tbuckley/cabot-search huggingface dataset:
Antibody response to core, envelope and nonstructural hepatitis C virus antigens: Comparison of immunocompetent and immunosuppressed patients
Authors: Anna S. F. Lok, David Chien, Qui-Lim Choo, Tak-Mao Chan, Edmond K. W. Chiu, Ignatius K. P. Cheng, Michael Houghton, George Kuo
Journal: Hepatology (1993)

Some immunosuppressed patients with hepatitis C virus infection do not have detectable levels of antibody to hepatitis C virus on second-generation enzyme immunoassay. Antibodies to the envelope and nonstructural region 5 proteins have not been examined. Four groups of patients with hepatitis C virus infection were studied: (a) 20 immunocompetent patients, (b) 15 hemodialysis patients, (c) 17 kidney transplant recipients and (d) 3 acute leukemia patients who underwent bone marrow transplantation. Serum samples were tested for antibody to hepatitis C virus with a second-generation enzyme immunoassay and multi-antigen enzyme immunoassays and for hepatitis C virus RNA with a nested polymerase chain reaction assay. All the immunocompetent patients reacted to C25, C22 and C33C; 90% reacted to nonstructural region 5 antigen and 80% reacted to C100-3. Only 55% reacted against yeast-derived e1 and e2 antigens, but all reacted against vaccinia virus--expressed N e1 and e2 antigens, indicating that the envelope epitopes are conformational and glycosylated. Sixty-five percent to 90% of dialysis and kidney transplant patients reacted to C25, C22 and N e1 and e2, but only 12% to 60% reacted to C100-3, C33C and nonstructural region 5 antigen. Diminution or loss of reactivity to hepatitis C virus antigens was observed after kidney and bone marrow transplantation, with C25 and N e1 and e2 less affected. Our data suggest that incorporation of C25 and N e1 and e2 antigens in the assay for antibody to hepatitis C virus would improve the detection of hepatitis C virus infection in immunosuppressed patients.
Treatment of osteomalacia associated with primary biliary cirrhosis with oral 1-alpha-hydroxy vitamin D3.
Authors: J E Compston, J P Crowe, L W Horton
Journal: BMJ (1979)

Treatment of osteomalacia associated with primary biliary cirrhosis with oral I-alpha-hydroxy vitamin D3 Osteomalacia sometimes occurs in chronic cholestatic liver disease and is usually treated with large doses of parenteral vitamin D, although oral treatment is also effective.'Treatment with oral lcx-hydroxy vitamin D3 (1ox-OHD,), a synthetic analogue of 1,25- dihydroxy vitamin D3, is of particular interest in liver disease since a therapeutic effect depends on its intestinal absorption and hepatic 25-hydroxylation,' both of which may be impaired in severe chronic cholestasis.We report the biochemical and histological responses to six months' treatment with oral lca-OHD3 in a patient with primary biliary cirrhosis (PBC) and severe osteomalacia. Case historyIn 1976 a 65-year-old woman presented with pruritus and jaundice.Liver biopsy showed changes consistent with late PBC, and antimitochondrial antibodies were present.Subsequently the serum bilirubin concentration remained between 50 and 103 4smol/l (2-9 and 6 0 mg/100 ml) (normal 3-20 ,umol/l; 0-2-1-2 mg/100 ml) and oesophageal varices developed.In April 1978 transiliac biopsy showed severe osteomnalacia, and in June treat- ment began with oral 1 oc-OHD3 2 ,ug daily.Serum calcium concentration was measured monthlyand a repeat bone biopsywas performed in December 1978.Renal function was normal throughout.She was also receiving frusemide 80 mg twice daily, potassium supplements, diphenoxylate, and parenteral vitamins A and K.Fasting serum alkaline phosphatase activity and calcium, albumin, phosphate, and bilirubin concentrations were measured on an autoanalyser (SMA 12/60), the serum calcium concentration being corrected for serum albumin value.3Plasma immunoreactive parathyroid hormone (PTH) values were measured by radioimmunoassay4 (MRC antiserum code BW 211/41).Undecalcified sections of transiliac biopsy specimens (8 ILm) were quantified with a Zeiss 25-point eyepiece graticule.Calcification fronts were shown both by 1 % toluidine-blue staining and by fluorescence microscopy of unstained sections after giving 900 mg demethylchlortetracycline by mouth 48 hours before biopsy.Hyperparathyroidism was assessed qualitatively.Control values
Effect of Treatment of Isolated Systolic Hypertension on Left Ventricular Mass
Authors: Elizabeth O. Ofili
Journal: JAMA (1998)

Context.—Left ventricular (LV) hypertrophy is a common problem among elderly patients with isolated systolic hypertension (ISH), but the effect of treatment of ISH on LV mass is not known.Objective.—To assess the ability of antihypertensive drug treatment to reduce LV mass in ISH.Design.—Echocardiographic Substudy of the Systolic Hypertension in the Elderly Program (SHEP).Patients.—A total of 104 participants at the St Louis SHEP site who had interpretable baseline echocardiograms, 94 of whom had 3-year follow-up echocardiograms.Intervention.—The SHEP participants were randomized to placebo or active treatment with chlorthalidone (12.5-25 mg/d), with atenolol (25-50 mg/d) added if necessary to maintain goal blood pressure.Main Outcome Measure.—Change in LV mass assessed by echocardiography.Results.—Minimum follow-up was 3 years. In the active treatment group, 91% and 80% of subjects were receiving treatment with chlorthalidone alone by the end of years 1 and 3, respectively. The LV mass index was 93 g/m2 in the active treatment group and 100 g/m2 in the placebo group (P<.001). The LV mass index declined by 13% (95% confidence interval, − 3% to − 23%) in the active treatment group compared with a 6% increase (95% confidence interval, − 3% to + 16%) in the placebo group over 3 years (P=.01).Conclusion.—Treatment of ISH with a diuretic-based regimen reduces LV mass.
Abstract 2010: Development of a cytotoxic peptide based on the C-terminal domain of Bax
Authors: Rebecca Boohaker, Ge Zhang, Kathleen Nemec, Annette R. Khaled
Journal: Cancer Research (2012)

Abstract The Bcl-2 family proteins maintain the balance of life and death in a cell. Bax, a pro-apoptotic member, translocates to the mitochondrial membrane in response to diverse death stimuli, initiating a cascade of programmed events that lead to cell death. Tumor progression involves deregulation of this process, in part, through mutations that cause aberrant expression of anti-apoptotic members of the Bcl-2 family that normally sequester and inhibit Bax. This study seeks to identify functional domains of Bax that can be developed into therapeutic peptides to promote the death of cancer cells resistant to existing chemotherapeutics. Our goal was to generate a peptide, much like antimicrobial peptides, that could target and disrupt mitochondrial membranes. To this end, we discovered that the C-terminal, alpha-9 helix of Bax (CT20), when tagged to EGFP or a destabilization domain (DD), could bind mitochondria and cause cell death, mimicking the activity of full-length Bax. Cell death was measured by morphological changes, such as membrane blebbing, as well as DNA fragmentation. Targeted mutagenesis of two adjacent lysines at the carboxyl end of the CT20 peptide demonstrated that these residues enabled mitochondrial membrane association. Expression of the CT20 peptide in the presence or absence of endogenous Bax resulted in cytotoxicity, indicating that the death mechanism engaged could function independently of the Bcl-2 family. These findings suggest the CT20 peptide has the potential to be developed into a viable therapeutic agent in the treatment of a broad range of cancer types. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2010. doi:1538-7445.AM2012-2010
Dietary Linolenic Acid Is Inversely Associated With Calcified Atherosclerotic Plaque in the Coronary Arteries
Authors: Luc Djoussé, Donna K. Arnett, J. Jeffrey Carr, John H. Eckfeldt, Paul N. Hopkins, Michael A. Province, R. Curtis Ellison
Journal: Circulation (2005)

High dietary intake of linolenic acid is associated with a lower risk of cardiovascular disease mortality. However, little is known about the association between linolenic acid and subclinical atherosclerosis.To examine the association between dietary linolenic acid measured by food frequency questionnaire and calcified atherosclerotic plaque in the coronary arteries (CAC) measured by cardiac CT, we studied 2004 white participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 32 to 93 years. The presence of CAC was defined on the basis of total CAC score of > or =100. We used generalized estimating equations to estimate odds ratios for the presence of CAC across quintiles of linolenic acid. The average consumption of dietary linolenic acid was 0.82+/-0.36 g/d for men and 0.69+/-0.29 g/d for women. From the lowest to the highest quintile of linolenic acid, adjusted odds ratios (95% CI) for the presence of CAC were 1.0 (reference), 0.61 (0.42 to 0.88), 0.55 (0.35 to 0.84), 0.57 (0.37 to 0.88), and 0.35 (0.22 to 0.55), respectively (P for trend <0.0001), after we controlled for age, gender, education, family risk group, smoking, fruit and vegetable intake, history of coronary artery disease, hypertension, diabetes mellitus, and statin use. When linolenic acid was used as a continuous variable, the multivariate adjusted odds ratio was 0.38 (95% CI, 0.24 to 0.46) per gram of linolenic acid intake. Use of different cut points for CAC score yielded similar results.Consumption of dietary linolenic acid is associated with a lower prevalence of CAC in a dose-response fashion in white men and women.
Mechanism of Rh prophylaxis: an experimental study on specificity of immunosuppression.
Authors: J C Woodrow, C A Clarke, W T Donohow, R Finn, R B McConnell, P M Sheppard, D Lehane, F M Roberts, T M Gimlette
Journal: BMJ (1975)

The mechanism by which Rh immunization is prevented by IgG anti-D was investigated by studying the specificity of immunosuppression. 62 D-negative Kell(K)-negative male volunteers were given two successive stimuli of 1 ml D-positive K-positive red cells. Thirty-one of the volunteers were also given 13-14 mug of IgG anti-K immediately after each stimulus, the others acting as controls. Anti-D developed in 11 of the 31 controls and in one of the 31 volunteers who had received anti-K. This marked suppression of the anti-D response by IgG anti-K was accompanied by the rapid clearance of the injected red cells to the spleen. This shows that the predominant mechanism that must be operating when IgG anti-D prevents Rh immunization is not antigen specific but is one that must involve the whole red cell, probably through destruction within splenic macrophages.
Scan Appearances in Hydatid Cysts of the Liver: Analysis of 55 Cases
Authors: A N JAIN, P RAMANATHAN, R D GANATRA
Journal: Clinical Nuclear Medicine (1980)

Liver scans done at our Centre between 1964 and 1977 were analyzed with reference to hydatid cysts in liver. Among the approximately 7200 patients analyzed, there were 55 suspected to have hydatid cysts. The criteria adopted in screening the patients for hydatid cysts were based upon clinical findings and liver scan findings. The cases were analyzed with respect to their histologic findings, locations of cold areas in the liver, and correlation with Casoni's test. We found that 1) the cystic involvement was most often in the right lobe of the liver; 2) Casoni's test does not rule out or establish the presence of hydatidosis; 3) radioisotopic vascular studies done in some cases contributed to the diagnosis; 4) although a positive liver scan does not indicate the cause of the disease, the scans showing large and totally photon-deficient cold areas along with good general condition of the patients help in the diagnosis of hydatid cysts in the liver.
Pre‐eminence and persistence of immature natural killer cells in acute myeloid leukemia patients in first complete remission
Authors: Nicolas Dauguet, Christian Récher, Cécile Demur, Jean‐Jacques Fournié, Mary Poupot, Rémy Poupot
Journal: American Journal of Hematology (2010)

Despite substantial progress in the treatment of AML, a proportion of patients do not achieve first complete remission (1(st) CR) with the induction chemotherapy, and, among patients achieving it, a majority is expected to relapse within three years. As allogeneic hematopoietic stem cell transplantation has been established as the most effective form of antileukemic therapy in patients with AML in remission, many studies have focused on the reconstitution and the functionality of the innate immune system in this context, especially regarding cytotoxic effectors such as natural killer (NK) cells. On the contrary, very few data are available concerning the innate immune system of patients in 1st CR. Herein we investigated the phenotype of autologous NK cells of AML patients in 1st CR. We showed that immature NK cells were pre-eminent in the blood of these patients and that this immature phenotype was persistent during the first months after 1st CR.
Health Insurance Exchanges — Key Link in a Better-Value Chain
Authors: Jon Kingsdale
Journal: New England Journal of Medicine (2010)

The focus on health insurance exchanges in the Patient Protection and Affordable Care Act (ACA) is one sign of just how politically mainstream the new law is. Not only are exchanges market-based, but also the ACA decentralizes them, delegating primary responsibility to the states. The states are eligible for federal financial support for developing statewide or multiple substate exchanges or forming multistate, regional exchanges. A state may even contract with a private, nonprofit entity to operate its exchange. Only if a state failed to act or to meet minimum standards would a federal exchange operate within its boundaries.Exchanges have . . .
Introduction to manipulation.
Authors: K A Keir, G C Goats
Journal: British Journal of Sports Medicine (1991)

OriginsThe art of manipulation was known to Hippocrates and the physicians of ancient Rome, and has passed down a long line of medical manipulators and bonesetters to present day practitioners; osteopaths, physiotherapists, chiropractors and manipulating physicians and surgeons.Osteopathy and chiropractic, unlike physiotherapy, at present remain outside orthodox medical practice in the UK The subject has always been contentious, often acrimonious, with much factional and interprofessional rivalry, but in the late 20th century the practice of manipulation is finally achieving scientific respect- ability through the application of biomechanical principles and recent advances in neurophysiology, together with a serious attempt to prove efficacy through controlled randomized clinical trials.Thus osteopathy and chiropractic may yet be extended a guarded welcome into the orthodox medical fold.This paper will describe briefly the terminology used in manipulation and discuss patient assess- ment, indications for treatment and the common manipulative techniques.A review of present knowledge of the physiological effects of manipu- lation will accompany a discussion of clinical outcomes based upon data from clinical research.
Aortoduodenal fistula. Primary repair with saphenous vein patch graft
Authors: F. S. Ray
Journal: JAMA (1976)

A successful primary repair of a fistula between the proximal aortic suture line and duodenum was performed in a 47-year-old man with the use of a saphenous vein patch graft with omental interposition between the aortic repair and the duodenum. Massive local and parenteral antibiotics were given. The patient remains completely well 3 1/2 years later.
Randomized trial of exercise effect on intrahepatic triglyceride content and lipid kinetics in nonalcoholic fatty liver disease
Authors: Shelby Sullivan, Erik P. Kirk, Bettina Mittendorfer, Bruce W. Patterson, Samuel Klein
Journal: Hepatology (2011)

Nonalcoholic fatty liver disease (NAFLD) and alterations in hepatic lipoprotein kinetics are common metabolic complications associated with obesity. Lifestyle modification involving diet-induced weight loss and regular exercise decreases intrahepatic triglyceride (IHTG) content and very low density lipoprotein (VLDL) triglyceride (TG) secretion rate. The aim of this study was to evaluate the weight loss-independent effect of following the physical activity guidelines recommended by the Department of Health and Human Services on IHTG content and VLDL kinetics in obese persons with NAFLD. Eighteen obese people (body mass index [BMI]: 38.1 ± 4.6 kg/m2) with NAFLD were randomized to 16 weeks of exercise training (45%-55% VO2peak, 30–60 minutes × 5 days/week; n = 12) or observation (control; n = 6). Magnetic resonance spectroscopy and stable isotope tracer infusions in conjunction with compartmental modeling were used to evaluate IHTG content and hepatic VLDL-TG and apolipoprotein B-100 (apoB-100) secretion rates. Exercise training resulted in a 10.3% ± 4.6% decrease in IHTG content ( P &lt; 0.05), but did not change total body weight (103.1 ± 4.2 kg before and 102.9 ± 4.2 kg after training) or percent body fat (38.9% ± 2.1% before and 39.2% ± 2.1% after training). Exercise training did not change the hepatic VLDL-TG secretion rate (17.7 ± 3.9 μmol/min before and 16.8 ± 5.4 μmol/min after training) or VLDL-apoB-100 secretion rate (1.5 ± 0.5 nmol/min before and 1.6 ± 0.6 nmol/min after training). Conclusion: Following the Department of Health and Human Services recommended physical activity guidelines has small but beneficial effects on IHTG content, but does not improve hepatic lipoprotein kinetics in obese persons with NAFLD.
Mastocytosis Manifested by Hepatosplenomegaly
Authors: Joseph S. Gonnella, Allen I. Lipsey
Journal: New England Journal of Medicine (1964)

CURRENT interest in the function and pathophysiology of the mast cell has been exemplified by a recent symposium on the subject.1 However, arguments over the derivation of the mast cell and its function and role in diseases remain unresolved.Pathologic states involving the mast cell can take several forms, which have been arbitrarily divided into benign and malignant varieties. Mastocytosis is a condition caused by systemic hyperplasia of mast cells, the skin being one of the organs primarily involved in the majority of cases. The cutaneous lesions may be of several types, and a definite diagnosis can only be made . . .
Increased gut permeability in Crohn's disease: is TNF the link?
Authors: P R Gibson
Journal: Gut (2004)

Evidence now implicates tumour necrosis factor α in global impairment of intestinal barrier function, and may be the link between the leaky gut and Crohn’s disease

Intestinal epithelial barrier function and Crohn’s disease are intimately related. An impaired barrier in association with active inflammation leads to increased exposure of the mucosal innate and acquired immune system to proinflammatory molecules. This has been implicated as a major driving force for mucosal inflammation. In active disease, macromolecules can permeate the barrier at an increased rate via, for example, breaks in the integrity of the epithelium (ulceration, erosions, or nests of apoptotic cells)1 via increased pinocytotic uptake of luminal proteins,2,3 and via increased proportion of M cells in the terminal ileum.4 Impaired barrier function may precede the clinical development of the disease and might represent a marker of increased susceptibility to Crohn’s disease. This notion derives from observations made in several centres using different techniques that paracellular permeability is abnormal in 10–20% of first degree relatives of patients with Crohn’s disease.8,9,11 That this reflects exposure to an environmental factor is supported by the observations from three studies that increased intestinal permeability is also found in 13–36% of spouses of patients with Crohn’s disease.8,9,11

Tumour necrosis factor α (TNF-α) and Crohn’s disease are intimately related. Mucosal levels and inflammatory cell production of TNF-α are elevated. Therapy with monoclonal antibodies to TNF-α, such as infliximab, leads …
Glutathione and Thioredoxin Antioxidant Pathways Synergize to Drive Cancer Initiation and Progression
Authors: Isaac S. Harris, Aislinn E. Treloar, Satoshi Inoue, Masato Sasaki, Chiara Gorrini, Kim Chung Lee, Ka Yi Yung, Dirk Brenner, Christiane B. Knobbe-Thomsen, Maureen A. Cox, Andrew Elia, Thorsten Berger, David W. Cescon, Adewunmi Adeoye, Anne Brüstle, Sam D. Molyneux, Jacqueline M. Mason, Wanda Y. Li, Kazuo Yamamoto, Andrew Wakeham, Hal K. Berman, Rama Khokha, Susan J. Done, Terrance J. Kavanagh, Ching-Wan Lam, Tak W. Mak
Journal: Cancer Cell (2015)
Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia
Authors: Menno D de Jong, Cameron P Simmons, Tran Tan Thanh, Vo Minh Hien, Gavin J D Smith, Tran Nguyen Bich Chau, Dang Minh Hoang, Nguyen Van Vinh Chau, Truong Huu Khanh, Vo Cong Dong, Phan Tu Qui, Bach Van Cam, Do Quang Ha, Yi Guan, J S Malik Peiris, Nguyen Tran Chinh, Tran Tinh Hien, Jeremy Farrar
Journal: Nature Medicine (2006)
Increased F<sub>2</sub> Isoprostanes in the Acute Chest Syndrome of Sickle Cell Disease as a Marker of Oxidative Stress
Authors: ELIZABETH S. KLINGS, BRIAN W. CHRISTMAN, JAMES McCLUNG, ARTHUR F. STUCCHI, LILLIAN McMAHON, MARC BRAUER, HARRISON W. FARBER
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Nitric oxide metabolism is altered during the acute chest syndrome of sickle cell disease. In the presence of oxygen and oxygen-related molecules, nitric oxide can preferentially form the powerful oxidants nitrite, nitrate, and peroxynitrite. We hypothesized that increased oxidative stress may contribute to the pathogenesis of acute chest syndrome and measured F2 isoprostanes, a nonenzymatically generated molecule resulting from free radical catalyzed lipid peroxidation in patients with sickle cell disease in various stages of disease. Plasma samples were obtained from nineteen patients with sickle cell disease during acute chest syndrome (pre- and postexchange transfusion), vasoocclusive crisis, and/or at baseline; 12 normal volunteers served as controls. F2 isoprostanes were measured by gas chromatography/mass spectrophotometry. There was a 9-fold increase in F2 isoprostanes in patients with acute chest syndrome as compared with normal volunteers. There was approximately a 50–60% decline in isoprostanes postexchange transfusion to a level similar to that of patients with sickle cell disease at baseline. There was no difference in isoprostanes between vasoocclusive crisis and patients with sickle cell disease at baseline. Increased oxidative stress, measured by generation of F2 isoprostanes, occurs during acute chest syndrome and may have an important role in the pathogenesis of this disease process.