tbuckley/cabot-search huggingface dataset:
Large Cell Neuroendocrine Carcinoma of the Mediastinum with α-Fetoprotein Production
Authors: Ken Takezawa, Isamu Okamoto, Junya Fukuoka, Kaoru Tanaka, Hiroyasu Kaneda, Hisao Uejima, Hyung-Eun Yoon, Masami Imakita, Masahiro Fukuoka, Kazuhiko Nakagawa
Journal: Journal of Thoracic Oncology (2008)
Predicting in-hospital mortality in patients with cirrhosis: Results differ across risk adjustment methods
Authors: Robert P. Myers, Hude Quan, James N. Hubbard, Abdel Aziz M. Shaheen, Gilaad G. Kaplan
Journal: Hepatology (2008)

Abstract Risk-adjusted health outcomes are often used to measure the quality of hospital care, yet the optimal approach in patients with liver disease is unclear. We sought to determine whether assessments of illness severity, defined as risk for in-hospital mortality, vary across methods in patients with cirrhosis. We identified 258,731 patients with cirrhosis hospitalized in the Nationwide Inpatient Sample between 2002 and 2005. The performance of four common risk adjustment methods (the Charlson/Deyo and Elixhauser comorbidity algorithms, Disease Staging, and All Patient Refined Diagnosis Related Groups [APR-DRGs]) for predicting in-hospital mortality was determined using the c-statistic. Subgroup analyses were conducted according to a primary versus secondary diagnosis of cirrhosis and in homogeneous patient subgroups (hepatic encephalopathy, hepatocellular carcinoma, congestive heart failure, pneumonia, hip fracture, and cholelithiasis). Patients were also ranked according to the probability of death as predicted by each method, and rankings were compared across methods. Predicted mortality according to the risk adjustment methods agreed for only 55%–67% of patients. Similarly, performance of the methods for predicting in-hospital mortality varied significantly. Overall, the c-statistics (95% confidence interval) for the Charlson/Deyo and Elixhauser algorithms, Disease Staging, and APR-DRGs were 0.683 (0.680–0.687), 0.749 (0.746–0.752), 0.832 (0.829–0.834), and 0.875 (0.873–0.878), respectively. Results were robust across diagnostic subgroups, but performance was lower in patients with a primary versus secondary diagnosis of cirrhosis. Conclusion: Mortality analyses in patients with cirrhosis require sensitivity to the method of risk adjustment. Because different methods often produce divergent severity rankings, analyses of provider-specific outcomes may be biased depending on the method used. (Hepatology 2008.)
Expression of the intestinal T‐lymphocyte‐associated‐molecule recognized by the HML‐1 antibody on mononuclear cells from HTLV‐I‐infected subjects
Authors: Maki Otsuka, Shuichi Hanada, Atae Utsunomiya, Kenji Ishitsuka, Kimiharu Uozumi, Terukatsu Arima
Journal: American Journal of Hematology (1995)

Abstract We investigated the expression of a monoclonal antibody (HML‐1) defined antigen that appears on human intestinal T‐lymphocytes in HTLV‐I‐related disease. We studied 25 ATL, and 24 healthy HTLV‐I carriers. Patients with acute ATL showed a variety of the expression of the HML‐1 antigen (range 0.4–74.8%). HML‐1 expression on mononuclear cells (MNCs) in blood from patients with chronic ATL ranged from 1.7–43.6% (mean 13.5%). This level of expression was less than that of patients with acute ATL, but not significantly. In patients with smoldering ATL, the degree of patients with acute ATL, but not significantly. In patients with smoldering ATL, the degree of expression ranged from 1.6–13.3% (mean 8.0%). In contrast to patients wtih acute ATL, MNCs from patients with acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL), and B‐cell type chronic lymphocytic leukemia (B‐CLL) did not express the HML‐1 antigen, except for the 2 patients with ALL. Healthy HTLV‐I carriers and healthy controls also were negative for HML‐1 reactivity. In acute ATL, patients with gastrointestinal tract infiltration tended to have high expression of the HML‐1 epitope. After stimulation with phytohemagglutinin (PHA), healthy HTLV‐I carriers showed significantly increased expression of the HML‐1 epitope ( P &lt; 0.05). Recently, the β7 integrin family has been found to play a specific role in mucosal localization or adhesion, and HML‐1 protein was found to match the deduced β7 N‐terminal sequence. We propose that the cellular gene responsible for HML‐1 epitope expression may, like IL‐2, IL‐2R, etc., be transactivated by infection with HTLV‐I, and that HML‐1 antigen gene expression by HTLV‐I infection may lead to infiltration of ATL cells with highly expressed HML‐1 epitope into the gut mucosa.
FLAGELLUM OF THE MICROORGANISM OF RAT-BITE FEVER
Authors: Kiyohisa Adachi
Journal: The Journal of Experimental Medicine (1921)

The work of previous investigators was confirmed in that the microorganism of rat-bite fever was found to have flagella which are clearly visible by dark-field illumination and which can be stained. The best staining is obtained with alkalinized Akashi solution, which is a modification of Giemsa's solution; the vapor of osmic acid gives the best fixation. The number of demonstrable flagella seems to vary with the technique. Sometimes many slender flagella unite into one large one or one large flagellum divides into several smaller ones. It may be concluded that commonly many slender flagella occur at the ends and that these may unite into one or several large flagella. In the living microorganism the flagella appear to be spiral. Their form in fixed preparations depends upon the method employed. Some long forms have flagella arising at the middle of the body; this seems to indicate that division is transverse and not longitudinal as generally believed. The rigid body, the signs of transverse division, and multiple flagella seem to distinguish the forms reported here from spirochetes and indicate that they are spirilla.
Quantitation of mitral valve tenting in ischemic mitral regurgitation by transthoracic real-time three-dimensional echocardiography
Authors: Nozomi Watanabe, Yasuo Ogasawara, Yasuko Yamaura, Takahiro Kawamoto, Eiji Toyota, Takashi Akasaka, Kiyoshi Yoshida
Journal: Journal of the American College of Cardiology (2005)
Immunology and Immunopathology of the Liver and Gastrointestinal Tract
Authors: Frank L. Iber
Journal: JAMA (1990)

Immunology of the gastrointestinal tract has exploded with advances in understanding of both normal regulatory function and pathophysiology. This multiauthored book reviews the current status of this massive field. There are six subdivisions covering normal function and pathology. Five chapters address the specific barriers to and facilitators of the entry of antigens and their interaction with lymphocytes, the migration of lymphocytes, and the production of humoral antibodies and cellular immunity. There is a chapter on regulation, five chapters on the pathology of the liver and biliary tract, and twelve chapters on the gastrointestinal (GI) tract. The chapter on the intestinal mucosal barrier and antigen uptake is well illustrated and extremely clearly presented, covering the process in newborns and the special properties of the Peyer's patch cells. Six schematic diagrams assist this presentation. However, a comparably well-illustrated chapter on antigen presentation is written in a manner that is almost impossible to
Osteonecrosis of the jaw associated with pamidronate therapy
Authors: Ryan Zarychanski, Erin Elphee, Paul Walton, James Johnston
Journal: American Journal of Hematology (2005)

Abstract Bisphosphonates are commonly used in the treatment and prevention of osteoporosis, and they are also an important therapeutic adjunct in multiple myeloma and other cancers metastatic to bone. Bisphosphonates are generally well tolerated and associated with minimal adverse effects; however, there exists a growing concern that intravenous bisphosphonate use is associated with osteonecrosis of the jaw (ONJ). We report the occurrence of osteonecrosis of the jaw associated with pamidronate therapy in 12 patients diagnosed with multiple myeloma, breast carcinoma, or renal cell carcinoma, all involving bone. At the onset of jaw osteonecrosis, pamidronate therapy was the single medication common to all 12 patients. The duration of therapy varied from 12 to 77 months before osteonecrosis was observed; 92% (11/12) of cases involved the posterior mandible and all cases have been refractory to a variety of medical therapies, including surgical debridement and systemic antibiotics. Available tissue biopsies revealed inflammation consistent with osteomyelitis. In one biopsy, Actinomyces spp. were recovered from culture, but treatment with an extended course of clindamycin conferred no clinical benefit. The persistence of exposed bone remains a significant source of morbidity and pain for each surviving patient. Discontinuation of pamidronate therapy has not helped reverse the presence of osteonecrosis, and surgical manipulation of the involved site appears to worsen the underlying bone pathology. ONJ is an important adverse outcome associated with bisphosphonate therapy, and physicians prescribing pamidronate or zoledronate must be aware of the association between these drugs and this serious clinical entity. Failure to recognize the signs of ONJ can lead to unnecessary surgical procedures, which ultimately exacerbate the condition and impact quality of life. The unremitting nature of this clinical development, and the long‐lasting morbidity associated with it suggests that patients should be counseled regarding the possible occurrence of ONJ prior to initiating therapy with pamidronate. Am. J. Hematol. 81:73–75, 2006. © 2005 Wiley‐Liss, Inc.
Termination of the Respiratory Burst in Human Neutrophils
Authors: Robert C. Jandl, Janine André-Schwartz, Linda Borges-Dubois, Ruby S. Kipnes, B. Jane McMurrich, Bernard M. Babior
Journal: Journal of Clinical Investigation (1978)

Recent evidence has suggested that a particulate O(2) (-)-forming system is responsible for the respiratory burst in activated neutrophils. The respiratory burst is normally a transient event, lasting only 30-60 min. To investigate the mechanism by which the burst is terminated, we examined the O(2) (-)-forming activity of neutrophil particles as a function of time in the presence and absence of agents known to affect the function of intact cells. Measurements of the O(2) (-)-forming capacity of the particles against time of exposure of neutrophils to opsonized zymosan, a potent stimulating agent, revealed a rapid fall in activity when exposure was continued beyond 3 min. Exposure to zymosan under conditions in which the myeloperoxidase system was inactive (i.e., in the presence of myeloperoxidase inhibitors, or in the absence of oxygen) resulted in a substantial increase in the initial O(2) (-)-forming activity of particles from the zymosan-treated cells, but did not prevent the sharp fall in activity seen when zymosan exposure exceeded 10 min. The fall in activity was, however, prevented when activation took place in the presence of cytochalasin B (1.5 mug/ml), an agent thought to act largely by paralyzing the neutrophil through an interaction with its microfilament network.We conclude from these findings that the termination of the respiratory burst results at least in part from the inactivation of the particulate O(2) (-)-forming system. This inactivation involves at least two processes which probably act simultaneously. One is the destruction of the system through the action of myeloperoxidase. The other appears to require active cell motility and is independent of oxygen. The current view holds that the O(2) (-)-forming system of the neutrophil is located in the plasma membrane. It may be that the second process involves the internalization and degradation of this membrane-bound system.
Diagnosis in dysmorphology: clues from the skin
Authors: S.F. Smithson, R.M. Winter
Journal: British Journal of Dermatology (2004)

Journal Article Diagnosis in dysmorphology: clues from the skin Get access S.F. Smithson, S.F. Smithson Department of Clinical Genetics, St Michael's Hospital, Southwell Street, Bristol BS2 8EG, U.K.The late Professor Robin Winter, formerly of the Mothercare Unit of Clinical Genetics and Fetal Medicine, Institute of Child Health, London, U.K Sarah Smithson. E‐mail: sarah.smithson@ubht.swest.nhs.uk Search for other works by this author on: Oxford Academic Google Scholar R.M. Winter R.M. Winter Department of Clinical Genetics, St Michael's Hospital, Southwell Street, Bristol BS2 8EG, U.K.The late Professor Robin Winter, formerly of the Mothercare Unit of Clinical Genetics and Fetal Medicine, Institute of Child Health, London, U.K Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 151, Issue 5, 1 November 2004, Pages 953–960, https://doi.org/10.1111/j.1365-2133.2004.06266.x Published: 01 November 2004 Article history Accepted: 08 May 2004 Published: 01 November 2004
ABSENCE OF THE RIGHT PINNA AND RIGHT TONSIL, WITH RIGHT FACIAL PARALYSIS
Authors: J. J. Healy
Journal: BMJ (1917)

within the aorta at its bifurcation.On the morning of August 12th the patient's condition did not seem the worse for the operations on-his thigh and loin under gas and oxygen, and the aspiration of 6 oz. of blood from the left pleural cavity.Pericardial friction was well marked, no increase of cardiac dullness could be made out, there was resonance in the left axilla, and the breath sounds were generally harsh on the left side.Hesdied at 6.25 p.m. this day.Necropsy.Tllere was surgical emphysema of face, neck, and thorax.The left chest conitained a small amount of blood.There was aan entrance wound in the left posterior axillary line.The pericardiumn contained -a small amount of blood and a small tear on the posterior inferior aspect.There was an exudate of fibrin over the anterior and left lateral walls.There was a small hole, surround,ed by haemorrhage into the myocardium, on the posterior wall of the left ventricle.The interior of the left ventricle was clear except that there was a ragged tear on the septal wall, and the chordae tendineae of the
Ultrastructure of experimental cocaine hepatotoxicity
Authors: Marcia R. Gottfried, Michelle W. Kloss, Doyle Graham, Elmer J. Rauckman, Gerald M. Rosen
Journal: Hepatology (1986)

Cocaine is a potent hepatotoxin in mice. It is converted in the liver by a minor oxidative pathway to the active metabolite, norcocaine nitroxide. Previous studies have shown evidence of a lipid peroxidative mechanism of toxicity, including increased conjugated diene absorption by hepatic microsomal lipids following a single 60 mg per kg i.p. dose of cocaine in DBA/2Ha mice. To explore this mechanism further, morphologic changesin the livers of DBA/2Ha mice were examined following the same dose of cocaine. The first ultrastructural change seen was dilatation of rough endoplasmic reticulum in centrilobular hepatocytes 1 hr following cocaine injection, coincident with the previously observed onset of increased conjugated diene absorption in microsomal lipids. During the previously observed period of peak conjugated diene absorption (2 to 4 hr), ultrastructural changes in centrilobular hepatocytes progressed. These included focal mitochondrial membrane disruption followed by more extensive mitochondrial swelling and disruption with increased swelling of rough endoplasmic reticulum. Changes in size, shape and concentration of histochemically labeled, morphometrically studied peroxisomes were also seen during this interval. Injury of centrilobular hepatocytes advanced to cell death in 6 to 8 hr. The time course and nature of these morphologic findings correlate with previously observed evidence of lipid peroxidation, supporting the hypothesis that this is the mechanism of cocaine hepatoxicity.
Recurrence of Primary Sclerosing Cholangitis Following Liver Transplantation
Authors: Ivo W. Graziadei, Russell H. Wiesner, Kenneth P. Batts, Paul J. Marotta, Nicholas F. LaRusso, Michael K. Porayko, Eileen J. Hay, Gregory J. Gores, Michael R. Charlton, Jurgen Ludwig, John J. Poterucha, Jeffery L. Steers, Ruud A. Krom
Journal: Hepatology (1999)

Recurrence of primary sclerosing cholangitis (PSC) following liver transplantation has been suggested; however, it has not been fully defined because of numerous complicating factors and the lack of diagnostic criteria. In the present study, we investigated the recurrence of PSC by developing strict criteria and applying them to a large cohort of PSC patients who underwent liver transplantation. Between March 1985 and June 1996, 150 PSC patients underwent liver transplantation at the Mayo Clinic; mean follow up was 55 months. The incidence of nonanastomotic biliary strictures and hepatic histologic findings suggestive of PSC were compared between patients transplanted for PSC and a non–PSC transplant control group. Our definition of recurrent PSC was based on characteristic cholangiographic and histologic findings that occur in nontransplant PSC patients. By using strict criteria, 30 patients with other known causes of posttransplant nonanastomotic biliary strictures were excluded leaving 120 patients for analysis of recurrence of PSC. We found evidence of PSC recurrence after liver transplantation in 24 patients (20%). Of these, 22 out of 24 patients showed characteristic features of PSC on cholangiography and 11 out of 24 had compatible hepatic histologic abnormalities with a mean time to diagnosis of 360 and 1,350 days, respectively. Both cholangiographic and hepatic histologic findings suggestive of PSC recurrence were seen in nine patients. The higher incidence and later onset of nonanastomotic biliary strictures in patients with PSC compared with a non–PSC control group is supportive of the fact that PSC does recur following liver transplantation. We were unable to identify specific clinical risk factors for recurrent PSC, and the overall patient and graft survival in patients with recurrent PSC was similar to those without evidence of recurrence. Our observations provide convincing evidence that PSC frequently recurs in the hepatic allograft using strict inclusion and exclusion criteria
HIGHER CHYMASE DEPENDENT ANGIOTENSIN II-FORMING ACTIVITY IN THE CIRCULATING MONONUCLEAR LEUKOCYTE IS A SIGNIFICANT CONTRIBUTING FACTOR FOR ATRIAL FIBRILLATION
Authors: Keisuke Okamura, Yukiko Inoue, Yoshinari Uehara, Kenzo Matsumoto, Seiyo Maruyama, Shunichiro Sumi, Yusuke Fukuda, Shodai Furuyama, Sunao Kodama, Chie Andoh, Hideya Niimura, Kazumitsu Kubota, Hideaki Tohjoh, Kei Miyoshi, Shinichiro Miura, Yoshio Yamanouchi, Keijiro Saku, Hidenori Urata
Journal: Journal of the American College of Cardiology (2010)
Insidious manifestation of large bowel perforation
Authors: S. Hac, J. Kobiela, W. Puzdrowski, Z. Sledzinski
Journal: Endoscopy (2007)

An 87-year-old woman presented at the emergency room with breathlessness and acute chest pain following an outpatient colonoscopy that was carried out 2 hours earlier. She suffered from chronic coronary disease and hypertension, and was taking medication for both conditions. The endoscopy was very painful. Abdominal discomfort was accompanied by a dull, heavy pain in the center and right side of the chest, radiating to the right shoulder. Retrosternal ailments were worsening (hypoxia, hypotension, tachycardia). Physical examination revealed moderately, dull respiratory murmur, and tympanic percussion note on the right side. Lower abdomen discomfort was also worsening. Radiographs revealed perforation, intestinal pneumatosis, and right-sided pneumothorax (Figure [1]). Concomitant myocardial infarction and other pathologies were excluded.
The Dixon Case.
Authors: G. G. Craig
Journal: JAMA (1897)

Rock Island, Ill., Nov. 22, 1897. <h3>To the Editor:</h3> —About a year ago I received a letter from a Springfield, Ill., physician asking me to contribute to the expense of carrying the Dixon case through the courts until a decision by the supreme court was obtained. I declined to do so except with the understanding that if the verdict should be against us that an effort would be made to organize the physicians of the State of Illinois pledged to fight everything that was against us, for I was quite sure that the decision in that case would be against us, when we would be worse off than we were before if we let it go at that. I received no reply to my letter. The reason for my belief that the decision would be against us was this: Probably twenty-five years ago Dr. Patrick Gregg of this city refused
ABC of psychological medicine: Chronic multiple functional somatic symptoms
Authors: C. Bass
Journal: BMJ (2002)

<h3>Objectives</h3> To assess the quality and impact of medication safety outputs issued by the National Patient Safety Agency (NPSA) to the NHS in England and Wales. <h3>Methods</h3> A multi-method study comprising (1) focus groups and interviews with NHS Chief Pharmacists and (2) an electronic survey of medical, nursing and clinical governance directors. <h3>Results</h3> Acute sector respondents agreed that the medication outputs had a major impact on patient safety. Pharmacists welcomed national support for medication safety improvement, despite the resulting workload. Medical Directors were much less likely to be aware of alerts and Rapid Response Reports (RRRs) than their nursing and clinical governance colleagues. One key finding was the inability of around half of NHS trusts to communicate effectively and reliably with their junior doctors. <h3>Conclusion</h3> Medication alerts issued by the NPSA have stimulated significant work to improve medication safety and are believed to have had an important impact on patient safety.
Abstract SY36-03: Hijacking homeostatsis: How heterogeneity drives tumor progression and treatment failure.
Authors: Alexander RA Anderson
Journal: Cancer Research (2013)

Abstract Heterogeneity in cancer is an observed fact, both genotypically and phenotypically. Cell-cell variation is seen in almost all aspects of cancer from early development all the way through to invasion and subsequent metastasis. Our current understanding of this heterogeneity has mainly focused at the genetic scale with little information on how this variation translates to actual changes in cell phenotypic behavior. Given that many genotypes can lead to the same cellular phenotype, it is important that we quantify the range and scope of this heterogeneity at the phenotypic scale as ultimately this variability will dictate the aggressiveness of the tumor and its treatability. Central to our understanding of this heterogeneity is how the tumor cells interact with each other and with their microenvironment. Since it is these very interactions that drive selection and that ultimately define the ecology of the tissue in which the tumor is developing. Considering an organ as an ecological system, means that we should view normal tissue homeostasis as an equilibrium that cancer cells must disrupt if they are to be successful. Disruption of this equilibrium is often one of the first events in cancer development, as the normal control mechanisms of the tissue are damaged or ignored. We will discuss the interplay between homeostasis, heterogeneity, evolution and ecology in cancer progression and treatment failure with an emphasis on the metabolism of breast cancer. Citation Format: Alexander RA Anderson. Hijacking homeostatsis: How heterogeneity drives tumor progression and treatment failure. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr SY36-03. doi:10.1158/1538-7445.AM2013-SY36-03
EFFECT OF EZETIMIBE PLUS LOW-DOSE ATORVASTATIN VERSUS DOUBLE-DOSE ATORVASTATIN ON INSULIN RESISTANCE AND LIPID METABOLISM IN CORONARY ARTERY DISEASE PATIENTS WITH OR WITHOUT METABOLIC SYNDROME
Authors: Keiko Goshima, Kazuki Fukui, Tomoaki Shimizu, Yukiko Morita, Atsushi Wada, Tomohiko Shigemasa, Yasuyuki Mochida, Reimin Sawada, Takei Takahiro, Noriaki Iwahashi, Satoshi Umemura, Kazuo Kimura
Journal: Journal of the American College of Cardiology (2010)