tbuckley/cabot-search huggingface dataset:
Shared Decision Making
Authors: Mack Lipkin
Journal: JAMA Internal Medicine (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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
Defective phosphorylation and hyaluronate binding of CD44 with point mutations in the cytoplasmic domain.
Authors: E Puré, R L Camp, D Peritt, R A Panettieri, A L Lazaar, S Nayak
Journal: The Journal of Experimental Medicine (1995)

CD44 is a cell surface adhesion molecule that plays a role in leukocyte extravasation, leukopoiesis, T lymphocyte activation, and tumor metastasis. The principal known ligand for CD44 is the glycosaminoglycan hyaluronate, (HA), a major constituent of extracellular matrices. CD44 expression is required but is not sufficient to confer cellular adhesion to HA, suggesting that the adhesion function of the receptor is regulated. We recently demonstrated that CD44 in primary leukocytes is phosphorylated in a cell type- and activation state-dependent fashion. In this study we demonstrate that serines 325 and 327 within the cytoplasmic domain of CD44 are required for the constitutive phosphorylation of CD44 in T cells. Furthermore, we demonstrate that cells expressing mutated CD44 containing a serine to glycine substitution at position 325 or a serine to alanine substitution at amino acid 327 are defective in HA binding, CD44-mediated adhesion of T cells to smooth muscle cells, as well as ligand-induced receptor modulation. The effect of these mutations can be partially reversed by a monoclonal anti-CD44 antibody that enhances CD44-mediated HA binding.
Multicenter clinical validation of an on-line monitor of dialysis adequacy.
Authors: T A Depner, P R Keshaviah, J P Ebben, P F Emerson, A J Collins, K K Jindal, A R Nissenson, J M Lazarus, K Pu
Journal: Journal of the American Society of Nephrology (1996)

Quantitation of hemodialysis by measuring changes in blood solute concentration requires careful timing when taking the postdialysis blood sample to avoid errors from postdialysis rebound and from recirculation of blood through the access device. It also requires complex mathematical interpretation to account for solute disequilibrium in the patient. To circumvent these problems, hemodialysis can be quantified and its adequacy assessed by direct measurement of the urea removed in the dialysate. Because total dialysate collection is impractical, an automated method was developed for measuring dialysate urea-nitrogen concentrations at frequent intervals during treatment. A multicenter clinical trial of the dialysate monitoring device, the Biostat 1000 (Baxter Healthcare Corporation, McGaw Park, IL) was conducted to validate the measurements of urea removed, the delivered dialysis dose (Kt/V), and net protein catabolism (PCR). The results were compared with a total dialysate collection in each patient. During 29 dialyses in 29 patients from three centers, the paired analysis of urea removed, as estimated by the dialysate monitor compared with the total dialysate collection, showed no significant difference (14.7 +/- 4.7 g versus 14.8 +/- 5.1 g). Similarly, measurements of Kt/V and PCR showed no significant difference (1.30 +/- 0.18 versus 1.28 +/- 0.19, respectively, for Kt/V and 42.3 +/- 15.7 g/day versus 52.2 +/- 17.4 g/day for PCR). When blood-side measurements during the same dialyses were analyzed with a single-compartment, variable-volume model of urea kinetics, Kt/V was consistently overestimated (1.49 +/- 0.29/dialysis, P < 0.001), most likely because of failure to consider urea disequilibrium. Because urea disequilibrium is difficult to quantitate during each treatment, dialysate measurements have obvious advantages. The dialysate monitor eliminated errors from dialysate bacterial contamination, simplified dialysate measurements, and proved to be a reliable method for quantifying and assuring dialysis adequacy.
PREKALLIKREIN DEFICIENCY IN MAN
Authors: Kirk D. Wuepper
Journal: The Journal of Experimental Medicine (1973)

Blood plasma obtained from an individual with abnormal thromboplastin formation, due to deficiency of Fletcher factor, was fully corrected by 2% of normal, Hageman factor- or PTA-deficient plasma. It was also reconstituted by addition of highly purified human or rabbit prekallikrein. The plasma failed to generate kinin upon exposure to kaolin, a defect which was also corrected by addition of prekallikrein. Prekallikrein antigen was not detectable in this plasma. Fletcher factor-deficient plasma did not support the normal generation of PF/dil when dilute plasma was incubated in glass vessels and injected intracutaneously. Small quantities of Fletcher factor-deficient or Hageman factor-deficient plasma corrected the ability of the other to generate PF/dil. The formation of plasmin in dilute, acidified plasma incubated with kaolin was also abnormal in Fletcher factor-deficient plasma. Plasmin generation was normalized by addition of prekallikrein or small quantities of Hageman factor-deficient plasma. The data support the identity of Fletcher factor and prekallikrein.
Identifying areas and risk groups with localised<i>Mycobacterium tuberculosis</i>transmission in northern England from 2010 to 2012: spatiotemporal analysis incorporating highly discriminatory genotyping data
Authors: María Saavedra-Campos, William Welfare, Paul Cleary, Andrew Sails, Andy Burkitt, Daniel Hungerford, Ebere Okereke, Peter Acheson, Marko Petrovic
Journal: Thorax (2015)

Information on geographical variation in localised transmission of TB can inform targeting of disease control activities. The aim of this study was to estimate the proportion of TB attributable to localised transmission for the period 2010-2012 in northern England and to identify case characteristics associated with spatiotemporal-genotypical clusters.We combined genotyping data with spatiotemporal scan statistics to define an indicator of localised TB transmission and identified factors associated with localised TB transmission thus defined in a multivariable logistics regression model.The estimated proportion of TB cases in northern England attributable to localised transmission was 10% (95% CI 9% to 12%). Clustered cases (cases which were spatiotemporally clustered with others of identical genotype) were on average younger than non-clustered cases (mean age 34 years vs 43 years; p value <0.05). Being UK born (adjusted OR (aOR) 3.6, 95% CI 2.9 to 6.0), presenting with pulmonary disease (aOR 2.2, 95% CI 1.3 to 3.6) and history of homelessness (aOR 2.8, 95% CI 1.2 to 6.8) or incarceration (aOR 2.6, 95% CI 1.2 to 5.9) were independently associated with being part of a spatiotemporal-genotypical cluster in a multivariable model. Belonging to an ethnic group other than white or mixed/other was also significantly associated with localised transmission. We identified localised transmission in 103/1958 middle super output areas mostly in urban areas.Incorporating highly discriminatory genotyping data into spatiotemporal analysis of TB incidence is feasible as part of routine surveillance and can provide valuable information on groups at greater risk and areas with localised transmission of TB, which could be used to inform control measures, such as intensified contact tracing.
Impaired Contractile Performance of Cultured Rabbit Ventricular Myocytes After Adenoviral Gene Transfer of Na <sup>+</sup> -Ca <sup>2+</sup> Exchanger
Authors: Wolfgang Schillinger, Paul M. L. Janssen, Shahriyar Emami, Scott A. Henderson, Robert S. Ross, Nils Teucher, Oliver Zeitz, Kenneth D. Philipson, Jürgen Prestle, Gerd Hasenfuss
Journal: Circulation Research (2000)

Na(+)-Ca(2+) exchanger (NCX) gene expression is increased in the failing human heart. We investigated the hypothesis that upregulation of NCX can induce depressed contractile performance. Overexpression of NCX was achieved in isolated rabbit ventricular myocytes through adenoviral gene transfer (Ad-NCX). After 48 hours, immunoblots revealed a virus dose-dependent increase in NCX protein. Adenoviral beta-galactosidase transfection served as a control. The fractional shortening (FS) of electrically stimulated myocytes was analyzed. At 60 min(-1), FS was depressed by 15.6% in the Ad-NCX group (n=143) versus the control group (n=163, P:<0.05). Analysis of the shortening-frequency relationship showed a steady increase in FS in the control myocytes (n=26) from 0.027+/-0.002 at 30 min(-1) to 0. 037+/-0.002 at 120 min(-1) (P:<0.05 versus 30 min(-1)) and to 0. 040+/-0.002 at 180 min(-1) (P:<0.05 versus 30 min(-1)). Frequency potentiation of shortening was blunted in NCX-transfected myocytes (n=27). The FS was 0.024+/-0.002 at 30 min(-1), 0.029+/-0.002 at 120 min(-1) (P:<0.05 versus 30 min(-1), P:<0.05 versus control), and 0. 026+/-0.002 at 180 min(-1) (NS versus 30 min(-1), P:<0.05 versus control). Caffeine contractures, which indicate sarcoplasmic reticulum Ca(2+) load, were significantly reduced at 120 min(-1) in NCX-transfected cells. An analysis of postrest behavior showed a decay of FS with longer rest intervals in control cells. Rest decay was significantly higher in the Ad-NCX group; after 120 seconds of rest, FS was 78+/-4% in control and 65+/-3% in the Ad-NCX group (P:<0.05) relative to steady-state FS before rest (100%). In conclusion, the overexpression of NCX in rabbit cardiomyocytes results in the depression of contractile function. This supports the hypothesis that upregulation of NCX can result in systolic myocardial failure.
Diagnostic detection of Streptococcus pneumoniae PpmA in urine
Authors: M.d.M. García-Suárez, L.E. Cron, B. Suárez-Álvarez, R. Villaverde, I. González-Rodríguez, F. Vázquez, P.W.M. Hermans, F.J. Méndez
Journal: Clinical Microbiology and Infection (2009)
High Incidence of Type 2 Diabetes in Peroxisome Proliferator–Activated Receptor γ2 Pro12Ala Carriers Exposed to a High Chronic Intake of <i>Trans</i> Fatty Acids and Saturated Fatty Acids
Authors: Raul Eduardo Pisabarro, Carlos Sanguinetti, Mario Stoll, Daniel Prendez
Journal: Diabetes Care (2004)

One of the most frequent polymorphisms of peroxisome proliferator–activated receptor (PPAR)γ2 is the Ala allele. Its incidence in the expression of obesity, insulin resistance, and type 2 diabetes is controversial (1–4). Recently it was suggested (5) that a gene-nutrient interaction at the PPARγ locus exists. We hypothesized that when exposed to a chronic environment of high trans fatty acid (FA) and saturated FA (SFAs) intake and sedentary lifestyle, 12Ala carriers express more type 2 diabetes at lower BMI and age than subjects without the polymorphism. This could be due to some weakness in the defenses against the ectopic storage of triglycerides, particularly in myocytes and β-cells. The current study is aimed at examining these possible relationships.

This is a pilot study. We have included 56 subjects (40 women and 16 men), all of them Caucasian, who consecutively visited our metabolic department seeking care for overweight and obesity, but not all were overweight or obese. It was a population with a wide age range (21–62 years) …
Development of pseudointima and stenosis after transjugular intrahepatic portasystemic shunts: Characterization of cell phenotype and function
Authors: Arun J. Sanyal, Melissa J. Contos, Dorn Yager, Ya-nan Zhu, Amy Willey, Martin F. Graham
Journal: Hepatology (1998)

The clinical utility of transjugular intrahepatic portasystemic shunts (TIPS) is frequently complicated by the ingrowth of tissue into the stent lumen, causing stent stenosis. These studies were undertaken to define the cellular and matrix components of the pseudointima, define the phenotype and function of the mesenchymal cells in the pseudointima and maintain them in culture, and to study the differences between stenotic and nonstenosed stents. A total of 35 stents were evaluated. TIPS pseudointima were examined histologically, by immunohistochemistry and in situ hybridization to determine the cellular and connective tissue constituents. Mesenchymal cells were grown from tissue within the TIPS and around it, and their phenotype was studied and compared with control smooth muscle cells and fibroblasts. Masson’s trichrome staining of histological sections demonstrated that TIPS tissue was composed of collagen and palisades of mesenchymal cells and was lined by an endothelium. Immunostaining demonstrated strong and uniform α-smooth muscle staining in TIPS mesenchymal cells and peri-TIPS cells. Type I procollagen mRNA expression was demonstrated in mesenchymal cells in and around the stent by in situ hybridization. TIPS mesenchymal cells secreted less radiolabeled fibronectin, and far more type III, relative to type I, collagen compared with peri-TIPS cells. TIPS cells also expressed high levels of type III procollagen mRNA compared with peri-TIPS cells. There was no difference between stenotic stents and nonstenosed stents with respect to clinical features, time from stenting, gross morphology, histology, presence of bile fistulae, and cell phenotype. However, smooth muscle cells (SMC) from stenotic stents demonstrated both greater cell proliferation and collagen I and III secretion compared with those from nonstenosed stents. These data demonstrate that TIPS stenosis results from an accumulation of collagen and proliferation of SMC within the stent lumen.
Peripheral Neuropathy Induced by Microtubule-Stabilizing Agents
Authors: James J. Lee, Sandra M. Swain
Journal: Journal of Clinical Oncology (2006)

Microtubule-stabilizing agents (MTSAs), including the taxanes and epothilones, are effective chemotherapeutic agents for the treatment of many cancers. Neuropathy is a major adverse effect of MTSA-based chemotherapy, with severe peripheral neuropathy (grade 3 or 4) occurring in as many as 30% of patients treated with a MTSA. MTSA-induced neuropathy usually resolves gradually after cessation of the treatment. The most reliable method to accurately assess MTSA-induced neuropathy is by clinical evaluation, although additional techniques are being developed and evaluated. Among MTSA-induced neuropathy, the most extensively studied is that induced by taxanes; such a neuropathy usually presents as sensory neuropathy and is more common with paclitaxel than docetaxel. The incidence of MTSA-induced neuropathy seems to depend on the MTSA dose per treatment cycle, the schedule of treatment, and the duration of the infusion. Although there have been several small clinical trials with neuroprotective agents, early recognition and supportive care are the best approaches for prevention and management of MTSA-induced neuropathy. In the future, research should focus on elucidating the mechanism of MTSA-induced neuropathy, developing reliable in vivo and in vitro preclinical models to study MTSA-induced neuropathy, developing a more reliable grading system for MTSA-induced neuropathy, developing more reliable methods for evaluating MTSA-induced neuropathy, and evaluating the efficacy of potential neuroprotective agents in clinical trials.
Does the cannabinoid dronabinol reduce central pain in multiple sclerosis? Randomised double blind placebo controlled crossover trial
Authors: Kristina B Svendsen, Troels S Jensen, Flemming W Bach
Journal: BMJ (2004)

<h3>Abstract</h3> <b>Objective</b> To evaluate the effect of the oral synthetic δ-9-tetrahydrocannabinol dronabinol on central neuropathic pain in patients with multiple sclerosis. <b>Design</b> Randomised double blind placebo controlled crossovertrial. <b>Setting</b> Outpatient clinic, University Hospital of Aarhus, Denmark. <b>Participants</b> 24 patients aged between 23 and 55 years with multiple sclerosis and central pain. <b>Intervention</b> Orally administered dronabinol at a maximum doseof 10 mg daily or corresponding placebo for three weeks (15-21days), separated by a three week washout period. <b>Main outcome measure</b> Median spontaneous pain intensity (numericalrating scale) in the last week of treatment. <b>Results</b> Median spontaneous pain intensity was significantlylower during dronabinol treatment than during placebo treatment(4.0 (25th to 75th centiles 2.3 to 6.0) <i>v</i> 5.0 (4.0 to 6.4),P = 0.02), and median pain relief score (numerical rating scale)was higher (3.0 (0 to 6.7) <i>v&gt;</i> 0 (0 to 2.3), P = 0.035). Thenumber needed to treat for 50% pain relief was 3.5 (95% confidenceinterval 1.9 to 24.8). On the SF-36 quality of life scale, thetwo items bodily pain and mental health indicated benefits fromactive treatment compared with placebo. The number of patientswith adverse events was higher during active treatment, especiallyin the first week of treatment. The functional ability of themultiple sclerosis patients did not change. <b>Conclusions</b> Dronabinol has a modest but clinically relevantanalgesic effect on central pain in patients with multiple sclerosis.Adverse events, including dizziness, were more frequent withdronabinol than with placebo during the first week of treatment.
Spontaneous Rupture of the Tendon of Extensor Pollicis Longus as a Complication of Rheumatoid Arthritis
Authors: R. Harris
Journal: Annals of the Rheumatic Diseases (1951)

Numerous authors have recently stressed the frequent clinical evidence of tendon involvement in rheumatoid arthritis.Edstrom (1945) found evidence of " tendinitis ", or " peritendinitis ", in 48 per cent. of 391 cases of chronic rheumatic polyarthritis.The long flexors to the fingers were involved in 38 per cent. of his cases, and the extensors in 10 per cent.Kellgren and Ball (1950) analysed 100 of their own cases, and found tendon lesions present in 42, in 37 of which the long flexors of the fingers were affected.Other tendons described as clinically affected were the extensors of the fingers, the tendons around the ankle, and Achilles' tendon, but no mention was made of the extensor pollicis longus.Fifteen of their cases were explored, and the clinical findings confirmed at operation.They emphasized that in most cases of rheumatoid arthritis the tendon lesions were only one aspect of " a generalized process involving joints, muscles, and occasionally viscera ", but that in rare cases the tendon lesions may be the chief cause of disability.The disabilities described were snapping fingers (Helweg, 1924; Sperling, 1949, 1950; Kellgren and Ball, 1950), weakness of grip (Edstrom, 1945), and inability to clench the fist.No cases of rupture of tendon were quoted, nor was this described as a possible occurrence.Kersley (1948), in a short paper, described two cases of spontaneous muscle rupture occurring in rheumatoid arthritic subjects.No similar cases have been described elsewhere.In his first case, the muscle ruptured was in the calf (? gastrocnemius); in the second, multiple lesions were described.In addition to the rupture of the quadriceps, which appeared to be at the musculo-tendinous junction, there were spontaneous ruptures of the extensor apparatus of the fourth digit of the right hand, and the flexor digitorum profundus of the third digit of the left hand.The patient's description of the spontaneous rupture of the extensor digitorum was " a slight pain, like an electric shock, running up the forearm ".The site ofthese lesions was considered to be in the forearm, probably at the musculo- tendinous junction.Both these cases were males, one aged 56, the other 54.In the first case, a typical rheumatoid arthritis had been present for one and a half years, in the second the quadriceps rupture occurred two years after the onset of the disease, the extensor rupture a further one and a half years later.298
On the Mechanism of Inhibition in Fluid Reabsorption by the Renal Proximal Tubule of the Volume-Expanded Rat
Authors: Barry M. Brenner, Julia L. Troy, Terrance M. Daugharty, I. F. Ueki, D. P. Nicholas, C. F. Wong
Journal: Journal of Clinical Investigation (1971)

We undertook to determine the extent to which the inhibition in absolute proximal fluid reabsorption in response to expansion of extracellular volume with noncolloid-containing solutions is the result of concomitant reductions in postglomerular (efferent arteriolar) protein concentration. Selective elevation of efferent arteriolar oncotic pressure in volume-expanded rats (Ringer's 10% body weight) to levels slightly in excess of normal by microperfusion with 9-10% albumin-Ringer's solution nearly completely reversed the inhibition in absolute and fractional reabsorption in adjacent proximal tubules. In contrast, during similar microperfusion with a 6-7% albumin solution, no increase in proximal reabsorption was measured. We interpret these findings to indicate that the bulk of the inhibition in absolute proximal reabsorption in response to volume expansion with colloid-free solutions is causally mediated by the accompanying parallel decline in postglomerular vascular protein concentration.
EBV-Positive Gastric Adenocarcinomas: A Distinct Clinicopathologic Entity With a Low Frequency of Lymph Node Involvement
Authors: Josine van Beek, Axel zur Hausen, Elma Klein Kranenbarg, Cornelis J.H. van de Velde, Jaap M. Middeldorp, Adriaan J.C. van den Brule, Chris J.L.M. Meijer, Elisabeth Bloemena
Journal: Journal of Clinical Oncology (2004)

Epstein-Barr virus (EBV) is detected in a substantial subgroup of gastric adenocarcinomas worldwide. We have previously reported that these EBV-positive gastric carcinomas carry distinct genomic aberrations. In the present study, we analyzed a large cohort of EBV-positive and EBV-negative gastric adenocarcinomas for their clinicopathologic features to determine whether they constitute a different clinical entity.Using a validated polymerase chain reaction/enzyme immunoassay-based prescreening method in combination with EBER1/2-RNA in situ hybridization, EBV was detected in the tumor cells of 7.2% (n = 41) of the gastric carcinomas from the Dutch D1D2 trial (N = 566; mean follow-up, 9 years). EBV status was correlated with clinicopathologic features collected for the Dutch D1D2 trial.EBV-positive gastric carcinomas occurred significantly more frequently in males (P <.0001) and in younger patients (P =.012). Most were of the intestinal type according to the Laurén classification (P =.047) or tubular according to the WHO classification (P =.006) and located in the proximal part of the stomach (P <.0001). A significantly lower tumor-node-metastasis system-stage (P =.026) was observed in the patients with EBV-carrying carcinomas, which was solely explained by less lymph node (LN) involvement (P =.034) in these cases. In addition, a better prognosis, as reflected by a longer disease-free period (P =.04) and a significant better cancer-related survival (P =.02), was observed for these patients, which could be explained by less LN involvement, less residual disease, and younger patient age.EBV-carrying gastric adenocarcinomas are a distinct entity of carcinomas, characterized not only by unique genomic aberrations, but also by distinct clinicopathologic features associated with significantly better prognosis.