tbuckley/cabot-search huggingface dataset:
Aggressive growth of epithelial carcinomas following treatment with nucleoside analogues
Authors: Christian Rifbjerg Larsen, Per Boye Hansen, Nielsaage Tøffner Clausen
Journal: American Journal of Hematology (2002)

Abstract Two patients, one with B‐cell chronic lymphocytic leukemia (CLL) and one with hairy‐cell leukemia (HCL), were treated with immunosuppressive chemotherapy. The patient with CLL was a 54‐year‐old female, who had had a squamous cell carcinoma (SCC) excised from her forehead 5 months before receiving the first course of fludarabine. During the fludarabine treatment, the patient developed a local SCC relapse and metastases in the neck. The carcinoma was treated by excision and radiotherapy, and further fludarabine treatment was withheld. Nevertheless, the SCC metastasized aggressively and the patient died 3 months after the start of fludarabine treatment, primarily due to respiratory failure. The autopsy revealed heavy SCC infiltrations involving the lungs, pleura, mediastinum, pericardium, and liver. The patient with HCL was a 69‐year‐old male. At the time of diagnosis of HCL, the patient had two solid tumors in the liver containing poorly differentiated epithelial carcinoma cells of unknown origin. During treatment with 2‐chlorodeoxyadenosine (2CdA), the tumors in the liver rapidly spread in multiple intrahepatic metastases, followed by liver failure and death within 1 month. Fludarabine and 2CdA cause a substantial suppression of all lymphocyte subsets, in particular the T‐cell line. T‐lymphocytes are believed to be responsible for the usually slow growth and the low metastatic rate of the SCC skin lesions. It is therefore assumed that fludarabine and 2CdA in these two cases triggered an exacerbation of both tumors due to the T‐cell depletion. Am. J. Hematol. 70:48–50, 2002. © 2002 Wiley‐Liss, Inc.
Case 39-1976
Authors: Richard C. Cabot, Robert E. Scully, James J. Galdabini, Betty U. McNeely, Edwin O. Wheeler, Stanley J. Robboy
Journal: New England Journal of Medicine (1976)

Presentation of CaseA 54-year-old man was admitted to the hospital because of aortic stenosis.He was well until two years previously, when glycosuria was found. Tolbutamide was administered briefly; he lost 24 kg on a weight-reduction diet, and the medication was discontinued. He was then well until five months before entry, when exertional syncope occurred, without sphincter incontinence. Syncope recurred, again associated with severe exertion, and he entered another hospital, where digoxin was begun. He had two more bouts of exertional syncope and two and a half months before entry was admitted to a second hospital, where right-sided and . . .
THE ELECTROCARDIOGRAM IN CLINICAL DIAGNOSIS
Authors: L. F. BARKER
Journal: JAMA (1910)

In the study of cardiac function by instrumental means, a number of methods have been employed, each of which has yielded information which was not obtainable with the others. The study of the arterial pulse has taught us much regarding the relation between cardiac output and peripheral resistance; the study of the blood-pressure has taught us to estimate accurately the force of the heart-beat and the factors which control it; the<i>x</i>-ray examination has given us a means of observing the changes in volume of the four chambers of the heart; and the study of the venous pulse has enabled us to detect many changes in the origin and propagation of the cardiac contraction. In spite of the great additions which these methods have made to the study of the heart, there is still much information that they are unable to
Inflammation and Activated Innate Immunity in the Pathogenesis of Type 2 Diabetes
Authors: John C. Pickup
Journal: Diabetes Care (2004)

There is increasing evidence that an ongoing cytokine-induced acute-phase response (sometimes called low-grade inflammation, but part of a widespread activation of the innate immune system) is closely involved in the pathogenesis of type 2 diabetes and associated complications such as dyslipidemia and atherosclerosis. Elevated circulating inflammatory markers such as C-reactive protein and interleukin-6 predict the development of type 2 diabetes, and several drugs with anti-inflammatory properties lower both acute-phase reactants and glycemia (aspirin and thiazolidinediones) and possibly decrease the risk of developing type 2 diabetes (statins). Among the risk factors for type 2 diabetes, which are also known to be associated with activated innate immunity, are age, inactivity, certain dietary components, smoking, psychological stress, and low birth weight. Activated immunity may be the common antecedent of both type 2 diabetes and atherosclerosis, which probably develop in parallel. Other features of type 2 diabetes, such as fatigue, sleep disturbance, and depression, are likely to be at least partly due to hypercytokinemia and activated innate immunity. Further research is needed to confirm and clarify the role of innate immunity in type 2 diabetes, particularly the extent to which inflammation in type 2 diabetes is a primary abnormality or partly secondary to hyperglycemia, obesity, atherosclerosis, or other common features of the disease.
HCV replication suppresses cellular glucose uptake through down-regulation of cell surface expression of glucose transporters
Authors: Daisuke Kasai, Tetsuya Adachi, Lin Deng, Motoko Nagano-Fujii, Kiyonao Sada, Masanori Ikeda, Nobuyuki Kato, Yoshi-Hiro Ide, Ikuo Shoji, Hak Hotta
Journal: Journal of Hepatology (2009)
Association Between Glycemia and Mortality in Diabetic Individuals on Renal Replacement Therapy in the U.K.
Authors: Amanda Adler, Anna Casula, Retha Steenkamp, Damian Fogarty, Martin Wilkie, Laurie Tomlinson, Dorothea Nitsch, Paul Roderick, Charles R.V. Tomson
Journal: Diabetes Care (2014)

In the U.K., one-third of patients receiving treatment with dialysis have diabetes. Guidelines from organizations representing patients with renal disease or diabetes advocate tight glycemic control in patients with end-stage renal disease, despite glucose-lowering trials having excluded these patients.Using national U.K. Renal Registry data, we tested whether glycemia as measured by hemoglobin (Hb) A(1c) (HbA(1c)) level is associated with death in adults with diabetes starting hemodialysis or peritoneal dialysis between 1997 and 2006, and observed for at least 6 months. Of 7,814 patients, we excluded those who had died within 6 months; had received transplants; were lost/recovered; or lacked measures of HbA1c, ethnicity, or Hb. Categorizing HbA1c measured in the first 6 months of starting dialysis as <6.5% (<48 mmol/mol), 6.5-7.4% (48-57 mmol/mol) (reference value), 7.5-8.4% (58-68 mmol/mol), and ≥8.5% (≥69 mmol/mol), we adjusted in proportional hazards models for age, sex, ethnicity, deprivation, year, dialysis type, and Hb, and tested for interactions.Of 3,157 patients observed for a median time of 2.7 years, 1,688 died. For patients ≥60 years of age, we found no association between HbA1c and death; among younger patients, relative to those with HbA(1c) values 6.5-7.4%, the hazard ratio for HbA(1c) level 7.5-8.4% was 1.2 (95% CI 0.9-1.5), and for HbA(1c) level >8.5% was 1.5 (1.2-1.9). The projected difference in median survival time between younger patients with a reference HbA1c value versus >8.5% was 1 year.In the absence of trials, and confounding notwithstanding, these observational data support improved glycemic control in younger patients prior to and during dialysis.
Cardiopulmonary resuscitation/Emergencies
Authors: A. Kalloghlian, N. T. Matthews, E. Quiňones, L. Yacelga, S. Campos, A. Dávalos, M. Cruz, Niranjan Kissoon, Talaat Abdelmoniem, Lindsey Johnson, Mariano Fiallos, Suzanne Murphy, Shala Masood, M. Tzareva, R. Nedialkova, B. Gerbaka, C. Hakme, C. Akatcherian, M. J. Ruíz López, J. Barja, M. A. García Teresa, B. Osona, I. Hinojosa, A. Ruíz Beltrán
Journal: Intensive Care Medicine (1996)
Adenocarcinoma of Small Intestine in Father and Daughter
Authors: D. B. E. Foster
Journal: BMJ (1944)

secretion.It is true that several cases have been reported in which unilateral infected nephrolithiasis has caused a general rise of blood pressure.It probably acts by effecting a chemical constriction of all arterioles, including efferent glomerular arterioles but excluding afferent arterioles (Pickering, 1943).Thus the glomerular pressure in the sound kidney should rise and, if anything, more urea should be excreted, because urea is probably secreted by a process of mechanical glomerular filtration and not by tubular secretion.In this patient another unknown mechanism -must have been involved, because there was no general rise of blood pressure and there was lessened urea excretion as judged by his raised blood urea.Summary A mobile renal calculus, according to its different positions, so changed the clinical picture that the following conditions were successively diagnosed: appendicitis, gall-stones, renal calculus, malaria.During the phase of infected early hydronephrosis the opposite healthy kidney was affected; no explanation has been found for this.A method is described for accurately locating the stone at operation.Thus only a small incision in the renal substance was needed; this minimized the risk of gross post-operative haemorrhage.
Stroke in a young man
Authors: D. Narayanan, A. Luvai, R. Barski, R. Sharma
Journal: BMJ (2013)

A 27 year old man was referred to the clinic for further evaluation after he developed sudden left sided facial droop, right sided visual loss, and slurred speech. Two months previously he had elective corneal transplantation of the left eye. At the age of 22 years he had experienced an episode of sagittal sinus thrombosis for which he had received short term anticoagulation, but he had made a full recovery. 

Investigations excluded JAK2 mutation, paroxysmal nocturnal haemoglobinuria, and thrombophilia. He had bilateral keratoconus and had high myopia. He was a non-smoker, did not drink alcohol, and had no family history suggestive of hypercoagulable states. His height was 175 cm and he had a body mass index of 23. 

Physical examination showed right sided central visual loss and left sided upper motor neurone facial palsy. A cranial computed tomogram and carotid Doppler study confirmed right hemisphere cerebral infarction as a result of a right cranial internal carotid artery thrombus. The visual loss was attributed to a retinal artery thrombosis. 

He was treated with anticoagulants. A secondary screen for stroke showed a plasma total homocysteine concentration of 341 µmol/L (reference range <18; 1 µmol/L=0.14 mg/L). Further investigations showed methionine concentration of 234 µmol/L (reference range 9-45; 1 µmol/L=0.01 mg/L) and urinary homocysteine concentration of 26 µmol/mmol creatinine (reference range <1).



### 1 What is the differential diagnosis for stroke in young patients?

#### Short answer

Strokes can be ischaemic or haemorrhagic. Ischaemic strokes are broadly classified as embolic or …
1034 COMBINATION OF TWO COMPLEMENTARY NUCLEOTIDE ANALOGUES PSI-7977 AND PSI-938 EFFECTIVELY CLEARS WILD TYPE AND NS5B:S282T HCV REPLICONS – COMPARISON WITH COMBINATIONS OF OTHER ANTIVIRAL COMPOUNDS
Authors: V. Zennou, A.M. Lam, M. Keilman, H.M. Micolochick Steuer, C. Espiritu, M.J. Sofia, P.G. Reddy, W. Chang, S. Rachakonda, M.J. Otto, P.A. Furman
Journal: Journal of Hepatology (2010)
Segregation and black/white differences in exposure to air toxics in 1990.
Authors: Russ Lopez
Journal: Environmental Health Perspectives (2002)

I examined non-Hispanic Black and non-Hispanic White differences in exposure to noncriteria air pollutants in 44 U.S. Census Bureau-defined metropolitan areas with populations greater than one million, using data on air toxics concentrations prepared for the U.S. Environmental Protection Agency as part of its Cumulative Exposure Project combined with U.S. census data. I measured differences in exposure to air toxics through the calculation of a net difference score, which is a statistical measure used in income inequality analysis to measure inequality over the whole range of exposures. The scores ranged from 11.52 to 83.60. In every metropolitan area, non-Hispanic Blacks are more likely than non-Hispanic Whites to be living in tracts with higher total modeled air toxics concentrations. To assess potential reasons for such a wide variation in exposure differences, I performed a multiple regression analysis with the net difference score as the dependent variable. Independent variables initially included were as follows: the dissimilarity index (to measure segregation), Black poverty/White poverty (to control for Black/White economic differences), population density and percentage of persons traveling to work who drive to work (alone and in car pools), and percentage of workforce employed in manufacturing (factors affecting air quality). After an initial analysis I eliminated from the model the measures of density and the persons driving to work because they were statistically insignificant, they did not add to the predictive power of the model, and their deletion did not affect the other variables. The final model had an R(2) of 0.56. Increased segregation is associated with increased disparity in potential exposure to air pollution.
Observations During Hypervolemic Hemodilution of Patients With Acute Focal Cerebral Ischemia
Authors: James H. Wood
Journal: JAMA (1982)

Infusions of 5% albumin and/or dextran 40 in nine patients with acute ischemic neurological deficits reduced mean hematocrit values from 41% to 32%, raised mean central venous pressure from 4 to 12 cm H2O, and reduced mean arterial BP from 101 to 94 mm Hg. Six alert patients had ischemic structural damage on cranial computed tomography. All six alert patients with upper arm paresis objectively improved and two others with only dysphasia also improved within 24 hours after infusion initiation. Although the improvement in two patients seemed to be temporarily dependent on the continuing of the infusion, all eight alert patients were eventually weaned without loss of regained function. This report of neurological improvement during hypervolemic hemodilution suggests that augmentation of collateral perfusion secondary to reduced blood viscosity may rapidly relieve cerebral ischemia, impede infarction, and allow time for compensatory mechanisms to maintain blood flow above ischemic thresholds.
Appendectomies During Physicians' Boycott
Authors: Vergil N. Slee
Journal: JAMA (1980)

ABSTRACT To the Editor.— The recent article by Pantell and Irwin (242:1627, 1979) reported results of a study on the incidence and quality of appendectomies performed during the May 1975 anesthesiologists' boycott in the San Francisco Bay area. Compared with May 1974 and January to June 1975, they found no change in the number of appendices removed during the boycott month. In another study (PAS Reporter 14:13, November 1976; Am Coll Surg Bull 61:18, 1976), the Commission on Professional and Hospital Activities (CPHA) examined the boycott's effect on the total number of patients operated on in 21 San Francisco Bay area hospitals participating in the Professional Activity Study (PAS). The PAS data showed a definite decrease in the number of patients operated on during May 1975 and most of the remainder of 1975, compared with the corresponding months of 1974. The number of patients operated on for each month of 1975
Vitamins C and E prevent endothelial VEGF and VEGFR-2 overexpression induced by porcine hypercholesterolemic LDL
Authors: J RODRIGUEZ, B NESPEREIRA, M PEREZILZARBE, E EGUINOA, J PARAMO
Journal: Cardiovascular Research (2004)

Objective: Vascular endothelial growth factor (VEGF) is believed to play a role in the development of atherosclerosis and has been found to be increased in hypercholesterolemia. We examined the hypothesis that endothelial VEGF and VEGF receptor-2 (VEGFR-2) expression is upregulated by hypercholesterolemic low-density lipoprotein (LDL) and, because it could be driven by oxidative stress, we tested whether vitamin C and E supplementation could modulate it. Methods: Native LDL were characterized after isolation from adult normal (C-LDL), hypercholesterolemic (HC-LDL) and hypercholesterolemic mini-pigs receiving vitamins C and E (HCV-LDL). VEGF, VEGFR-2, HIF-1α and superoxide anion (O2−) productions were measured in porcine coronary endothelial cells (ECs) incubated for 48 h with native LDL. The effect of exogenous ascorbic acid and α- or β-tocopherol was also studied. Results: HC-LDL, with high cholesterol (P<0.05) and reduced tocopherol/cholesterol ratio (P<0.05), increased significantly VEGF and VEGFR-2 (p<0.001) in EC, associated with higher O2− and HIF-1α expression, in comparison with C-LDL and HCV-LDL. The addition of vitamin C and α- or β-tocopherol to the culture medium prevented the induction of VEGF and VEGFR-2 expression by HC-LDL, both at mRNA and protein levels. Conclusions: Our data suggest HC-LDL induce endothelial VEGF and VEGFR-2 overexpression at least by increasing oxidative stress, and HIF-1α is one of the signaling mechanisms involved. Prevention of VEGF and VEGFR-2 upregulation could help explain the beneficial effects of vitamins C and E in hypercholesterolemia-induced experimental atherosclerosis.
Ragweed Allergy Immunotherapy Tablet Reduces Use of Ocular Antihistamines in Patients with Ragweed Pollen–Induced Allergic Rhinoconjunctivitis
Authors: David I. Bernstein, Hendrik Nolte, Peter Creticos, Amarjot Kaur, Nancy Liu, Gary D. Berman, Jacques Hebert, Jennifer Maloney
Journal: Journal of Allergy and Clinical Immunology (2013)
Interleukin-13–regulated M2 Macrophages in Combination with Myeloid Suppressor Cells Block Immune Surveillance against Metastasis
Authors: Pratima Sinha, Virginia K. Clements, Suzanne Ostrand-Rosenberg
Journal: Cancer Research (2005)

Abstract CD1-deficient mice reject established, disseminated 4T1 metastatic mammary cancer and survive indefinitely if their primary mammary tumors are surgically removed. This highly effective immune surveillance is due to three interacting mechanisms: (a) the generation of inducible nitric oxide synthase (iNOS)–producing M1 macrophages that are tumoricidal for 4T1 tumor cells; (b) a rapid decrease in myeloid-derived Gr1+CD11b+ suppressor cells that are elevated and down-regulate the CD3ζ chain when primary tumor is present and that suppress T cells by producing arginase; and (c) production of activated lymphocytes. Macrophages from wild-type BALB/c mice are polarized by interleukin-13 (IL-13) towards a tumor-promoting M2 phenotype, thereby inhibiting the generation of tumoricidal M1 macrophages. In contrast, CD1−/− mice, which are deficient for IL-13 because they lack IL-13–producting NKT cells, generate M1 macrophages that are cytotoxic for 4T1 via the production of nitric oxide. Although tumoricidal macrophages are a necessary component of immune surveillance in CD1−/− mice, they alone are not sufficient for tumor resistance because IL-4Rα−/− mice have M1 macrophages and retain high levels of myeloid suppressor cells after surgery; in addition, they are susceptible to 4T1 metastatic disease. These results show that effective immune surveillance against established metastatic disease is negatively regulated by IL-13 and requires the induction of tumoricidal M1 macrophages and lymphocytes combined with a reduction in tumor-induced myeloid suppressor cells. (Cancer Res 2005; 65(24): 11743-51)
Chronic dynamic exercise improves a functional abnormality of the G stimulatory protein in cardiomyopathic BIO 53.58 Syrian hamsters.
Authors: T Tomita, T Murakami, T Iwase, K Nagai, J Fujita, S Sasayama
Journal: Circulation (1994)

BACKGROUND The effects of chronic exercise training on myocardial contractility and beta-adrenergic signal transduction in hearts with left ventricular dysfunction have not been determined. METHODS AND RESULTS Fourteen-week-old cardiomyopathic BIO 53.58 and normal F1B Syrian hamsters underwent 10 weeks of treadmill training and were compared with 24-week-old BIO 53.58 and F1B untrained controls. Left ventricular isovolumic maximum positive dP/dt and peak developed pressure were significantly lower in BIO 53.58 than in F1B controls. Exercise training improved left ventricular contractile indices in BIO 53.58 but not F1B hamsters. The left ventricular beta-adrenergic receptor number (Bmax) was similar in BIO 53.58 and F1B controls. Basal adenylate cyclase activity (ACA) and ACAs stimulated by isoproterenol, 5'-guanylylimidodiphosphate (GppNHp), sodium fluoride, and forskolin were significantly lower in BIO 53.58 than in F1B controls. The functional activity of stimulatory guanine nucleotide-binding protein (Gs), as determined by reconstitution with S49 lymphoma cyc- cell membranes, was significantly lower in BIO 53.58 controls. After 10 weeks of exercise training, Bmax and basal and isoproterenol-stimulated ACAs were unchanged in either BIO 53.58 or F1B hamsters compared with controls. However, in F1B hamsters, training decreased ACAs stimulated by GppNHp, sodium fluoride, and forskolin, with a reduced functional activity of Gs. In contrast, these ACAs increased significantly in association with an enhanced Gs activity in cardiomyopathic BIO 53.58 hamsters after training. CONCLUSIONS Chronic exercise training does not change receptor-mediated beta-adrenergic responsiveness in either F1B or BIO 53.58 hamsters. However, exercise training reduces Gs activity in normal F1B hamsters and improves the functional abnormality of Gs in cardiomyopathic BIO 53.58 hamsters. This improvement may potentially contribute to augmented left ventricular contractility in BIO 53.58 after training.
Is it lymphoma or lymphomatoid papulosis?
Authors: Marie-France Demierre, Lynne J. Goldberg, Marshall E. Kadin, Howard K. Koh
Journal: Journal of the American Academy of Dermatology (1997)

Distinguishing malignancy from premalignant conditions can be difficult.Controversy surrounds both the clinical and histologic criteria used to distinguish lymphomatoid papulosis, a benign disorder, from CD30 ÷ anaplastic large-cell lymphoma.Three case histories illustrate important points in categorizing different lymphoproliferative disorders as benign or malignant.We emphasize a multidisciplinary approach to improve diagnosis and patient management.(J Am Acad Dennatol 1997;36:765-72.)Distinguishing malignancy from premalignant conditions can be challenging.1-3 This distinction within cutaneous lymphoproliferative disorders has become even more difficult with the recent description of CD30 ÷ anaplastic large-cell lymphoma of the skin.First described 11 years ago, 4, 5 this lymphoma can arise either secondarily from lymphomatoid papulosis (LYP), 6, 7 a clinically benign disorder with histologic features suggestive of malignant lymphoma, 8 or as a result of a transformation from mycosis fungoides.9 It can also appear de novo, as primary cutaneous CD30 ÷ large-cell lymphoma, 9-H or as a primary systemic lymphoma.12 Because not all CD30 + large-cell lymphomas are anaplastic and the differentiation between morphologic subtypes of primary cutaneous CD30 ÷ large-cell lymphomas (anaplastic vs nonanaplastic) does not appear to be clinically or prognostically relevant, we will refer to this group as CD30 + large-cell lymphoma (CD30 ÷ L C L ) .13-15Controversy surrounds both the clinical and histologic diagnostic criteria used to distinguish LYP from CD30 ÷ LCL. 13 Both contain CD30 ÷ cells.There is no uniform approach to the management and treatment of these patients.A classification of primary cutaneous CD30 ÷ lymphoproliferative dis-