuse trauma exposure, and genetic ancestry. This genetic interaction was also paralleled by FKBP5 genotype-dependent and PTSD-dependent effects on glucocorticoid receptor sensitivity, measured by the dexamethasone suppression test.<h3>Conclusions</h3>Four SNPs of the FKBP5 gene interacted with severity of child abuse as a predictor of adult PTSD symptoms. There were no main effects of the SNPs on PTSD symptoms and no significant genetic interactions with level of non–child abuse trauma as predictor of adult PTSD symptoms, suggesting a potential gene-childhood environment interaction for adult PTSD.
Regulation of gene expression by thyroid hormone.
Authors: H H Samuels, B M Forman, Z D Horowitz, Z S Ye
Journal: Journal of Clinical Investigation (1988)

The thyroid hormones (3,5,3',5'-tetraiodo-L-thyronine [L-T4]' and 3,5,3'triiodo-L-thyronine [L-T3]) have marked effects on the growth, development, and metabolic function of virtually all organ systems and tissues of human beings and other higher organisms (1-3).L-T4 was one of the first hormones to be isolated and its structure determined (4-6).Several decades later L-T3 was identified in the circulation (7-9).Although L-T3 is secreted by the thyroid gland, a significant amount is derived from peripheral conversion of L-T4 to L-T3 by 5'- deiodinases in various tissues (10).L-T3 is about 10-fold more active than L-T4 on a molar basis (3).Because of its higher intrinsic biologic activity, its conversion from L-T4 in various tissues, and its lower affinity for serum binding proteins, L-T3 plays a more dominant role than L-T4 in maintaining the normal euthyroid state (2).Because of the marked alterations in the rate of oxygen consumption identified in hypothyroid- ism and hyperthyroidism, initial studies on the mechanism of action ofthe thyroid hormones were focused on mitochondrial function.In vitro studies indicated that iodothyronines could alter the function of isolated mitochondria (1, 1 1).However, this occurred only at iodothyronine concentrations 100,000- fold higher than those found in the euthyroid state, and L-T3 was less active than L-T4 (1 1).In the 1960s Tata and co-workers showed that thyroid hormone administration increased the rate of RNA synthesis in rat liver suggesting that L-T3 and L-T4 might act by control- ling gene expression (12, 13).Research over the past decade using intact animals and cultured cells has provided compel- ling evidence that the thyroid hormones exert their effects in various cells and tissues by stimulating the accumulation of mRNAs which code for specific proteins.The following thy- roid hormone-dependent effects have been studied in detail: stimulation of growth hormone synthesis in the rat anterior pituitary in vivo ( 14); regulation of growth hormone gene ex- pression in cultured rat pituitary cell lines (15-24); stimulation
Cortisol Secretion in Patients With Type 2 Diabetes: Relationship With Chronic Complications
Authors: Iacopo Chiodini, Guido Adda, Paolo Beck-Peccoz, Emanuela Orsi, Bruno Ambrosi, Maura Arosio
Journal: Diabetes Care (2007)

Several papers focused on the possible link between cortisol secretion and physiological and pathological cerebral aging (1,2). The neurological (mainly limbic-hippocampal) degenerative modification during aging has been suggested to be responsible for a hyperactivity of hypothalamic-pituitary-adrenal (HPA) axis, and an age-related decrease of HPA sensitivity to cortisol feedback has been reported (2).

In our study (3 …
Oral Apixaban for the Treatment of Acute Venous Thromboembolism
Authors: Giancarlo Agnelli, Harry R. Buller, Alexander Cohen, Madelyn Curto, Alexander S. Gallus, Margot Johnson, Urszula Masiukiewicz, Raphael Pak, John Thompson, Gary E. Raskob, Jeffrey I. Weitz
Journal: New England Journal of Medicine (2013)

Apixaban, an oral factor Xa inhibitor administered in fixed doses, may simplify the treatment of venous thromboembolism.In this randomized, double-blind study, we compared apixaban (at a dose of 10 mg twice daily for 7 days, followed by 5 mg twice daily for 6 months) with conventional therapy (subcutaneous enoxaparin, followed by warfarin) in 5395 patients with acute venous thromboembolism. The primary efficacy outcome was recurrent symptomatic venous thromboembolism or death related to venous thromboembolism. The principal safety outcomes were major bleeding alone and major bleeding plus clinically relevant nonmajor bleeding.The primary efficacy outcome occurred in 59 of 2609 patients (2.3%) in the apixaban group, as compared with 71 of 2635 (2.7%) in the conventional-therapy group (relative risk, 0.84; 95% confidence interval [CI], 0.60 to 1.18; difference in risk [apixaban minus conventional therapy], -0.4 percentage points; 95% CI, -1.3 to 0.4). Apixaban was noninferior to conventional therapy (P<0.001) for predefined upper limits of the 95% confidence intervals for both relative risk (<1.80) and difference in risk (<3.5 percentage points). Major bleeding occurred in 0.6% of patients who received apixaban and in 1.8% of those who received conventional therapy (relative risk, 0.31; 95% CI, 0.17 to 0.55; P<0.001 for superiority). The composite outcome of major bleeding and clinically relevant nonmajor bleeding occurred in 4.3% of the patients in the apixaban group, as compared with 9.7% of those in the conventional-therapy group (relative risk, 0.44; 95% CI, 0.36 to 0.55; P<0.001). Rates of other adverse events were similar in the two groups.A fixed-dose regimen of apixaban alone was noninferior to conventional therapy for the treatment of acute venous thromboembolism and was associated with significantly less bleeding (Funded by Pfizer and Bristol-Myers Squibb; ClinicalTrials.gov number, NCT00643201).
Amyloid Imaging With Carbon 11–Labeled Pittsburgh Compound B for Traumatic Brain Injury
Authors: Young T. Hong, Tonny Veenith, Deborah Dewar, Joanne G. Outtrim, Vaithianadan Mani, Claire Williams, Sally Pimlott, Peter J. A. Hutchinson, Adriana Tavares, Roberto Canales, Chester A. Mathis, William E. Klunk, Franklin I. Aigbirhio, Jonathan P. Coles, Jean-Claude Baron, John D. Pickard, Tim D. Fryer, William Stewart, David K. Menon
Journal: JAMA Neurology (2013)

To image amyloid deposition in patients with traumatic brain injury (TBI) using carbon 11-labeled Pittsburgh Compound B ([11C]PiB) positron emission tomography (PET) and to validate these findings using tritium-labeled PiB ([3H]PiB) autoradiography and immunocytochemistry in autopsy-acquired tissue.In vivo PET at tertiary neuroscience referral center and ex vivo immunocytochemistry of autopsy-acquired brain tissue from a neuropathology archive. [11C]PiB PET was used to image amyloid deposition in 11 controls (median [range] age, 35 [24-60] years) and in 15 patients (median [range] age, 33 [21-50] years) between 1 and 361 days after a TBI. [3H]PiB autoradiography and immunocytochemistry for β-amyloid (Aβ) and β-amyloid precursor protein in brain tissue were obtained from separate cohorts of 16 patients (median [range] age, 46 [21-70] years) who died between 3 hours and 56 days after a TBI and 7 controls (median [range] age, 61 [29-71] years) who died of other causes.We quantified the [11C]PiB distribution volume ratio and standardized uptake value ratio in PET images. The distribution volume ratio and the standardized uptake value ratio were measured in cortical gray matter, white matter, and multiple cortical and white matter regions of interest, as well as in striatal and thalamic regions of interest. We examined [3H]PiB binding and Aβ and β-amyloid precursor protein immunocytochemistry in autopsy-acquired brain tissue.Compared with the controls, the patients with TBI showed significantly increased [11C]PiB distribution volume ratios in cortical gray matter and the striatum (corrected P < .05 for both), but not in the thalamus or white matter. Increases in [11C]PiB distribution volume ratios in patients with TBI were seen across most cortical subregions, were replicated using comparisons of standardized uptake value ratios, and could not be accounted for by methodological confounders. Autoradiography revealed [3H]PiB binding in neocortical gray matter, in regions where amyloid deposition was demonstrated by immunocytochemistry; white matter showed Aβ and β-amyloid precursor protein by immunocytochemistry, but no [3H]PiB binding. No plaque-associated amyloid immunoreactivity or [3H]PiB binding was seen in cerebellar gray matter in autopsy-acquired tissue from either controls or patients with TBI, although 1 sample of cerebellar tissue from a patient with TBI showed amyloid angiopathy in meningeal vessels.[11C]PiB shows increased binding following TBI. The specificity of this binding is supported by neocortical [3H]PiB binding in regions of amyloid deposition in the postmortem tissue of patients with TBI. [11C]PiB PET could be valuable in imaging amyloid deposition following TBI.
Inhibition of cyclic 3'-5'-guanosine monophosphate-specific phosphodiesterase selectively vasodilates the pulmonary circulation in chronically hypoxic rats.
Authors: A H Cohen, K Hanson, K Morris, B Fouty, I F McMurty, W Clarke, D M Rodman
Journal: Journal of Clinical Investigation (1996)

While it is known that nitric oxide (NO) is an important modulator of tone in the hypertensive pulmonary circulation, the roles of cyclic 3'-5'-guanosine monophosphate (cGMP) and cGMP-phosphodiesterase (PDE) are uncertain. We found that isolated lung perfusate levels of cGMP were over ninefold elevated in hypertensive vs. normotensive control rats. 98-100% of lung cGMP hydrolytic activity was cGMP-specific PDE5, with no significant decrease in PDE activity in hypertensive lungs, suggesting that the elevation in cGMP was due to accelerated production rather than reduced degradation. In pulmonary hypertensive rat lungs, in vitro, cGMP-PDE inhibition by E4021[1-(6-chloro-4-(3,4-methylbenzyl) amino-quinazolin-2-yl)piperdine-4-carboxylate], increased perfusate cGMP threefold, reduced hypoxic vasoconstriction by 58 +/- 2%, and reduced baseline pulmonary artery pressure by 37 +/- 5%. In conscious, pulmonary hypertensive rats, intravenous administration of E4021 reduced hypoxic vasoconstriction by 68 +/- 8%, pulmonary artery pressure by 12.6 +/- 3.7% and total pulmonary resistance by 13.1 +/- 6.4%, with no significant effect on cardiac output, systemic pressure, and resistance. Comparison of E4021 to inhaled nitric oxide demonstrated that cGMP-PDE inhibition was as selective and as effective as inhaled NO.