tbuckley/cabot-search huggingface dataset:
Identification of Patients With Diabetes From the Text of Physician Notes in the Electronic Medical Record
Authors: Alexander Turchin, Isaac S. Kohane, Merri L. Pendergrass
Journal: Diabetes Care (2005)

In this report, we describe a software tool that rapidly and reliably identifies a diagnosis of diabetes documented in physician notes in the electronic medical record.

Diabetes care in the U.S. is suboptimal: 20–40% of diabetic patients have inadequate glycemic or blood pressure control or do not have annual eye or foot examinations (1–3). Effective public health surveillance is mandatory to address this problem. It is crucial for the assessment of prevalence of diabetes, its economic and social costs, and evaluation of the dynamics of disease care measures and outcomes (4,5).

Disease surveillance can be significantly hampered by the difficulty in identifying the target population (6). A number of approaches have been used to identify patients with diabetes, including death certificates (7,8), billing data (9,10), and surveys (11,12). Each of these methods has its own shortcomings, and sensitivity remains relatively low. Consequently, manual chart review remains the gold standard for the identification of individuals diagnosed with a particular disease. This is a labor-intensive process that is not scalable to the level needed in public health surveillance.

Because most elements of the patient chart are increasingly available in digital format, there have been a number of attempts to …
Agranulocytic Angina: A Case of the Relapsing Type
Authors: A. D. Briscoe
Journal: BMJ (1936)

274t W A I;Y~- Aic 7~LitAffAt suspicious of any-such surgical procedures.Histopathological examination confirmed the view that the nerves were abnormal, for extensive myelinic degeneration was found to be present.The patient was discharged to her own home convinced that her pains had gone and that the head noises were less severe, presumably due to lowered nervous tension generally.Unfortunately, before the progress of the case could be further observed, she developed influenza and died from bronchopneumonia.
Bimodal Distribution of Glucose Is Not Universally Useful for Diagnosing Diabetes
Authors: Dorte Vistisen, Stephen Colagiuri, Knut Borch-Johnsen
Journal: Diabetes Care (2008)

Bimodality in the distribution of glucose has been used to define the cut point for the diagnosis of diabetes. Previous studies on bimodality have primarily been in populations with a high prevalence of type 2 diabetes, including one study in a white Caucasian population. All studies included participants with known diabetes. The aim of this study was to assess whether a bimodal structure is a general phenomenon in fasting plasma glucose (FPG) and 2-h plasma glucose that is useful for deriving a common cut point for diabetes in populations of different origin, both including and excluding known diabetes.The Evaluation of Screening and Early Detection Strategies for Type 2 Diabetes and Impaired Glucose Tolerance (DETECT-2) project is an international collaboration pooling surveys from all continents. These studies include surveys in which plasma glucose was measured during an oral glucose tolerance test; in total, 43 studies (135,383 participants) from 27 countries were included. A mixture of two normal distributions was fitted to plasma glucose levels, and a cut point for normal glycemia was estimated as their intersection. In populations with a biologically meaningful cut point, bimodality was tested for significance.Distributions of FPG and 2-h plasma glucose did not, in general, produce bimodal structures useful for deriving cut points for diabetes. When present, the cut points produced were inconsistent over geographical regions.Deriving cut points for normal glycemia from distributions of FPG and 2-h plasma glucose does not appear to be suitable for defining diagnostic cut points for diabetes.
<scp>NSAID</scp>‐exacerbated respiratory disease: a meta‐analysis evaluating prevalence, mean provocative dose of aspirin and increased asthma morbidity
Authors: D. R. Morales, B. Guthrie, B. J. Lipworth, C. Jackson, P. T. Donnan, V. H. Santiago
Journal: Allergy (2015)

Abstract Background The prevalence and mean provocative dose of oral aspirin ( MPDA ) triggering respiratory reactions in people with asthma have been inconsistently reported, and the relationship between NSAID ‐exacerbated respiratory disease ( NERD ) and asthma morbidity was less well quantified. Methods A systematic review was performed by identifying studies diagnosing NERD using blinded, placebo‐controlled oral provocation challenge tests ( OPCT s) or by self‐reported history in people with asthma. Data were extracted, and effect estimates for changes in respiratory function, MPDA and asthma morbidity were pooled using random‐effects meta‐analysis. Results The prevalence of NERD in adults with asthma was 9.0% (95% CI 6–12%) using OPCT s and 9.9% (95% CI 9.4–10.5%) using self‐reported history from questionnaires. The MPDA in adults with NERD was 85.8 mg (95% CI 73.9–97.6). In people with NERD , the risk of: uncontrolled asthma was increased twofold ( RR 1.96 (95% CI 1.25–3.07)); severe asthma and asthma attacks was increased by 60% ( RR 1.58 (95% CI 1.15–2.16) and RR 1.59 (95% CI 1.21–2.09), respectively); emergency room visits was increased by 80% ( RR 1.79 (95% CI 1.29–2.49)); and asthma hospitalization was increased by 40% ( RR 1.37 (95% CI 1.12–1.67)) compared to people with NSAID‐tolerant asthma. Conclusions Respiratory reactions triggered by oral aspirin in people with asthma are relatively common. At the population level, the prevalence of NERD was similar when measured using appropriately conducted OPCT s or by self‐reported history. On average, respiratory reactions were triggered by clinically relevant doses of oral aspirin. Asthma morbidity was significantly increased in people with NERD who potentially require more intensive monitoring and follow‐up.
Role of Bone Marrow Biopsy in the Staging of Diffuse Large B-Cell Lymphoma in the PET/CT Era
Authors: Musa F. Alzahrani, Tarec Christoffer El-Galaly, Martin Hutchings, Jakob Werner Hansen, Peter de Nully Brown, Annika Loft, Hans E Johnsen, Victor Iyer, Don Wilson, Laurie H. Sehn, Kerry J. Savage, Joseph M. Connors, Diego Villa
Journal: Blood (2014)
The Bradshaw Lecture on Modern Abdominal Surgery
Authors: T. S. Wells
Journal: BMJ (1890)

cases might lessen the danger.The distinction of hypertrophic and atrophic was good if used without necessarily employing a different causation."Hypertrophic" should not be used as synonymous with "biliary."The "publican's liver" was often a large one.The ascites was probably not due to purely mechanical causes.The extent of liver dulness was not by any means a good guide as to the size of the liver.Although not denying that in those ex- ceptional cases in which the inferior vena cava was surrounded by liver tissue, cedema of the lower extremities followed as a direct r*Eult, he was doubtful if cirrhosis could ever be regarded as a mechanical cause of cedema of the lower extremities.-Dr. HUTCHINsON (Scarborough) drew attention to the very lengthy list of causes of ascites, and was very much relieved to fina on listening to the debate that most of them had no symptoms, and that after all the alcoholic form was the one which practical men had to face.He drew attention to the fact that cirrhosis had a tendency to generally lower the general tone of health, and that therefore small congestions here and there, in the lungs or kidneys, were very difficult to cure, hence the temptation to send the cases abroad for change.He mentioned a case which had been sent abroad on this account.Sea-sickness brought onhbemorrhage which ended in death, and he appealed to physicians to go a little more into cases before with a light heart sending them across the seas.-Dr.RATCLIFFB said, in reply to Dr. Griffith, that Dr. Wil- son and he had purposely refrained from mentioning the collateral correlations other than the important one through the coronary, esophageal, and pericesophageal plexus, into the diaphragmatlc
Anti-thrombopoietin antibodies suppress megakaryocytic colony formation in vitro in patients with systemic lupus erythaematosus
Authors: P D Ziakas, H A Papadaki, M Psyllaki, M Voulgarelis
Journal: Annals of the Rheumatic Diseases (2008)

Autoantibodies against thrombopoietin (TPO) have been implicated in systemic lupus erythaematosus (SLE) thrombocytopoenia.1 2 To investigate their pathophysiological significance, we have evaluated the effect of SLE sera on megakaryocytic colony formation in vitro.

A total of 35 randomly selected SLE sera were initially screened for the presence of antiplatelet antibodies (APAs), using a commercially available assay (PAK12, GTI Diagnostics, Wauksesha, Wisconsin, USA). In all, 16 sera tested positive and were excluded from the analysis. Only sera negative for APAs have been evaluated in the current study, since APAs have been reported to inhibit megakaryopoiesis in vitro.3 Of the remaining 19 samples, 7 tested positive for anti-TPO antibodies and 12 were negative. TPO concentration was then measured by a …
DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice
Authors: Lisiane B. Meira, James M. Bugni, Stephanie L. Green, Chung-Wei Lee, Bo Pang, Diana Borenshtein, Barry H. Rickman, Arlin B. Rogers, Catherine A. Moroski-Erkul, Jose L. McFaline, David B. Schauer, Peter C. Dedon, James G. Fox, Leona D. Samson
Journal: Journal of Clinical Investigation (2008)

Chronic inflammation increases cancer risk. While it is clear that cell signaling elicited by inflammatory cytokines promotes tumor development, the impact of DNA damage production resulting from inflammation-associated reactive oxygen and nitrogen species (RONS) on tumor development has not been directly tested. RONS induce DNA damage that can be recognized by alkyladenine DNA glycosylase (Aag) to initiate base excision repair. Using a mouse model of episodic inflammatory bowel disease by repeated administration of dextran sulfate sodium in the drinking water, we show that Aag-mediated DNA repair prevents colonic epithelial damage and reduces the severity of dextran sulfate sodium-induced colon tumorigenesis. Importantly, DNA base lesions expected to be induced by RONS and recognized by Aag accumulated to higher levels in Aag-deficient animals following stimulation of colonic inflammation. Finally, as a test of the generality of this effect we show that Aag-deficient animals display more severe gastric lesions that are precursors of gastric cancer after chronic infection with Helicobacter pylori. These data demonstrate that the repair of DNA lesions formed by RONS during chronic inflammation is important for protection against colon carcinogenesis.
ADAP–SLP-76 Binding Differentially Regulates Supramolecular Activation Cluster (SMAC) Formation Relative to T Cell–APC Conjugation
Authors: Hongyan Wang, Fiona E. McCann, John D. Gordan, Xiang Wu, Monika Raab, Talat H. Malik, Daniel M. Davis, Christopher E. Rudd
Journal: The Journal of Experimental Medicine (2004)

T cell–APC conjugation as mediated by leukocyte function-associated antigen-1 (LFA-1)–intercellular adhesion molecule (ICAM)-1 binding is followed by formation of the supramolecular activation cluster (SMAC) at the immunological synapse. The intracellular processes that regulate SMAC formation and its influence on T cell function are important questions to be addressed. Here, using a mutational approach, we demonstrate that binding of adaptor adhesion and degranulation promoting adaptor protein (ADAP) to SLP-76 differentially regulates peripheral SMAC (pSMAC) formation relative to conjugation. Although mutation of the YDDV sites (termed M12) disrupted SLP-76 SH2 domain binding and prevented the ability of ADAP to increase conjugation and LFA-1 clustering, M12 acted selectively as a dominant negative (DN) inhibitor of pSMAC formation, an effect that was paralleled by a DN effect on interleukin-2 production. ADAP also colocalized with LFA-1 at the immunological synapse. Our findings identify ADAP–SLP-76 binding as a signaling event that differentially regulates SMAC formation, and support a role for SMAC formation in T cell cytokine production.
Tuberculosis sanatorium regimen in the 1940s: a patient's personal diary
Authors: R. Hurt
Journal: Journal of the Royal Society of Medicine (2004)

This article reproduces extracts from a diary that was begun in 1944 and was written spontaneously as events and treatment permitted.The first part describes the thoughts and emotions of a professional woman of 32 who was suddenly separated from her husband, Bill, and fifteen-month-old baby, Mark.The second part narrates the strict routine of sanatorium treatment for pulmonary tuberculosis in the 1940s before the introduction of streptomycin therapy.The diary covers a period before the introduction of the National Health Service and gives an insight into the financial implications of medical practice at that time.References to family and current events have been excluded.
Risk Factors for Coronary Heart Disease in Type 1 Diabetic Patients in Europe
Authors: Sabita S. Soedamah-Muthu, Nish Chaturvedi, Monika Toeller, Barry Ferriss, Paolo Reboldi, Georges Michel, Christos Manes, John H. Fuller
Journal: Diabetes Care (2004)

OBJECTIVE—The goal of the study was to examine risk factors in the prediction of coronary heart disease (CHD) and differences in men and women in the EURODIAB Prospective Complications Study. RESEARCH DESIGN AND METHODS—Baseline risk factors and CHD at follow-up were assessed in 2,329 type 1 diabetic patients without prior CHD. CHD was defined as physician-diagnosed myocardial infarction, angina pectoris, coronary artery bypass graft surgery, and/or Minnesota-coded ischemic electrocardiograms or fatal CHD. RESULTS—There were 151 patients who developed CHD, and the 7-year incidence rate was 8.0 (per 1,000 person-years) in men and 10.2 in women. After adjustment for age and/or duration of diabetes, the following risk factors were related to CHD in men: age, GHb, waist-to-hip ratio (WHR), HDL cholesterol, smoking, albumin excretion rate (AER), and autonomic neuropathy. The following risk factors were related to CHD in women: age, systolic blood pressure (BP), fasting triglycerides, AER, and retinopathy. Multivariate standardized Cox proportional hazards models showed that age (hazard ratio 1.5), AER (1.3 in men and 1.6 in women), WHR (1.3 in men), smoking (1.5 in men), fasting triglycerides (1.3 in women) or HDL cholesterol (0.74 in women), and systolic BP (1.3 in women) were predictors of CHD. CONCLUSIONS—This study supports the evidence for a strong predictive role of baseline albuminuria in the pathogenesis of CHD in type 1 diabetes. Furthermore, sex-specific risk factors such as systolic BP, fasting triglycerides (or HDL cholesterol), and WHR were found to be important in the development of CHD.
Immunosuppressive Myeloid Cells Induced by Chemotherapy Attenuate Antitumor CD4+ T-Cell Responses through the PD-1–PD-L1 Axis
Authors: Zhi-Chun Ding, Xiaoyun Lu, Miao Yu, Henrique Lemos, Lei Huang, Phillip Chandler, Kebin Liu, Matthew Walters, Antoni Krasinski, Matthias Mack, Bruce R. Blazar, Andrew L. Mellor, David H. Munn, Gang Zhou
Journal: Cancer Research (2014)

In recent years, immune-based therapies have become an increasingly attractive treatment option for patients with cancer. Cancer immunotherapy is often used in combination with conventional chemotherapy for synergistic effects. The alkylating agent cyclophosphamide (CTX) has been included in various chemoimmunotherapy regimens because of its well-known immunostimulatory effects. Paradoxically, cyclophosphamide can also induce suppressor cells that inhibit immune responses. However, the identity and biologic relevance of these suppressor cells are poorly defined. Here we report that cyclophosphamide treatment drives the expansion of inflammatory monocytic myeloid cells (CD11b(+)Ly6C(hi)CCR2(hi)) that possess immunosuppressive activities. In mice with advanced lymphoma, adoptive transfer (AT) of tumor-specific CD4(+) T cells following cyclophosphamide treatment (CTX+CD4 AT) provoked a robust initial antitumor immune response, but also resulted in enhanced expansion of monocytic myeloid cells. These therapy-induced monocytes inhibited long-term tumor control and allowed subsequent relapse by mediating functional tolerization of antitumor CD4(+) effector cells through the PD-1-PD-L1 axis. PD-1/PD-L1 blockade after CTX+CD4 AT therapy led to persistence of CD4(+) effector cells and durable antitumor effects. Depleting proliferative monocytes by administering low-dose gemcitabine effectively prevented tumor recurrence after CTX+CD4 AT therapy. Similarly, targeting inflammatory monocytes by disrupting the CCR2 signaling pathway markedly potentiated the efficacy of cyclophosphamide-based therapy. Besides cyclophosphamide, we found that melphalan and doxorubicin can also induce monocytic myeloid suppressor cells. These findings reveal a counter-regulation mechanism elicited by certain chemotherapeutic agents and highlight the importance of overcoming this barrier to prevent late tumor relapse after chemoimmunotherapy.
Palmitoyl protein thioesterase-1 deficiency impairs synaptic vesicle recycling at nerve terminals, contributing to neuropathology in humans and mice
Authors: Sung-Jo Kim, Zhongjian Zhang, Chinmoy Sarkar, Pei-Chih Tsai, Yi-Ching Lee, Louis Dye, Anil B. Mukherjee
Journal: Journal of Clinical Investigation (2008)

Neuronal ceroid lipofuscinoses represent the most common childhood neurodegenerative storage disorders. Infantile neuronal ceroid lipofuscinosis (INCL) is caused by palmitoyl protein thioesterase-1 (PPT1) deficiency. Although INCL patients show signs of abnormal neurotransmission, manifested by myoclonus and seizures, the molecular mechanisms by which PPT1 deficiency causes this abnormality remain obscure. Neurotransmission relies on repeated cycles of exo- and endocytosis of the synaptic vesicles (SVs), in which several palmitoylated proteins play critical roles. These proteins facilitate membrane fusion, which is required for neurotransmitter exocytosis, recycling of the fused SV membrane components, and regeneration of fresh vesicles. However, palmitoylated proteins require depalmitoylation for recycling. Using postmortem brain tissues from an INCL patient and tissue from the PPT1-knockout (PPT1-KO) mice that mimic INCL, we report here that PPT1 deficiency caused persistent membrane anchorage of the palmitoylated SV proteins, which hindered the recycling of the vesicle components that normally fuse with the presynaptic plasma membrane during SV exocytosis. Thus, the regeneration of fresh SVs, essential for maintaining the SV pool size at the synapses, was impaired, leading to a progressive loss of readily releasable SVs and abnormal neurotransmission. This abnormality may contribute to INCL neuropathology.
Influence of Convection on the Diffusive Transport and Sieving of Water and Small Solutes across the Peritoneal Membrane
Authors: Ramzana B Asghar, Ann M Diskin, Patrik Spanel, David Smith, Simon J Davies
Journal: Journal of the American Society of Nephrology (2005)

The three-pore model of peritoneal membrane physiology predicts sieving of small solutes as a result of the presence of a water-exclusive pathway. The purpose of this study was to measure the diffusive and convective components of small solute transport, including water, under differing convection. Triplicate studies were performed in eight stable individuals using 2-L exchanges of bicarbonate buffered 1.36 or 3.86% glucose and icodextrin. Diffusion of water was estimated by establishing an artificial gradient of deuterated water (HDO) between blood/body water and the dialysate. (125)RISA (radio-iodinated serum albumin) was used as an intraperitoneal volume marker to determine the net ultrafiltration and reabsorption of fluid. The mass transfer area coefficient (MTAC) for HDO and solutes was estimated using the Garred and Waniewski equations. The MTAC of HDO calculated for 1.36% glucose and icodextrin were similar (36.8 versus 39.7 ml/min; P = 0.3), whereas for other solutes, values obtained using icodextrin were consistently higher (P < 0.05). A significant increase in the MTAC of HDO was demonstrated with an increase in the convective flow of water when using 3.86% glucose (mean value, 49.5 ml/min; P < 0.05). MTAC for urea was also increased with 3.86% glucose. The identical MTAC for water using 1.36% glucose and icodextrin indicates that diffusion is predominantly through small pores, whereas the difference in MTAC for the remaining solutes is a reflection of their sieving. The increase in the MTAC of water and urea associated with an increase in convection is most likely due to increased mixing within the interstitium.
Congruence of total and perfused capillary network in rat brains.
Authors: U Göbel, H Theilen, W Kuschinsky
Journal: Circulation Research (1990)

In awake normocapnic rats, the density of the total and of the perfused capillary network was determined in 10 brain areas. The density of perfused capillaries was measured by using fluorescein isothiocyanate (FITC) globulin or Evans blue as intravenous marker and by fluorescent microscopy. The density of morphologically existing capillaries was determined according to either the histochemical alkaline phosphatase method or a newly developed immunohistochemical fluorescent method that allows marking of the capillary wall constituent fibronectin with a primary antibody directed against fibronectin. This antibody is made visible by a second FITC-coupled antibody (indirect immunofluorescence). Comparison of perfused and existing capillary counts revealed high congruence when fluorescent results were compared. In contrast, the alkaline phosphatase technique yielded capillary counts that were consistently 30% lower than the fibronectin and the FITC globulin counts. The identity of the perfused and the morphologically existing capillary network could be confirmed by a newly developed double-staining technique. First, the perfused capillaries were quantified by intravascular Evans blue. Then, the existing capillaries were relocated in the same measuring field by the fibronectin technique. Such double staining resulted in identical capillary counts in 97% of all cases. The following conclusions have been reached: 1) Fluorescent methods show a perfusion of virtually all capillaries in the brain of the awake normocapnic rat. 2) The alkaline phosphatase technique appears to underestimate the capillary density in the rat brain.