tbuckley/cabot-search huggingface dataset:
Infarct Cavities in a Hepatic Allograft
Authors: J Ludwig, G J Gores
Journal: New England Journal of Medicine (1995)

Figure 1. A 49-year-old man underwent liver transplantation in 1989 for alcoholic cirrhosis. In 1994, ischemic cholangitis developed with strictures and signs of ascending cholangitis, leading to a second transplantation. Three weeks later, blood cultures were positive for Clostridium clostridiiforme. Angiography and ultrasonography revealed hepatic-artery thrombosis. A computed tomographic scan (Panel A) of the second allograft showed intrahepatic cavities. A culture from a cavity contained Enterococcus faecalis and coagulase-negative staphylococci. Because of these complications, the second allograft had to be removed. The specimen contained large, multiloculated ischemic infarcts with extensive central cavitation (Panel B). The patient is doing well . . .
Changing patterns and mortality of acute myocardial infarction in a coronary care unit.
Authors: D Hunt, G Sloman, D Christie, C Penington
Journal: BMJ (1977)

Three groups of patients who had been admitted to a coronary care unit with infarction at different periods since 1963 were reviewed to assess whether the outcome in such patients had improved over 12 years. There was a significant reduction in mortality among consecutive patients with mild or severe infarction between 1969-70 and 1974-5. Classifying the patients in all three groups according to their risk factors showed that for each risk factor mortality had decreased since 1963. The incidence of arrhythmias and conduction defects decreased between 1969-70 and 1974-5, and mortality among patients with each arrhythmia also fell. The reduction in mortality may reflect a changing pattern in the natural history of the disease as well as a benefit of improved treatment.
Language, cognition, and the nature of modularity: Evidence from aphasia
Authors: Rosemary Varley, Michael Siegal
Journal: Behavioral and Brain Sciences (2002)

We examine Carruthers’ proposal that sentences in logical form serve to create flexibility within central system modularity, enabling the combination of information from different modalities. We discuss evidence from aphasia and the neurobiology of input-output systems. This work suggests that there exists considerable capacity for interdomain cognitive processing without language mediation. Other challenges for a logical form account are noted.
High prevalence of thrombocytopenia in SLE patients with a high level of anticardiolipin antibodies combined with lupus anticoagulant
Authors: Junzo Nojima, Etsuji Suehisa, Hirohiko Kuratsune, Takashi Machii, Masayuki Toku, Hisato Tada, Kouzi Yamaguti, Takao Koike, Yuzuru Kanakura, Teruo Kitani, Nobuyuki Amino
Journal: American Journal of Hematology (1998)

The relationship between thrombocytopenia and the level of anticardiolipin antibodies (aCL) and/or the existence of lupus anticoagulant (LA) ware studied in 146 patients with systemic lupus erythematosus (SLE). These patients were divided into six groups: A, those LA positive with a high level of aCL (>10 U/ml) (10 cases); B, those LA positive with a low level of aCL (3–10 U/ml) (15 cases); C, those LA positive but aCL negative (<3 U/ml) (12 cases); D, LA negatives with a high level of aCL (12 cases); E, LA negatives with a low level of aCL (16 cases); and F, aCL and LA double negatives (81 cases). The prevalence of thrombocytopenia (platelet count ≦ 100 × 109/L) was by far the highest in group A (9/10 cases, 90.0%, P < 0.005, Fisher's exact probability test) as compared with group B (4/15 cases, 26.7%), group C (4/12 cases, 33.3%), group D (1/12 cases, 8.3%), group E (4/16 cases, 25.5%), and group F (9/81 cases, 11.1%). When the relationship between moderate thrombocytopenia and arterial or venous thrombosis was studied in these patients with SLE, thrombocytopenia was detected in 10 (83.3%, P < 0.005, Fisher's exact probability test) of 12 patients with arterial thrombosis; however, it was present in only 4 (23.5%) of 17 patients with venous thrombosis and in 14 (12.3%) of 114 patients without thrombosis. These findings suggest that a high aCL activity combined with LA positively reflects a high risk for both thrombocytopenia and arterial thrombosis. Am. J. Hematol 58:55–60, 1998. © 1998 Wiley-Liss, Inc.
Random suppression of T cells that bear specific T cell receptor Vβ sequences in adult T cell leukemia/lymphoma (ATLL) patients at each clinical stage: Carrier, smoldering, chronic, and acute
Authors: Koichi Ohshima, Junji Suzumiya, Masahiro Kikuchi, Morishige Takeshita, Kotaro Tashiro, Nobuhiro Kimura
Journal: American Journal of Hematology (1996)

Human T cell leukemia virus type I (HTLV-I) is associated with adult T cell leukemia/lymphoma (ATLL), which is well known as a T cell malignancy. In order to clarify whether HTLV-I plays a role as a virus-encoded superantigen in the neoplastic process, we examined the TCR Vβ families in the peripheral blood at four different clinical stages: carrier, smoldering leukemia, chronic leukemia, and acute leukemia. An increased number of CD4 T cells was found in each of the four clinical stages. However, we found neither uniform specific losses nor uniform clonal expansion of particular TCR Vβ gene families in any case from the four clinical stages. However, a suppression of the random TCR Vβ families was found. Our data did not therefore directly suggest the existence of a common superantigen model of HTLV-I which induces an increase in CD4 T cells. The random suppression in the TCR Vβ repertoire is most likely caused by the influence of HTLV-I neoplastic pathogenesis rather than by virus-encoded superantigens. In the patients with acute leukemia, one or two families of the Vβ repertoires were very strongly expressed, while in chronic leukemia, no such repertoire of strong expression was observed. The immunological reaction of the hosts might thus be different between the above described groups. © 1996 Wiley-Liss, Inc.
Doctor who injected adrenaline against advice found guilty of manslaughter
Authors: C. Dyer
Journal: BMJ (2009)

A doctor who killed a patient more than 10 years ago with an injection of adrenaline (epinephrine) against the advice of colleagues has been convicted of manslaughter and given a suspended jail sentence of six months.

Priya Ramnath, aged 40, walked free after the judge, Mrs Justice Rafferty, told her that the interests of justice did not require her to be sent to prison. The judge said that Dr Ramnath’s defining error was not to listen to a nurse working with her who had urged her not to give the injection to Patricia Leighton. “Arrogance has cost you your reputation,” she said.

Mrs Leighton, aged 51, who had arthritis, had been transferred to the intensive therapy unit of Stafford District General Hospital in septic shock after having a reaction to …
Surgery of the Biliary Tract
Authors: Richard B. Cattell, Kenneth W. Warren
Journal: New England Journal of Medicine (1956)

THIS survey is concerned with recent advances in the field of surgery of the gall bladder and bile ducts. The report is not limited to any rigid interval of time, but most of the references are to articles that have appeared within the last five years. The cumulative literature in this area is so extensive that comment is confined to papers that seemed to be of original or authoritative interest.In editorial assessment of much of the material referred to in this communication we have drawn upon our own clinical experience for comparison.AnatomyAn excellent book by Michels1 contains . . .
INHIBITORY AND STIMULATORY EFFECTS OF CONCANAVALIN A ON THE RESPONSE OF MOUSE SPLEEN CELL SUSPENSIONS TO ANTIGEN
Authors: Richard W. Dutton
Journal: The Journal of Experimental Medicine (1972)

The presence of concanavalin A (Con A) inhibits the immune response of mouse spleen cell suspensions to erythrocyte antigens, stimulates the incorporation of tritiated thymidine, and increases cell recovery. Con A also restores the depressed response of cell preparations treated to remove thymus-derived cells. The dose-response curve for all four effects shows peak activity at 2 microg/ml. The depressed in vitro response of spleen cell suspensions from adult thymectomized, irradiated, bone marrow-restored mice is also restored by Con A. Here the dose-response curve is quite different with activity over a much wider range of concentration. The restoration of thymus-derived cell-depleted cultures by Con A is inhibited by the addition of untreated, unirradiated, mouse spleen cell suspensions, but is not inhibited by untreated, irradiated cells. Small numbers of spleen cells that have been preincubated with Con A and washed will inhibit the response of fresh, untreated cells to antigen. If the mouse spleen cell suspensions are incubated for 24 hr before the addition of Con A, the response to antigen is no longer inhibited but is stimulated instead. The data are compatible with the hypothesis that there are at least two cell targets for the action of Con A. One cell, that mediates the inhibitor effect, is a short-lived, radiosensitive, thymus-derived cell. The other cell, that mediates the stimulating effect, cannot be identified from the data presented here but may also be of thymus origin on the basis of studies by other investigators.
IMMUNE RESPONSE TO A HAPTEN COUPLED TO A NONIMMUNOGENIC CARRIER
Authors: Jon R. Schmidtke, Frank J. Dixon
Journal: The Journal of Experimental Medicine (1972)

Cooperation between two or more cell types is an essential feature of the immune response to some antigens (1).These cell types are commonly referred to as thymus derived (T) and bone marrow derived (B).Furthermore, in the immune response to a hapten bound to a carrier protein these two cell types perform quite separate and distinct cooperative functions (2-5).The T cell is responsible for recognition of the carrier and has been termed the helper cell (5, 6) ; the B cell synthesizes antibody to the hapten.In another series of observations lipopolysaccharide (LPS), endotoxin, from Gram-negative bacteria was shown to alter thymic-deficient mice so that they could respond with antibody formation to thymic-dependent antigens.Mice that were thymectomized, lethally irradiated, and bone marrow reconstituted (TxB) responded to heterologous red cells coated with LPS (7).Also, lethally irradiated, bone marrow reconstituted mice responded to injections of sheep red blood cells (SRBC) when accompanied by LPS (8).LPS alone acted as a mitogen on B cells (9, 10).Thus, when antigen is present LPS might substitute for T cell function by direct stimulation of B cells which are then able to form antibody to the antigen resulting in an immune response.If a h a p t e n such as trinitrophenyl ( T N P ) were coupled to a n o n i m m u n o g e n i c carrier such as isologous mouse red blood cells ( M R B C ) , no i m m u n e response would be expected from the injected host because the T, or helper, cell would not recognize M R B C as a foreign carrier.However, if L P S did stimulate B cells directly, it m i g h t be hypothesized that, in the presence of L P S , an i m m u n e response to a hapten on a n o n i m m u n o g e n i c carrier could be induced.
How To Do It: Participate in an international conference
Authors: W. A M Cutting
Journal: BMJ (1995)

Attending an international conference should be instructive and fun.But it can also be alarming and lonely.Although participating in scientific conferences is now almost essential to medical career development, no medical school describes how to make the most of the opportunity as part of its curriculum.Here are some hints on how to get yourself organised so that the experience can be both scientifically productive and enjoyable.In essence, you should travel, see places, meet people, make friends, and identify one or two ideas that you can apply in your own work or research. Objectives ofparticipating in a conferenceEducation is the most obvious objective, the one that you declare on the application form even if the location is the Bahamas and the company you have in mind is not purely professional.However, brushing up on forgotten facts and obtaining the latest information in your specialty may seem more attractive away from the pressures of your own job.
Hepatitis B virus-DNA level and basal core promoter A1762T/G1764A mutation in liver tissue independently predict postoperative survival in hepatocellular carcinoma
Authors: Chau-Ting Yeh, Mary So, Jennifer Ng, Han-Wen Yang, Ming-Ling Chang, Ming-Wei Lai, Tse-Ching Chen, Chun-Yen Lin, Ta-Sen Yeh, Wei-Chen Lee
Journal: Hepatology (2010)

Hepatitis B virus (HBV) is a major etiological factor of hepatocellular carcinoma (HCC). However, the postoperative prognostic value of the virological factors assayed directly from liver tissue has never been investigated. To address this issue, 185 liver samples obtained from the noncancerous part of surgically removed HBV-associated HCC tissues were subjected to virological analysis. Assayed factors included the amount of HBV-DNA in the liver tissues; genotype; and the presence of the HBV precore stop codon G1896A mutation, basal core promoter A1762T/G1764A mutation, and pre-S deletions/stop codon mutation. All virological factors and clinicopathological factors were subjected to Cox proportional hazard model analysis to estimate postoperative survival. It was found that an HBV-DNA level >3.0 × 107 copies/g of liver tissue and the presence of the basal core promoter mutation independently predicted disease-free (adjusted hazard ratio 1.641 [95% confidence interval (CI) 1.010-2.667] and 2.075 [95% CI 1.203-3.579], respectively) and overall (adjusted hazard ratio 2.807 [95% CI 1.000-7.880] and 5.697 [95% CI 1.678-19.342], respectively) survival. Kaplan-Meier survival analysis indicated that in-frame, short stretch (<100 bp) pre-S deletions, but not large fragment (>100 bp) pre-S deletions, were significantly associated with poorer disease-free (P = 0.005) and overall (P = 0.020) survival. A hot deletion region located between codons 107 and 141 of the pre-S sequence was identified for the short stretch pre-S deletion mutants. Conclusion: The amount of HBV-DNA in liver tissue and the presence of the basal core promoter mutation were two independent predictors for postoperative survival in HCC. A short stretch pre-S deletion located between codons 107 and 141 was strongly associated with a poorer postoperative prognosis. (Hepatology 2010)
PSYCHIATRIC DISORDERS IN MULTIPLE SCLEROSIS
Authors: FREDERICK LEMERE
Journal: American Journal of Psychiatry (1966)

The incidence of psychiatric disorders in multiple sclerosis is higher than is generally recognized. The majority of multiple sclerosis patients show emotional instability, denial, personality disintegration and, in the late stages, deterioration. The emotional instability is manifested by irritability, anxiety and depression, as well as euphoria, even to the extent of a manic or depressive psychosis. Denial is manifested by querulousness and projection of frustration and hostility onto other people, or by unrealistic optimism. Personality disintegration is manifested by subjectivity, lability, inappropriateness and poor coordination of emotional reactions with the rest of the personality and the reality of the situation. The organic interruption of subcortical pathways by demyelinization produces variable loss of emotional control and disorganization of the total personality. This threat to personality functioning produces the compensatory psychological defense mechanisms of denial and projection. Emotional instability may precede the onset of neurologic findings, and the final diagnosis may be obscure for months or years. Although emotional stress does not cause multiple sclerosis, it can precipitate exacerbations and have a deleterious effect on the course of the disease. Because there is no definitive treatment, psychotherapy is an important, if not the most important, part of the treatment of multiple sclerosis. Psychiatrists are, therefore, especially qualified to treat patients with multiple sclerosis.
Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.
Authors: W Ptak, D Rozycka, P W Askenase, R K Gershon
Journal: The Journal of Experimental Medicine (1980)

Three outcomes pertinent to contact sensitivity (CS) follow immunization with various forms of trinitrophenylated (TNP) substrates: (a) specific immunological unresponsiveness for CS is induced when immunization favors activation of splenic suppressor cells. This state is achieved by intravenous injection of trinitrophenyl-conjugated to various types of cells, such as peritoneal exudate cells (PEC). (b) A short-lived or evanescent form of CS is induced when immunization reduces activation of the suppressor circuit. This can be achieved by subcutaneous immunization with trinitrophenyl conjugated to syngeneic PEC, by pretreatment with cyclophosphamide to diminish suppression before intravenous immunization, or by altering the mode of antigen presentation by using TNP-substrate that has undergone phagocytosis. (c) A long-lived form of CS is induced when trinitrophenyl is presented to the immune system on skin cells either by contact skin painting with reactive trinitrophenyl, or by subcutaneous, or even intravenous injection of trinitrophenyl-conjugated epidermal cells. In fact, trinitrophenyl-conjugated epidermal cells induced CS even when the suppressor circuit was activated by intravenous coadministration of TNP-PEC. This implies that antigen presentation on epidermal cells induces sensitized cells that are relatively resistant to suppression. The cell type(s) in the skin that are primarily responsible for this potent form of antigen presentation are most likely Langerhans cells, because they can be concentrated by virtue of their Fc receptors and they are Ia positive. Thus, both the anatomical site where antigen is first encountered by the immune apparatus, as well as the nature of the cells which present the antigen, determine whether a CS response will ensue, as well as whether it will be evanescent or long-lasting.
Overdose How excessive government regulation stifles pharmaceutical innovation
Authors: David B. Ross
Journal: Journal of Clinical Investigation (2007)

In Overdose: how excessive government regulation stifles pharmaceutical innovation, Richard Epstein confronts the many problems besieging pharmaceutical companies — accusations of unethical and illegal marketing practices, plummeting credibility with health care providers and patients, and calls for more rigorous government regulation — and declares the industry the victim of creeping government paternalism. Epstein, a law professor at the University of Chicago and a consultant to pharmaceutical companies, ascribes the industry’s woes to too much government scrutiny. In eighteen chapters discussing intellectual property issues, FDA regulation of drug development and marketing, and tort claims related to drug safety, Epstein advocates one consistent solution: replace government oversight of drug companies, wherever possible, with marketplace success or failure. He describes the FDA as an economically inefficient behemoth that deprives patients of the freedom to take whatever drugs they think will help them. He argues that drug manufacturers should be free to market their products without first proving that they work — in essence, dismantling the current U.S. drug regulatory framework.
Moxalactam and Hemorrhage
Authors: STEPHEN R. JONES
Journal: Annals of Internal Medicine (1983)

Letters and Corrections1 July 1983Moxalactam and HemorrhageSTEPHEN R. JONES, M.D., ROBERT C. KIMBROUGH III, M.D.STEPHEN R. JONES, M.D.Search for more papers by this author, ROBERT C. KIMBROUGH III, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-99-1-126_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Bleeding disorders associated with antibiotic treatment may be due to distinct pathophysiologic events (1). Platelet functional defects caused by beta-lactam antibiotic agents have been well documented (2). Bleeding difficulties in patients receiving moxalactam, a new beta-lactam antibiotic agent, have been reported. Both hypoprothrombinemia and platelet abnormalities have been implicated as the cause of bleeding (3). The manufacturer states that the reports of bleeding difficulties in patients receiving moxalactam are difficult to evaluate because of complex underlying illnesses and multiple drug treatment (4). We report the case of a patient with diverticulitis who received moxalactam as single-drug therapy...References1. Antimicrobials and hemostasis [Editorial]. Lancet. 1983;1:510-1. MedlineGoogle Scholar2. BROWN C, NATELSON E, and BRADSHAW M. The hemostatic defect produced by carbenicillin. N Engl J Med. 1974;291:265-70. CrossrefMedlineGoogle Scholar3. NEU H. Adverse effects of new cephalosporins [Letter]. Ann Intern Med. 1983;98:415. LinkGoogle Scholar4. KAMMER R. Antibiotic-Associated Coagulopathy. Indianapolis, Indiana: Lilly Research Laboratories; 1983. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: STEPHEN R. JONES, M.D.; ROBERT C. KIMBROUGHIII, M.D.Affiliations: Good Samaritan Hospital & Medical Center Portland, OR 97210 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byImpaired hemostasis caused by beta-lactam antibioticsCefoperazone-Induced CoagulopathyAutoimmune Diseases of the Liver: Chronic Active Hepatitis and Primary Biliary CirrhosisMoxalactam Disodium-Induced Pulmonary HemorrhageSevere Bleeding Diathesis Associated with Moxalactam AdministrationNEW EXAMPLES OF VITAMIN K-DRUG INTERACTION 1 July 1983Volume 99, Issue 1Page: 126-126KeywordsAntibioticsDiverticulitisDrugsHemorrhagePlatelets ePublished: 1 December 2008 Issue Published: 1 July 1983 PDF downloadLoading ...
Electronic Fetal Monitoring
Authors: Stephen B. Thacker
Journal: JAMA (1981)

<h3>To the Editor.—</h3> We are writing in reference to the SPECIAL COMMUNICATION, "Impact of Electronic Fetal Monitoring on Obstetric Management" by Orvan W. Hess, MD (1980;244:682). Dr Hess' review is incomplete and biased, as well as inaccurate in some instances, recurrently demonstrating his position as an advocate of universal electronic fetal monitoring (EFM). It is difficult, for example, to understand why he omitted results from three of the four randomized controlled clinical trials (RCTs) of EFM.<sup>1-3</sup>He also inappropriately labeled Dr Wennberg's study an RCT (Dr Hess' reference 15). Dr Hess alludes to our work several times but fails to reference articles that appear in the scientific literature.<sup>4-6</sup>We think that it is only fair to offer readers the opportunity to judge what we have written and draw their own conclusions. After thorough review of the issues involved in EFM, we concur with the conclusion of the
FATAL PULMONARY EMBOLISM FOLLOWING VARICOSE VEIN INJECTION
Authors: Eugene F. Traub
Journal: JAMA (1942)

<h3>To the Editor:—</h3> Drs. Vaughn and Lees have contributed much to medical science by publishing and evaluating a case of "Fatal Pulmonary Embolism Following Varicose Vein Injection" (The Journal, April 11, p. 1293). They deserve the highest appreciation for their honesty and courage. The mechanism of occlusion of the vein after the injection of different obliterating solutions has been studied microscopically by many authors (McPheeters, H. O.: Injection Treatment of Varicose Veins, Philadelphia, F. A. Davis Company, 1938, chapter 29, pp. 133-145). It requires several days' time from the onset of the injury of the endothelial lining of the varicose vein to the point at which the whole lumen of the vein is tightly filled with a well attached thrombus. As a rule, after the injection of the sclerosing solution not the entire endothelial lining of the vein is injured uniformly. Islands of destroyed endothelium have been found with stratified