tbuckley/cabot-search huggingface dataset:
A CASE OF ACTINOMYCOSIS OF THE PELVIS.
Authors: FRANK McMORROW
Journal: JAMA (1907)

down near the bladder, where the small bowel, three feet from the cecum, was adherent to the anterior abdominal wall.Within this adherent bowel the nail3 could be felt running forward to the abdominal wall and firmly fixed thereto.On breaking up the adhesions the larger nail was left behind firmly fastened in the abdominal wall by its point, while its head was still within the gut.This nail was pushed back, loosened and removed, and the opening in the gut sutured.The other nail had been displaced some eight inches toward the cecum, but was easily found and removed (Fig. 3).The whole abdomen was explored by the introduced hand, and no other foreign boaies could be found.The stomach was examined with special care, and no evidences of induration or dilatation were discovered.Postoperative History.-Recovery was uneventfi.ilexcept for a colon bacillus abscess which developed on the sixth day and opened through the lower corner of the incision, apparently arising from the abdominal wall at the site of the nail puncture.The nails removed were not corroded like those previously removed from the stomach, showing that they had undoubt- edly passed directly by gravity through the gastroenterostomy into the gut.
Neurology training around the world: asking the trainees
Authors: Konrad Rejdak, Axel Petzold, Karl Ng, Judit Afra, Irena Dujmovic, Zbigniew Stelmasiak, Danuta Ryglewicz, Hubert Kwiecinski, Wolfgang Grisold, Laszlo Vecsei
Journal: The Lancet Neurology (2009)
Abstract 3997: TUSC3 (N33) affects protein N-glycosylation and proliferation of prostate cancer cells
Authors: Peter Horak, Erwin Tomasich, Mariam Anees, Maximilian Marhold, Marion Gerschpacher, Dietmar Pils, Michael Krainer
Journal: Cancer Research (2012)

Abstract Prostate cancer is the most prevalent cancer in males in developed countries. Molecular aberrations in the pathogenesis of this disease are numerous, though losses on the short arm of chromosome 8 are highly prevalent. In our previous studies, hypermethylation and diminished TUSC3 expression turned out to be significantly associated with poor progression free and overall survival in ovarian cancer. Additionally, expression profiling of TUSC3 negative cancer cell lines revealed deregulation of genes involved in ‘cell structure and motility’ and ‘development processes’, further supporting our hypothesis of TUSC3 as a tumor suppressor. In silico prediction of TUSC3 shows a high homology of TUSC3 to the Ost3p subunit of the oligosaccharyltransferase (OST) complex in yeast, hinting to its role in protein glycosylation. In this project, we characterized TUSC3 (N33), a putative tumor suppressor gene on 8p, in prostate cancer. To study the prognostic role of TUSC3 in prostate cancer we used a comprehensive prostate cancer tissue microarray, comprised of samples from 143 prostate cancer patients. Serum DNA methylation was studied in an additional cohort of 67 prostate cancer patients. Statistical analysis demonstrated low or missing TUSC3 protein expression in 56.6% of prostate cancer patients based on immunohistochemical staining. Methylation of the TUSC3 promoter was observed in 38.8% of prostate cancer patients’ serum DNA, confirming our previous findings of TUSC3 promoter hypermethylation as a possible epigenetic regulatory mechanism. In our prostate cancer cohorts, however, neither expression nor hypermethylation of TUSC3 had a significant effect on overall survival, possibly due to the relatively short follow-up period. Next, we studied the function of TUSC3 in N-glycosylation and in particular its influence on carcinogenesis using a cell culture model. We downregulated TUSC3 expression in prostate cancer cell lines DU145 and PC3 using shRNA mediated knockdown and analyzed them for their proliferative and carcinogenic properties in vitro. We could show that loss of TUSC3 expression confers growth advantage of prostate cancer cell lines, in particular under conditions of serum starvation. We also observed increased migratory properties of prostate cancer cell lines upon TUSC3 knockdown. Further, influence of TUSC3 downregulation on several putative targets of N-linked glycosylation has been analyzed in vitro. In our study, we characterized TUSC3 expression and/or methylation in prostate cancer patients and obtained a first mechanistic insight into its function in N-glycosylation and carcinogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3997. doi:1538-7445.AM2012-3997
Bacteremia Associated With Angiography
Authors: Thomas H. Shawker
Journal: JAMA (1974)

Positive bacterial cultures were obtained from catheters and guide wires or blood, or both, during 23 of 100 angiographic procedures. Most frequently contaminated were the catheters. In 11 cases, the organisms isolated were of low virulence (diphtheroids, coagulase-negative staphylococci, and an aerobic Gram-positive rod) and may have represented air or skin contaminants. In 12 cases, however, Gram-negative bacilli of known pathogenicity were recovered. Transient bacteremia was demonstrated in four cases, but in none did local infection of puncture or cutdown sites, or prolonged bacteremia leading to sepsis develop. Postprocedure temperature elevations were not proved to be related to catheter-induced infection.  ( JAMA 229:1090-1092, 1974)
Monoconjugated bilirubin is a major component of hemolysis-induced gallstones in mice
Authors: Bruce W. Trotman, Rajagopalan C. Nair, Seldon E. Bernstein
Journal: Hepatology (1988)

The role of bilirubin conjugates in the formation of pigment gallstones is not known. In this study, we completely solubilized and then analyzed by high-performance liquid chromatography specimens of black pigment gallstones from eight nb/nb mice with hereditary hemolytic anemia. Each dried gallstone specimen of about 200 μg was dissolved in 5 ml of dimethyl sulfoxide/0.15 M HCl/50 m M disodium-EDTA (8:1:1 by volume) at room temperature. Stone dissolution was complete by 30 min as monitored by the A 456 and direct observation, and no oxidative products of bilirubin were observed in the visible spectrum, 350 to 750 nm. By high-performance liquid chromatography, the intact tetrapyrroles were separated as diconjugated and monoconjugated bilirubins; unconjugated bilirubin was resolved as XIII, IX and III α-isomers. The isocratic solvent system used was 0.1 M di- n -dodecylamine acetate/0.1 M di- n -octylamine acetate (4:1, v/v) in methanol, pH 7.4, at a flow of 1 ml per min. Diconjugated bilirubin accounted for 6.0 ± 2.4 molar % (mean ± S.E.), monoconjugated bilirubin for 37.4 ± 8.4% and unconjugated bilirubin for 56.3 ± 8.9% of the solubilized pigments. The IX α-isomer represented 96 ± 1.9% of the unconjugated bilirubin. The presence of bilirubin conjugates in gallstones was confirmed by ethylanthranilate diazotization: the conjugated azodipyrrole in stone had the same retention time as that of conjugated azodipyrrole from rat and mouse bile. A majority of the bilirubin conjugates was sensitive to β-glucuronidase of liver origin, indicating that the C-1 glucuronide ester was present. We conclude that (i) monoconjugated bilirubins are a significant component of black pigment gallstones from mice with hereditary hemolytic anemia, and (ii) the IX α-isomer is the predominant unconjugated bilirubin isomer in these gallstones. Monoconjugated bilirubin may play a role in black pigment stone formation as a coprecipitant and source of unconjugated bilirubin.
Toxicity following methoxyflurane anesthesia. I. Clinical and pathological observations in two fatal cases
Authors: B. J. Panner
Journal: JAMA (1970)

Two patients who received methoxyflurane anesthesia during abdominal surgery developed polyuric renal failure within 24 hours after their operations. Both patients died after complicated clinical courses which were dominated by renal failure. Toxic effects to the kidneys suspected of being related to methoxyflurane were characterized by polyuria and progressive azotemia. Postmortem examination in both cases revealed crystals resembling calcium oxalate in renal tubules. The possibility of concurrent toxic effects to the liver is also considered.
Rescue of Skeletal Muscles of γ-Sarcoglycan- Deficient Mice with Adeno-Associated Virus-Mediated Gene Transfer
Authors: Laurence Cordier, Andrew A. Hack, Marion O. Scott, Elisabeth R. Barton-Davis, Guang-ping Gao, James M. Wilson, Elizabeth M. McNally, H.Lee Sweeney
Journal: Molecular Therapy (2000)

In humans, a subset of cases of Limb–girdle muscular dystrophy (LGMD) arise from mutations in the genes encoding one of the sarcoglycan (α, β, γ, or δ) subunits of the dystrophin–glycoprotein complex. While adeno-associated virus (AAV) is a potential gene therapy vector for these dystrophies, it is unclear if AAV can be used if a diseased muscle is undergoing rapid degeneration and necrosis. The skeletal muscles of mice lacking γ-sarcoglycan (gsg−/− mice) differ from the animal models that have been evaluated to date in that the severity of the skeletal muscle pathology is much greater and more representative of that of humans with muscular dystrophy. Following direct muscle injection of a recombinant AAV [in which human γ-sarcoglycan expression is driven by a truncated muscle creatine kinase (MCK) promoter/enhancer], we observed significant numbers of muscle fibers expressing γ-sarcoglycan and an overall improvement of the histologic pattern of dystrophy. However, these results could be achieved only if injections into the muscle were prior to the development of significant fibrosis in the muscle. The results presented in this report show promise for AAV gene therapy for LGMD, but underscore the need for intervention early in the time course of the disease process.
ADAPTATION OF THE ANGER CAMERA FOR CHROMATOGRAPHIC QUALITY CONTROL OF NUCLIDE BINDING AFFINITY
Authors: Mary E. Thompson, Thomas D. Kay, Douglas V. Porter, David L. Johnson, David Romo, Sandy J. Riahi
Journal: Clinical Nuclear Medicine (1982)

Romo, David; Kay, Thomas D.; Neufeld, Gwynne K.; Johnson, David L.; Thompson, Mary E.; Riahi, Sandy J.; McGranahan, George M. Jr. Author Information
Electric Pulses Help With Chemotherapy, May Open New Paths for Other Agents
Authors: Tracy Hampton
Journal: JAMA (2011)

FOR NEARLY 3 DECADES, BASIC SCIence researchers have used electric pulses to make cell membranes transiently permeable to deliver DNA and other molecules into cells. Now, clinical investigators are applying this method to introduce chemotherapeutics to cancer cells by inserting electrodes into a tumor. Such electrochemotherapy has proven to be an effective local treatment for various types of tumors, particularly when electric pulses are applied with chemotherapeutics that pass through the cell membrane with difficulty or not at all. “Electrochemotherapy has great potential in the treatment of many different cancer histologies and stages,” said Julie Gehl, MD, of the University of Copenhagen at Herlev Hospital, in Denmark. Gehl has been treating patients with electrochemotherapy for more than a dozen years and was trained under the guidance of the investigator who first conceptualized and coined the term electrochemotherapy, Lluis M. Mir, PhD, DSc, of the Institut GustaveRoussy, in Villejuif, France. “It’s highly efficient, it’s quick, patient acceptance is high, and cost is low,” Gehl said. Researchers hope that the technology might also be applied to the delivery of other agents, such as DNA or inhibitory nucleic acids.
Acquired copy-neutral loss of heterozygosity of chromosome 1p as a molecular event associated with marrow fibrosis in MPL-mutated myeloproliferative neoplasms
Authors: Elisa Rumi, Daniela Pietra, Paola Guglielmelli, Roberta Bordoni, Ilaria Casetti, Chiara Milanesi, Emanuela Sant’Antonio, Virginia Ferretti, Alessandro Pancrazzi, Giada Rotunno, Marco Severgnini, Alessandro Pietrelli, Cesare Astori, Elena Fugazza, Cristiana Pascutto, Emanuela Boveri, Francesco Passamonti, Gianluca De Bellis, Alessandro Vannucchi, Mario Cazzola
Journal: Blood (2013)
Future Roles and Training of Internal Medicine Subspecialists
Authors: Lynn O. Langdon
Journal: Annals of Internal Medicine (1996)

While fellowship training programs are being reduced in size to better conform to societal needs, the training of subspecialist basic scientists and clinical investigators must be protected to ensure continued discovery and the scholarly application of knowledge to patient care.Fewer subspecialist clinicians must be appropriately trained to serve as consultants, as principal care providers, and as scholarly leaders and educators in their subspecialties. This article describes the recommendations of the American Board of Internal Medicine for subspecialty training. To encourage physicians to choose careers as investigators, overlapping but different training paths are delineated for subspecialist clinicians and investigators. More didactic coursework is recommended for both paths. To maximize the contribution of fewer subspecialists, it is essential to provide rigorous training that is appropriately relevant and realistically matched with career opportunities. *The American Board of Internal Medicine Task Force on Subspecialty Internal Medicine includes P.P. Toskes, MD (University of Florida College of Medicine, Gainesville, Florida); J.C. Bennett, MD (University of Alabama at Birmingham, Birmingham, Alabama); W.M. Bennett, MD (Oregon Health Sciences University, Portland, Oregon); G.D. Braunstein, MD (Cedars-Sinai Medical Center, Los Angeles, California); P.A. Cassileth, MD (University of Miami School of Medicine, Miami, Florida); M.D. Cheitlin, MD (San Francisco General Hospital, San Francisco, California); D.R. Dantzker, MD (Long Island Jewish Medical Center, New Hyde Park, New York); M. Feldman, MD (Dallas Veterans Administration Medical Center, Dallas, Texas); H.M. Golomb, MD (University of Chicago Medical Center, Chicago, Illinois); M.R. Green, MD (University of California at San Diego School of Medicine, San Diego, California); J.P. Kassirer, MD (The New England Journal of Medicine, Boston, Massachusetts); M.A. Kelley, MD (University of Pennsylvania Medical Center, Philadelphia, Pennsylvania); M.S. Klempner, MD (Tufts University School of Medicine, Boston, Massachusetts); R.W. Moskowitz, MD (Case Western Reserve University School of Medicine, Cleveland, Ohio); M.I. Surks, MD (Montefiore Medical Center, Bronx, New York); S.I. Wasserman, MD (University of California at San Diego School of Medicine, San Diego, California); and D.P. Zipes, MD (Indiana University School of Medicine, Indianapolis, Indiana).
TESTS FOR PNEUMOCOCCUS HYPERSENSITIVENESS IN DOGS AFTER RECOVERY FROM EXPERIMENTAL PNEUMOCOCCUS LOBAR PNEUMONIA
Authors: Lowell T. Coggeshall
Journal: The Journal of Experimental Medicine (1935)

The data derived from the above described investigations indicate that dogs do not develop hypersensitivity to the pneumococcus as the result of experimental lobar pneumonia. This inference is based on the following findings: 1. Fifteen dogs were given Type I and Type II pneumococcus lobar pneumonia and following recovery were tested for hypersensitiveness by means of intrabronchial and intracutaneous injections of the autolysate made from the homologous pneumococcus. 2. Seven dogs showed a pulmonary lesion discernible with the X-ray at site of the autolysate inoculation; three of these dogs were normal controls. 3. No evidence of a positive skin reaction was found in any of the fifteen dogs, many of which received repeated infections and intradermal autolysate injections. 4. Subsequent infections in the same animals were definitely milder than the initial infection. 5. The infections following the administration of intrapulmonary and cutaneous autolysate were practically of the same intensity as the initial infection. 6. Temperature, pulse rates, white blood counts and differential blood pictures showed no significant variations following intrapulmonary injection of autolysate. 7. Tests for the acquisition of humoral immune bodies following autolysate injection and recovery from the experimental disease showed the presence of these substances in some of the dogs and their absence in others. 8. Study of the pathology of the pulmonary lesions produced by the autolysate failed to reveal histological changes characteristic of an allergic reaction. However, the presence of perivascular accumulations of large mononuclear cells observed in the lesions of the recovered dogs does suggest a locally accelerated reactivity of the fixed tissue cells to the products of the pneumococcus.
Abstract 3851: The nuclear guanine nucleotide exchange factors Ect2 and Net1 regulate RhoB-mediated cell death after DNA damage
Authors: Melissa C. Srougi, Keith Burridge
Journal: Cancer Research (2011)

Abstract Commonly used antitumor treatments, including radiation and chemotherapy, function by damaging the DNA of rapidly proliferating cells. However, resistance to these agents is a predominant clinical problem. A member of the Rho family of small GTPases, RhoB has been shown to be integral in mediating cell death after ionizing radiation (IR) or other DNA damaging agents in Ras-transformed cell lines. In addition, RhoB protein expression increases after genotoxic stress, and loss of RhoB expression causes radio- and chemotherapeutic resistance. However, the signaling pathways that govern RhoB-induced cell death after DNA damage remain enigmatic. Here, we show that RhoB activity increases in human breast and cervical cancer cell lines after treatment with DNA damaging agents. Furthermore, RhoB activity is necessary for DNA damage-induced cell death, as the stable loss of RhoB protein expression using shRNA partially protects cells and prevents the phosphorylation of c-Jun N-terminal kinases (JNKs) and the induction of the pro-apoptotic protein Bim after IR. The increase in RhoB activity after genotoxic stress is associated with increased activity of the nuclear guanine nucleotide exchange factors (GEFs), Ect2 and Net1, but not the cytoplasmic GEFs p115 RhoGEF or Vav2. Importantly, loss of Ect2 and Net1 via siRNA-mediated protein knock-down inhibited IR-induced increases in RhoB activity, reduced apoptotic signaling events, and protected cells from IR-induced cell death. Collectively, these data suggest a mechanism involving the nuclear GEFs Ect2 and Net1 for activating RhoB after genotoxic stress, thereby facilitating cell death after treatment with DNA damaging agents. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3851. doi:10.1158/1538-7445.AM2011-3851
Long-term Risks of Subsequent Primary Neoplasms Among Survivors of Childhood Cancer
Authors: Raoul C. Reulen
Journal: JAMA (2011)

Survivors of childhood cancer are at excess risk of developing subsequent primary neoplasms but the long-term risks are uncertain.To investigate long-term risks of subsequent primary neoplasms in survivors of childhood cancer, to identify the types that contribute most to long-term excess risk, and to identify subgroups of survivors at substantially increased risk of particular subsequent primary neoplasms that may require specific interventions.British Childhood Cancer Survivor Study--a population-based cohort of 17,981 5-year survivors of childhood cancer diagnosed with cancer at younger than 15 years between 1940 and 1991 in Great Britain, followed up through December 2006.Standardized incidence ratios (SIRs), absolute excess risks (AERs), and cumulative incidence of subsequent primary neoplasms.After a median follow-up time of 24.3 years (mean = 25.6 years), 1354 subsequent primary neoplasms were ascertained; the most frequently observed being central nervous system (n = 344), nonmelanoma skin cancer (n = 278), digestive (n = 105), genitourinary (n = 100), breast (n = 97), and bone (n = 94). The overall SIR was 4 times more than expected (SIR, 3.9; 95% confidence interval [CI], 3.6-4.2; AER, 16.8 per 10,000 person-years). The AER at older than 40 years was highest for digestive and genitourinary subsequent primary neoplasms (AER, 5.9 [95% CI, 2.5-9.3]; and AER, 6.0 [95%CI, 2.3-9.6] per 10,000 person-years, respectively); 36% of the total AER was attributable to these 2 subsequent primary neoplasm sites. The cumulative incidence of colorectal cancer for survivors treated with direct abdominopelvic irradiation was 1.4% (95% CI, 0.7%-2.6%) by age 50 years, comparable with the 1.2% risk in individuals with at least 2 first-degree relatives affected by colorectal cancer.Among a cohort of British childhood cancer survivors, the greatest excess risk associated with subsequent primary neoplasms at older than 40 years was for digestive and genitourinary neoplasms.
IgM and IgG antibodies to human T cell lymphotropic retrovirus (HTLV-III) in lymphadenopathy syndrome and subjects at risk for AIDS in Italy.
Authors: F Aiuti, P Rossi, M C Sirianni, M Carbonari, M Popovic, M G Sarngadharan, L Contu, M Moroni, S Romagnani, R C Gallo
Journal: BMJ (1985)

A study was performed to assess the prevalence of specific antibodies to human T cell lymphotropic retrovirus (HTLV-III) in patients with lymphadenopathy syndrome, patients with the acquired immune deficiency syndrome (AIDS), and those at risk of AIDS. Serum samples were obtained from these groups and from healthy controls in selected cities in Italy, and antibodies to HTLV-III were measured by immunofluorescence assay and, in a few patients, by Western blotting. In addition, IgM antibody values were measured in 82 of those positive for HTLV-III. Altogether, 235 out of 320 patients with lymphadenopathy syndrome had antibodies to HTLV-III, the proportions being highest in haemophiliacs, homosexuals, and drug addicts from Rome; 11 out of 12 patients with AIDS had antibodies; 78 out of 439 subjects at risk for AIDS had antibodies; and six out of 30 patients with lymphadenopathy syndrome and positive for HTLV-III antibodies and nine of 52 patients at risk of AIDS had a detectable titre of IgM. HTLV-III is widespread in groups at risk of AIDS in Italy, and antibodies to HTLV-III are highly prevalent in patients with lymphadenopathy syndrome. A higher proportion of drug abusers were positive for antibodies than in previous studies. HTLV-III "infection" would appear to be spread mainly in compromised hosts, as none of the controls were positive for antibodies.
Alternatives to using fetal tissue from induced abortions
Authors: J. W. LO
Journal: JAMA (1990)

To the Editor.—  The article 1 by the American Medical Association's Council on Scientific Affairs and Council on Ethical and Judicial Affairs emphasizes the advantages of using human fetal tissue for transplantation and provides ethical and legal guidelines. But there are obstacles and concerns such as Prolife objections, federal moratoria in the United States, and doubts about strict adherence to guidelines. However, there may be alternatives to using fetal tissue from induced abortions.  First, spontaneous abortions and ectopic pregnancies could be sources, not only of intraembryonic tissue, but also of placental and yolk sac tissue. Ectopic pregnancies have increased in incidence and are not uncommon in some large hospitals. Improvements in technology have facilitated earlier diagnoses of ectopic pregnancies, which would permit recovery of viable gestational tissue more frequently and at an earlier stage with the attendant advantages of greater immaturity. Another advantage of ectopic pregnancies is that the frequency