tbuckley/cabot-search huggingface dataset:
Fibrinogen Stony Brook, a heterozygous A alpha 16Arg----Cys dysfibrinogenemia. Evaluation of diminished platelet aggregation support and of enhanced inhibition of fibrin assembly.
Authors: D K Galanakis, A Henschen, E I Peerschke, M Kehl
Journal: Journal of Clinical Investigation (1989)

Assessed by high performance liquid chromatographic and amino acid sequence determinations, approximately one half (n = 4) of A peptide in fibrinogen Stony Brook (phi SB) contained the A alpha 16Arg----Cys substitution. To examine its functional behavior, mutant molecule-rich soluble subfractions that partly or fully lacked their normal A peptide were obtained from cryoprecipitates or from incoagulable material, respectively. Such subfractions consistently induced a more pronounced decrease (n = 3) in the turbidity of normal polymerizing fibrin than that induced by normal fibrinogen, by whole phi SB (n = 4) or by fibrinogen from an unrelated homozygous proband. These subfractions also exhibited decreased (12-50% of normal controls, fibrinogen 30-590 nM, n = 5) ADP-induced aggregation support of gel-sieved platelets, a decrease not demonstrable by whole phi SB, by fibrinogen from the homozygous proband, or by enrichment of the latter with normal soluble fibrin. A single isolate displaying diminished platelet aggregation support was 125I-labeled and examined further. It exhibited decreased binding to platelets, and Scatchard analysis indicated decreased binding affinity but normal maximum binding. We infer that phi SB contained heterodimers that exhibited these distinct functional properties when their normal A peptide had been cleaved.
Cerebral and Peripheral Emboli Caused by Cervical Ribs
Authors: H. S. Shucksmith
Journal: BMJ (1963)

Barker, N. W., Cromer, H. E., Hum, M., and Waugh, J. M. (1945). Surgery, 17. 207. Barritt, D. W., and Jordan, S. C. (1960). Lancet, 1, 1309. Bauer, G. (1946). J. Amer. med. Ass., 131, 196. Byrne, J. J. (I960). Ibid., 174. 113. Coon, W. W., MacKenzie, J. W., and Hodgson, P. E. (1958). Surg. Gynec. Obstet., 106, 129. de Bakey, M. E. (1954). Int. Abst. Surg., 98. 1. Eskeland, G. (1962). Lancet, ?, 1035 Gibbs, N. M. (1957). Brit. J. Surg., 45. 209. (1959). Ibid., 47. 282. Harvey, W. P., and Finch, C. A. (1950). New Engt. J. Med., 242, 208. Henderson, E. F. (1927). Arch. Surg., 15, 231. Hermann, R. E., Davis, J. H., and Holden, W. D. (1961). Amer. J. Surg., 102. 19. Honey, G. E., and Truelove, S. C. (1957). Lancet, 1. H55. Lam, C. R., and Hooker. D. H. (1946). Ann. Surg., 123. 221. McLachlin, A. D., McLachlin, J. A., Jory, T. A., and Rawling, E. G. (1960). Ibid., 152. 678. Meister, H. (1960). Frankfurt. Z. Path., 70. 640. Ochsner, A., de Bakey, M. E., De Camp, P. T., and da Rocha, E. (1951). Ann. Surg., 134. 405. Payling Wright, H., and Osborn, S. B. (1952). Brit. Heart J.t 14, 325. Sevitt, S., and Gallagher, N. G. (1959). Lancet, 2, 981. Zeitlhofer, J., and Reiffenstuhl, G. (1952). Wein. klin. Wschr.. 64. 446. Zilliacus, H. (1946). Acta med. se and., Suppl. No. 171, p. 1.
Na+- and Cl–-coupled active transport of nitric oxide synthase inhibitors via amino acid transport system B0,+
Authors: Takahiro Hatanaka, Takeo Nakanishi, Wei Huang, Frederick H. Leibach, Puttur D. Prasad, Vadivel Ganapathy, Malliga E. Ganapathy
Journal: Journal of Clinical Investigation (2001)

Nitric oxide synthase (NOS) inhibitors have therapeutic potential in the management of numerous conditions in which NO overproduction plays a critical role. Identification of transport systems in the intestine that can mediate the uptake of NOS inhibitors is important to assess the oral bioavailability and therapeutic efficacy of these potential drugs. Here, we have cloned the Na+ - and Cl- -coupled amino acid transport system B(0,+) (ATB(0,+)) from the mouse colon and investigated its ability to transport NOS inhibitors. When expressed in mammalian cells, ATB(0,+) can transport a variety of zwitterionic and cationic amino acids in a Na+ - and Cl- -coupled manner. Each of the NOS inhibitors tested compete with glycine for uptake through this transport system. Furthermore, using a tritiated analog of the NOS inhibitor N(G)-nitro-L-arginine, we showed that Na+ - and Cl- -coupled transport occurs via ATB(0,+). We then studied transport of a wide variety of NOS inhibitors in Xenopus laevis oocytes expressing the cloned ATB(0,+) and found that ATB(0,+) can transport a broad range of zwitterionic or cationic NOS inhibitors. These data represent the first identification of an ion gradient-driven transport system for NOS inhibitors in the intestinal tract.
Treatment of Heart Failure with Emphasis on the Use of Diuretics
Authors: Charles K. Friedberg
Journal: JAMA (1960)

In the treatment of heart failure it is necessary to make use of all available therapeutic agents, to adapt them to the individual patient, and to adjust them to changing conditions. Overdigitalization, especially common in the presence of sinus rhythm, is as bad as inadequate digitalization. The reduction of sodium intake is important, but not all patients require extreme sodium restriction. Similarly the regulation of water intake, the administration of diuretics, and the use of acidifying agents like ammonium chloride and lysine monohydrochloride, to potentiate mercurial diuretics must all be individualized and adjusted by constant observation of the clinical manifestations and the patient's responses.
Unexpected Death during Treatment of Uncomplicated Diabetic Ketoacidosis
Authors: T. M. Hayes, C. J. Woods
Journal: BMJ (1968)

Unexpected Death during Treatment of Uncomplicated Diabetic Ketoacidosis Brit.med.1968, 4, 32-33 Ketotic coma accounts for only 1 % of deaths in diabetics (Entmacher and Marks, 1965), but the mortality of diabetic coma remains around 10% (Nabarro, 1965).The majority of those who die in diabetic coma do so of vascular or renal com- plications, but a small number die of uncomplicated ketosis which fails to respond to routine therapy.Recently there have been reports of young patients in diabetic ketosis who died after an initial improvement, both clinical and biochemical.FitzGerald et al. (1961) reported two cases and Young and Bradley (1967) a further two in which this course of events occurred and in which cerebral oedeema was found at necropsy.We report a case in which cerebral oedema developed during diabetic coma and which failed to respond to treatment. CASE REPORTA 28-year-old housewife was admitted to hospital as an emergency with a history of vomiting and dyspnoea for 24 hours.Diabetes mellitus had been diagnosed two years previously and she had been controlled with insulin zinc suspension and soluble insulin.On examination she was conscious but drowsy and dehydrated.Acetone was detectable in the breath and she was overbreathing.There were no other abnormal physical signs and no signs of infec- tion.Her blood pressure was 120/80 and her temperature 96' F.(35.6°C.).Laboratory data on admission included: blood sugar 490 mg./ 100 ml., alkali reserve 11 mEq/l., serum sodium 130 mEq/l., serum potassium 6.2 mEq/l., serum chloride 87 mEq/l., and blood urea 75 mg./100ml.Her plasma gave a strongly positive reaction for ketones and her urine contained 2% glucose and was strongly positive to Acetest tablets.Treatment was started with intravenous normal saline and sodium bicarbonate.She was given 100 units of soluble insulin intra- venously and during the first two hours had I litre of saline and 100 mEq of sodium bicarbonate.By this time her blood sugar had
Observations on MORTALITY IN ACUTE APPENDICULAR DISEASE
Authors: D. P. D. Wilkie
Journal: BMJ (1931)

I make no apology for takinig up a subject which has been dealt with repeatedly in recent years.We are faced with the fact that despite improved education, the greater appreciation by the public of the dangers of the disease, the extended hospital facilities, the vastly improved transport service, and the increased number of capable operating surgeons, the death rate in acute appendicular disease is as high to-day as it was twenty years ago.There can be no doubt that early operation is now practised the country over to a degree greatly exceeding that of two decades ago.How are we, then, to reconcile our advocacy of early operation with this persistently hligh mortality?To mv mind the explanation is clear, and permits of no doubt-namely, that the majority of the patients now operated on early are of the class which did not contribute to the mortality, while in the dangerous and fatal type of case operation occurs little, if at all,
Warfarin Dosage and Vitamin K in Osmolite
Authors: ELLIS LADER
Journal: Annals of Internal Medicine (1980)

Letters and Corrections1 August 1980Warfarin Dosage and Vitamin K in OsmoliteELLIS LADER, M.D., LEE YANG, B.A., ALLAN CLARKE, R. PH.ELLIS LADER, M.D.Search for more papers by this author, LEE YANG, B.A.Search for more papers by this author, ALLAN CLARKE, R. PH.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-93-2-373_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: A cause of warfarin antagonism is unappreciated inclusion of vitamin K analogues in commercial dietary supplements. The following case report is pertinent to this point.A 60-year-old woman had undergone aortic-valve replacement surgery 15 years before admission and had been anticoagulated thereafter with sodium warfarin. Satisfactory anticoagulation has been maintained chronically with daily administration of 5 mg of warfarin. With institution of dietary supplementation with Osmolite (Ross Laboratories, Columbus, Ohio), up to 1200 mL (12 kcal) daily, the patient's prothrombin time fell to control levels within 1 week. Stepwise increments in her daily warfarin dose to 15...References1. FRICK P, RIEDLER G, and BRÖGLI H. Dose response and minimal daily requirement for vitamin K in man. J Appl Physiol. 1967;23:387-9. CrossrefMedlineGoogle Scholar2. WESSLER S and ALEXANDER B. A Guide to Anticoagulant Therapy. New York: American Heart Association; 1970:14. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ELLIS LADER, M.D.; LEE YANG, B.A.; ALLAN CLARKE, R. PH.Affiliations: State University of New York Buffalo, NY 14215 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byWarfarin Sodium – White LotionDrug–Nutrient Interactions in Patients Receiving Enteral NutritionDrug-Nutrient Interactions in Patients Receiving Enteral NutritionVitamin K: A Practical Guide to the Dietary Management of Patients on WarfarinVitamin K: A Practical Guide to the Dietary Management of Patients on WarfarinOral AnticoagulantsOral Anticoagulant DrugsWarfarin Resistance and Enteral FeedingsDrug-nutrient interaction counseling programs in upper Midwestern hospitals: 1986 survey resultsWarfarin resistance linked to enteral nutrition productsFamilial Warfarin ResistanceDrugs affecting blood clotting, fibrinolysis and hemostasisWarfarin Resistance and Vitamin KMARY LEE, PHARM.D., ROWEENA N. SCHWARTZ, ROOHOLLAH SHARIFI, M.D. 1 August 1980Volume 93, Issue 2 Page: 373-374 Keywords Prothrombin time Sodium Surgery Vitamin K ePublished: 1 December 2008 Issue Published: 1 August 1980 PDF downloadLoading ...
Points: In praise of the Basuto pony
Authors: I Kennedy
Journal: BMJ (1984)

Choosing a practice SIR,-The last section in the paper by Dr Brian Beaumont and Dr Malcolm McCoubrie (10 March, p 761) gives a varied list of "practice progonistic signs," but unfortunately the authors do not state the significance of these qualities.We are a coffee drinking, Christmas party giving practice, devoid of drug firm goodies and with a smoking partner.Our trainee is confused as to whether these signs bode good or ill for the future.
Analysis of Environmental Chemical Mixtures and Non-Hodgkin Lymphoma Risk in the NCI-SEER NHL Study
Authors: Jenna Czarnota, Chris Gennings, Joanne S. Colt, Anneclaire J. De Roos, James R. Cerhan, Richard K. Severson, Patricia Hartge, Mary H. Ward, David C. Wheeler
Journal: Environmental Health Perspectives (2015)

There are several suspected environmental risk factors for non-Hodgkin lymphoma (NHL). The associations between NHL and environmental chemical exposures have typically been evaluated for individual chemicals (i.e., one-by-one).
Doppler-Derived Ejection Intraventricular Pressure Gradients Provide a Reliable Assessment of Left Ventricular Systolic Chamber Function
Authors: Raquel Yotti, Javier Bermejo, M. Mar Desco, J. Carlos Antoranz, José Luis Rojo-Álvarez, Cristina Cortina, Carmen Allué, Hugo Rodríguez-Abella, Mar Moreno, Miguel A. García-Fernández
Journal: Circulation (2005)

Ejection intraventricular pressure gradients are caused by the systolic force developed by the left ventricle (LV). By postprocessing color Doppler M-mode (CDMM) images, we can measure noninvasively the ejection intraventricular pressure difference (EIVPD) between the LV apex and the outflow tract. This study was designed to assess the value of Doppler-derived EIVPDs as noninvasive indices of systolic chamber function.CDMM images and pressure-volume (conductance) signals were simultaneously acquired in 9 minipigs undergoing pharmacological interventions and acute ischemia. Inertial, convective, and total EIVPD curves were calculated from CDMM recordings. Peak EIVPD closely correlated with indices of systolic function based on the pressure-volume relationship: peak elastance (within-animal R=0.98; between-animals R=0.99), preload recruitable stroke work (within-animal R=0.81; between-animals R=0.86), and peak of the first derivative of pressure corrected for end-diastolic volume (within-animal R=0.88; between-animals R=0.91). The correlation of peak inertial EIVPD with these indices was also high (all R>0.75). Load dependence of EIVPDs was studied in another 5 animals in which consecutive beats obtained during load manipulation were analyzed. During caval occlusion (40% EDV reduction), dP/dtmax, ejection fraction, and stroke volume significantly changed, whereas peak EIVPD remained constant. Aortic occlusion (40% peak LV pressure increase) significantly modified dP/dtmax, ejection fraction, and stroke volume; a nearly significant trend toward decreasing peak EIVPD was observed (P=0.06), whereas inertial EIVPD was unchanged (P=0.6). EIVPD beat-to-beat and interobserver variabilities were 2+/-12% and 5+/-11%, respectively.Doppler-derived EIVPDs provide quantitative, reproducible, and relatively load-independent indices of global systolic chamber function that correlate closely with currently available reference methods.
The Emerging p53 Gene Family
Authors: W G Kaelin
Journal: JNCI Journal of the National Cancer Institute (1999)

Perturbation of p53 protein function is a common, if not universal, finding in human cancer. Tumor suppression by p53 is due, at least in part, to its ability to activate transcription of certain genes involved in cell cycle control and apoptosis (programmed cell death). Two additional members of the mammalian p53 family, p73 and p51, which is also known as p40, p63, KET, or p73L, were recently identified. Both of these proteins share substantial sequence homology with p53 and can, at least when overproduced, activate p53-responsive promoters and induce apoptosis. Nonetheless, data on differences between these proteins and p53 are emerging. For example, p73 is not induced by DNA damage and is not targeted for inactivation by viral oncoproteins such as simian virus 40 (SV40) T antigen, adenovirus E1B 55K, and human papillomavirus E6. In contrast to p53, neither p73 nor p51 appears to be frequently mutated in human cancers on the basis of the limited studies reported to date. Finally, unlike p53, cells produce multiple p73 and p51 isoforms as a result of alternative splicing, and production of p73 and p51 appears to be restricted to certain tissues. Additional studies are required to determine the role, if any, that p73 and p51 play in cell growth control and carcinogenesis.
OT1-02-01: Phase II Neoadjuvant Trial of Anthracycline Based Regimens Followed by a Combination with Nanoparticle Almumin-Bound Paclitaxel and Trastuzumab in Patients with Operable T2-3,N0-1,Her2 Positive Breast Cancer.
Authors: M Iwamoto, Y Takahashi, K Kimura, S Tanaka, K Uchiyama
Journal: Cancer Research (2011)

Abstract Background: Anthracycline and taxane have been widely used and studied in neoadjuvant setting for treatment of locally advanced breast cancer. Various regimens have explored the addition of newer agents to determine safety and efficacy, and pathological complete response(pCR) has been demonstrated to be associated with favorable overall survival in primary breast cancer. In addition, Three year median follow-up data of the TECHNO Trial revealed that the neoadjuvant combination of trastuzumab and chemotherapy resulted in a high chance for a pCR. We conducted a clinical Phase II neoadjuvant trial of Anthracycline based regimens(EC,AC,FEC) followed by a combination with nanoparticle albumin-bound Paclitaxel and Trastuzumab in patients with operable T2-3,N0-1,Her2 positive breast cancer. Patients and Methods: The study is designed to evaluate EC or AC or FEC followed a combination of nanoparticle almumin-bound Paclitaxel and Trastuzumab as neoadjuvant therapy in patients with Her2 positive locally advanced(T2-3,N0-1) breast cancer. Patients are treated with neoadjuvant EC(Epirubicin 90 mg/m2, Cyclophosphamide 600 mg/m2) or AC(Doxorubicin 90 mg/m2, Cyclophosphamide 600 mg/m2) or FEC(Fluorouracil 500mg/m2, Epirubicin 100 mg/m2, Cyclophosphamide 500 mg/m2) q21d x 4, follosed by a combination with nanoparticle almumin-bound Paclitaxel(260 mg/m2) and Trastuzumab q21d x 4. Patients undergo surgery 4–6 weeks later from completing chemotherapy. pCR, the primary endpoint is defined as no evidence of invasive tumors in the final surgical sample both in the breast and axillary lymph nodes. Secondary endpoints include objective clinical response rate, disease-free interval, overall survival, rate of breast concerving surgery, and the safety of the treatment. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr OT1-02-01.
SAGITTAL SPINAL CURVATURES AND PELVIC TILT OF FEMALE DANCERS IN STANDING POSTURE
Authors: F Esparza-Ros, R Vaquero-Cristóbal, F Alacid, E Martínez-Ruiz, PA López-Miñarro
Journal: British Journal of Sports Medicine (2014)

Background A good control of the spinal posture may induce greater ability to change spinal angles in several positions. The spinal posture influences vertebral loading during daily activities. Neutral postures have been associated to lower spinal forces in the intervertebral joints. Objective To compare the spinal posture and pelvic tilt between relaxed standing and active alignment while standing in elementary education dancers. Design Comparative study. Setting Dance Conservatory professional. The sample included dance students of 4th year. Participants 46 female dancers (mean±SD, age: 12.07±1.01 years-old) were recruited for this study. All participants had at less 4 years of experience in the Dance Conservatory. Risk factor assessment Not applicable. Main outcome measurements Thoracic kyphosis, lumbar lordosis and pelvic tilt were measured in relaxed standing and during active alignment of spinal curvatures using a Spinal Mouse ® . Results Thoracic and lumbar curvatures and pelvic tilt values while relaxed standing were 18.72±11.11°, -25.52±7.14° and 19.52±5.10°, respectively. Mean values in the active alignment were: 4.96±13.54°, -3.76±12.12° and 4.57±7.06°, respectively. Significant differences between both postures were found in the thoracic (t=6.39; P&lt;.001) and lumbar curvatures (t=−10.33; P&lt;.001), and pelvic tilt (t=12.29; P&lt;.001). Conclusions Dance is associated with a large control of spinal posture in standing position. Dance training is related to a great curvature change when active alignment of spinal curves is required. This control of spinal curvatures may reduce the risk of injury in dance and daily activities.
Effects of DNA Damage in Smooth Muscle Cells in Atherosclerosis
Authors: Kelly Gray, Sheetal Kumar, Nichola Figg, James Harrison, Lauren Baker, John Mercer, Trevor Littlewood, Martin Bennett
Journal: Circulation Research (2014)

DNA damage and the DNA damage response have been identified in human atherosclerosis, including in vascular smooth muscle cells (VSMCs). However, although double-stranded breaks (DSBs) are hypothesized to promote plaque progression and instability, in part, by promoting cell senescence, apoptosis, and inflammation, the direct effects of DSBs in VSMCs seen in atherogenesis are unknown.To determine the presence and effect of endogenous levels of DSBs in VSMCs on atherosclerosis.Human atherosclerotic plaque VSMCs showed increased expression of multiple DNA damage response proteins in vitro and in vivo, particularly the MRE11/RAD50/NBS1 complex that senses DSB repair. Oxidative stress-induced DSBs were increased in plaque VSMCs, but DSB repair was maintained. To determine the effect of DSBs on atherosclerosis, we generated 2 novel transgenic mice lines expressing NBS1 or C-terminal deleted NBS1 only in VSMCs, and crossed them with apolipoprotein E(-/-) mice. SM22α-NBS1/apolipoprotein E(-/-) VSMCs showed enhanced DSB repair and decreased growth arrest and apoptosis, whereas SM22α-(ΔC)NBS1/apolipoprotein E(-/-) VSMCs showed reduced DSB repair and increased growth arrest and apoptosis. Accelerating or retarding DSB repair did not affect atherosclerosis extent or composition. However, VSMC DNA damage reduced relative fibrous cap areas, whereas accelerating DSB repair increased cap area and VSMC content.Human atherosclerotic plaque VSMCs show increased DNA damage, including DSBs and DNA damage response activation. VSMC DNA damage has minimal effects on atherogenesis, but alters plaque phenotype inhibiting fibrous cap areas in advanced lesions. Inhibiting DNA damage in atherosclerosis may be a novel target to promote plaque stability.
Community Screening for Diabetes: Low detection rate in a low-risk population
Authors: William P Newman, Rik Nelson, Kurt Scheer
Journal: Diabetes Care (1994)

To evaluate glucose-based community screening for diabetes with regard to detection rate.A retrospective analysis of a community-screening questionnaire data base that included a screening for blood glucose. Referred subjects had fasting glucose levels > 6.4 mM (115 mg/dl) or postprandial levels > or = 8.9 mM (160 mg/dl). An attempt was made to contact referred subjects and to ascertain whether follow-up was undertaken and current status. A random sample of subjects not meeting the glucose criteria (nonreferred) also was contacted in an analogous fashion to referred subjects.In 2,016 questionnaires, glucose-based referral criteria were exhibited by 148 (7.3%) individuals, and subsequent evaluation data were available for 111. Of those 111 individuals, 37 (33%) knew they had diabetes before the screening, and 39 (36%) did not seek further evaluation. Of the remaining 35 subjects, 6 (13%) were told of their new diagnosis of diabetes, and 29 were told they did not have diabetes. Three of 50 nonreferred subjects knew of their diabetes before screening. Thirty percent (14 out of 47) of nonreferred subjects underwent subsequent evaluation, although they were not told to do so. A single new case of diabetes occurred in the nonreferred group.Community screening for diabetes that is based on measured glucose is of low yield. The known problems of glucose-based screening, coupled with its low yield, make a glucose-based approach difficult to justify. These results indicate that glucose-based community screening should be done only under the careful supervision of a health professional who is trained both in glucose measurement instrumentation and in screening.