tbuckley/cabot-search huggingface dataset:
Surgery of the Stomach and Duodenum
Authors: Craig R. Reckard
Journal: JAMA (1978)

Complications of Gastric Surgery, by David Fromm, 163 pp, with illus, $18, New York, Wiley, 1977.  Both of these volumes are of value to surgeons, internists, and students interested in upper gastrointestinal (GI) disease and its surgical management. The third edition of Surgery of the Stomach and Duodenum succeeds the second edition by eight years (1969) and is written by 62 contributors, many of whom are new since the last edition. Consisting of 28 chapters, the volume is well written and well illustrated. New chapters have been added in the rapidly expanding areas of treatment of the upper GI tract, endocrine physiology and pathophysiology, acute gastritides, and parietal cell vagotomy in the treatment of duodenal ulcer disease. All chapters have undergone revision since the previous edition, and each is completed with comments by specialists in the field. The chapter on massive upper GI tract bleeding is particularly well written and
Why are small bowel tumours rare? An experimental model
Authors: K. C. Calman
Journal: Gut (1974)

It is a well known clinical observation that small bowel tumours are rarer than tumours of the stomach or colon. The fluidity and relative sterility of small bowel contents, and rapid transit time and of the relative sterility of the small bowel itself have been suggested as possible factors contributing to this relatively low incidence. A further mechanism, that of a local immune response against malignant cells, has also been suggested and this investigation is the subject of this paper. A transplantable tumour (Gardner lymphosarcoma) was injected either into the stomach or small bowel of CBA mice, and the incidence of subsequent tumour growth was studied when the immune status of the host mouse was altered. Normal mice, mice `deprived9 by thymectomy and irradiation (T-cell-deficient mice), and `reconstituted mice9 (prepared as the `deprived9 animals but given a thymus graft) were used. The results showed that in normal and reconstituted mice more tumours arise in the stomach than in the small bowel but that in deprived mice the incidence of tumours was the same in both sites. This could be taken to suggest that local immune responses can suppress the development of tumours of the small bowel.
The transcriptional regulator Aire coopts the repressive ATF7ip-MBD1 complex for the induction of immunotolerance
Authors: Michael Waterfield, Imran S Khan, Jessica T Cortez, Una Fan, Todd Metzger, Alexandra Greer, Kayla Fasano, Marc Martinez-Llordella, Joshua L Pollack, David J Erle, Maureen Su, Mark S Anderson
Journal: Nature Immunology (2014)
Trends and Factors Associated With Infant Bed Sharing, 1993-2010
Authors: Eve R. Colson, Marian Willinger, Denis Rybin, Timothy Heeren, Lauren A. Smith, George Lister, Michael J. Corwin
Journal: JAMA Pediatrics (2013)

A strong association between infant bed sharing and sudden infant death syndrome or unintentional sleep-related death in infants has been established. Occurrences of unintentional sleep-related deaths among infants appear to be increasing.
Enhanced CT and FDG PET/CT Findings of Splenic Hamartoma
Authors: Aisheng Dong, Yang Wang, Jianping Lu, Changjing Zuo
Journal: Clinical Nuclear Medicine (2013)

Splenic hamartomas are very rare benign vascular tumors. A 67-year-old man was referred after an incidental detection of a splenic lesion. Abdominal-enhanced CT showed a splenic lesion with progressive enhancement. This lesion showed intense FDG uptake with an SUVmax of 9.2. The patient underwent splenectomy. Splenic hamartoma was confirmed by pathologic evaluation. In this tumor, the disorganized splenic sinus contained a large amount of lymphocytes and plasma cells, which may contribute to the intense FDG uptake. This case indicates that splenic hamartoma should be included in the differential diagnosis of focal FDG accumulation along with tumor and nontumor conditions.
Pneumococcal Vaccine — Past, Present, and Future
Authors: Claire V. Broome, Robert F. Breiman
Journal: New England Journal of Medicine (1991)

IN this issue of the Journal, Shapiro and colleagues present the results of a case–control study of the efficacy of pneumococcal polysaccharide vaccine.1 In their carefully designed and implemented study, the vaccine had an efficacy of 61 percent (95 percent confidence interval, 47 percent to 72 percent) in immunocompetent persons. The large size of the study allowed an elegant analysis of the variables that affect the efficacy of the vaccine. The results confirm and extend the findings from a number of studies conducted in the 14 years since the initial 14-valent vaccine was licensed.2 This history illustrates the often . . .
My Anatomy Teacher
Authors: Veronica K. Piziak
Journal: JAMA (1984)

I was a new intern with the creases hardly out of my lab coat when one of my patients, an elderly gentleman with pneumonia, died. I heard his autopsy announced over the page system. The page operator droned, "Doctor Mortimer Post"—the hospital's attempt at medical humor—but appropriate for an autopsy. I had come from a large medical school where we were required to attend our patients' autopsies; therefore, a large crowd of people used to assemble and some jostling usually occurred among the medical students to get a spot in the back row where they would not have to answer questions fired by the pathologist. At the university, the important remains of the patient were exhibited in a large specimen pan; hence the name "Man in the Pan" conferences. The value of these conferences escaped me then, and now my presence was not even required. I was tired, having been
Intraalveolar Expression of Tumor Necrosis Factor- α Gene during Conventional and High-Frequency Ventilation
Authors: MASAO TAKATA, JUN ABE, HIROYUKI TANAKA, YOSHIHIRO KITANO, SHOUZABUROH DOI, TAKAO KOHSAKA, KATSUYUKI MIYASAKA
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

The effects of conventional mechanical ventilation (CMV) and high-frequency oscillatory ventilation (HFO) on intraalveolar expression of the tumor necrosis factor-alpha (TNF-alpha) gene were studied in surfactant-depleted rabbits. After lung lavage with saline, 13 rabbits were administered either CMV (n = 6) or HFO (n = 7) for 1 h at an FiO2 of 1.0 and a mean airway pressure of 13 cm H2O. Lung lavage was then repeated. The rabbits' RNA was extracted from the lavage cells, and mRNA for TNF-alpha was quantitated by reverse-transcription polymerase chain reaction using glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as an internal standard. At 1 h of ventilation, PaO2 was slightly lower with CMV than HFO, while lavage cell counts and cytology were similar between the two groups. The ratio of TNF-alpha mRNA to GAPDH mRNA increased with CMV (control, 0.48 +/- 0.04 [SE] versus 1 h, 1.02 +/- 0.14, p < 0.01) but did not change with HFO (0.55 +/- 0.07 versus 0.73 +/- 0.09). In a separate series of experiments, ten surfactant-depleted rabbits continued to be ventilated for 4 h either by CMV (n = 5) or HFO (n = 5). Conventional mechanical ventilation resulted in a progressive hypoxemia, decreased lung compliance, increased number of neutrophils in lung lavage fluid, and substantial morphological changes including hyaline membrane formation and neutrophil accumulation, whereas HFO was associated with minimal changes in such physiological and pathological abnormalities. These results suggest that activation of alveolar macrophages and production of proinflammatory cytokines may play a pivotal role in the early stage of ventilator-induced lung injury, and that ventilator mode (CMV or HFO) substantially modulates macrophage activation and hence the degree of lung injury.
ATP-Dependent Activation of the Atrial Acetylcholine-Induced K <sup>+</sup> Channel Does Not Require Nucleoside Diphosphate Kinase Activity
Authors: Steve Sorota, Michael Chlenov, Xiao-Yi Du, Michael Kagan
Journal: Circulation Research (1998)

Abstract —Prior reports by others have shown that cytoplasmically applied ATP can activate the acetylcholine-induced K + channel in inside-out atrial membrane patches when no guanine nucleotides are present in the solution bathing the cytosolic face of the membrane. A nucleoside diphosphate kinase mechanism was proposed to explain the activation by ATP. We show in the present study that cytoplasmic adenylylimidodiphosphate mimics the activation by ATP. Unlike ATP, the activation by adenylylimidodiphosphate does not subside on washout. Although commercially available adenylylimidodiphosphate is contaminated by guanylylimidodiphosphate, the activation by adenylylimidodiphosphate still occurs after HPLC purification to remove guanine nucleotide contamination. Adenylylimidodiphosphate does not support phosphotransferase activity by nucleoside diphosphate kinase. Therefore, nucleoside diphosphate kinase activity cannot explain the activation of atrial acetylcholine-induced K + current by ATP and adenylylimidodiphosphate. We hypothesize that the activation by millimolar concentrations of ATP is due to binding of adenine nucleotide to the guanine nucleotide binding site of the G protein(s) responsible for stimulating the acetylcholine-induced K + current.
Superficial and Muscle-Invasive Bladder Cancer: Principles of Management for Outcomes Assessments
Authors: Dipen J. Parekh, Bernard H. Bochner, Guido Dalbagni
Journal: Journal of Clinical Oncology (2006)

Bladder cancer is a heterogeneous disease. Non-muscle-invasive bladder cancer embraces a spectrum of tumors with varying degrees of clinical behavior. Transurethral resection remains the surgical mainstay for the treatment of non-muscle-invasive bladder cancer. In an attempt to decrease the recurrence or progression rate, intravesical chemotherapy or immunotherapy is also used. Radical cystectomy with bilateral pelvic lymph node dissection remains the gold standard for treating muscle-invasive bladder cancer. Over the last decade, the orthotopic neobladder has gained widespread popularity as the preferred mode of urinary diversion in both males and females with similar oncologic and functional outcomes. Well-designed trials with effective chemotherapy have shown a beneficial role for neoadjuvant chemotherapy.
Determinants of efficacy and safety in epicutaneous allergen immunotherapy: summary of three clinical trials
Authors: G. Senti, S. Moos, F. Tay, N. Graf, P. Johansen, T. M. Kündig
Journal: Allergy (2015)

The results of our third trial on epicutaneous allergen-specific immunotherapy (EPIT) will be presented and discussed in the context of our previous trials. This monocentric, placebo-controlled, double-blind phase I/IIa trial included 98 patients with grass pollen rhinoconjunctivitis. Prior to the pollen season 2009, patients received six patches (allergen extract: n = 48; placebo: n = 50) with weekly intervals, administered onto tape-stripped skin. Allergen EPIT produced a median symptom improvement of 48% in 2009 and 40% in the treatment-free follow-up year 2010 as compared to 10% and 15% improvement after placebo EPIT (P = 0.003). After allergen EPIT but not placebo EPIT, conjunctival allergen reactivity was significantly decreased and allergen-specific IgG4 responses were significantly elevated (P < 0.001). In conclusion, our three EPIT trials found that allergen EPIT can ameliorate hay fever symptoms. Overall, treatment efficacy appears to be determined by the allergen dose. Local side-effects are determined by the duration of patch administration, while risk of systemic allergic side-effects is related to the degree of stratum corneum disruption.
842 A RANDOMIZED TRIAL OF ENDOSCOPIC BAND LIGATION VERSUS CYANOACRYLATE INJECTION IN THE MANAGEMENT OF BLEEDING JUNCTIONAL VARICES
Authors: H. El Amin, L. Abdel Baki, Z.E.A. Sayed, Y.M. Fouad, E. Abdel-Mohsen, K.A. Eid, H.R. El-Khayat
Journal: Journal of Hepatology (2010)
Analysis of Bevacizumab (Bev) Therapy, Bisphosphonate Use and Osteonecrosis of the Jaw (ONJ) in >1900 Patients Treated in Two Randomized, Controlled Trials.
Authors: V. Guarneri, D. Miles, N. Robert, V. Dieras, J. Glaspy, I. Smith, C. Thomssen, L. Biganzoli, T. Taran, P. Conte
Journal: Cancer Research (2009)

Abstract Background: Long-term bisphosphonate therapy is known to increase the risk of ONJ. A 16% incidence of ONJ was reported in a retrospective analysis of 116 patients receiving bisphosphonates with anti-angiogenic therapy (Bev or sunitinib) for bone metastases from breast, colon, or renal cell cancers.Methods: To assess the incidence of ONJ with Bev, we analyzed data from &amp;gt;3500 patients with locally recurrent or metastatic breast cancer (LR/MBC) treated in three large trials of Bev-containing therapy: AVADO (Bev in combination with docetaxel); RIBBON-1 (Bev in combination with taxane, anthracycline-based combination therapy, or capecitabine); and MO19391 (single-arm safety study of &amp;gt;2000 patients receiving Bev-containing therapy in the general oncology practice context). The incidence of ONJ was compared in patients treated with Bev versus placebo and in patients with or without bisphosphonate exposure.Results: Data from the blinded phase of two randomized, placebo-controlled trials demonstrated an ONJ incidence of 0.3%. ONJ was more common in patients who also received bisphosphonate therapy than in those who received no bisphosphonates (Table). This observation is supported by data from 2216 patients treated in the single-arm MO19391 study (2.4% with bisphosphonate versus 0% without). AVADO*RIBBON-1**TotalIncidence of ONJ, no. of pts (%)Bev (n=492)Pla (n=238)Bev (n=817)Pla (n=412)Bev (n=1309)Pla (n=650)Overall population receiving Bev (n=1309)3 (0.6%)O1 (0.1%)O4 (0.3%)OBisphosphonate (n=233)1 (1.2%)O1 (0.6%)O2 (0.9%)ONo bisphosphonate (n=1076)2 (0.5%)OOO2 (0.2%)O *Bev 15 and 7.5 mg/kg arms pooled**Taxane/anthracycline and capecitabine cohorts pooledConclusions: This is the largest analysis of ONJ in patients receiving Bev for LR/MBC. The 0.3% incidence of ONJ with Bev is considerably lower than previously reported by Christodoulou et al. with anti-angiogenic therapy. As in the general population, the risk of ONJ is increased in patients exposed to bisphosphonates. The 0.9–2.4% incidence seen here in a large population of patients receiving Bev and bisphosphonate therapy is substantially lower than the 16% observed in a small cohort of patients from a retrospective analysis and within the range reported in the literature for bisphosphonates alone (1–4%). Good oral hygiene, dental examination and avoidance of invasive dental procedures remain important in patients receiving bisphosphonates, irrespective of Bev treatment. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 208.
Genetics and respiratory disease bullet 2: Alpha1-antitrypsin deficiency, cirrhosis and emphysema
Authors: R. Mahadeva, D. A Lomas
Journal: Thorax (1998)

Emphysema is a chronic progressive lung disease characterised by abnormal permanent enlargement of airspaces as a result of destruction of alveolar walls.1 Most patients develop emphysema as a consequence of smoking but 1–2% of patients with emphysema develop the condition as a result of a genetic deficiency of the plasma proteinase inhibitor α1-antitrypsin. The two common deficiency variants of α1-antitrypsin, S and Z, result from point mutations in the α1-antitrypsin gene2-4 and are named on the basis of their slower electrophoretic mobility on isoelectric focusing analysis compared with the normal M allele.5 S α1-antitrypsin (264Glu→Val) is found in up to 28% of Southern Europeans and, although it results in plasma α1-antitrypsin levels that are 60% of the M allele, it is not associated with any pulmonary sequelae. The Z variant (342Glu→Lys) results in a more severe deficiency that is characterised, in the homozygote, by plasma α1-antitrypsin levels of 10% of the normal M allele and by levels of 60% in the MZ heterozygote (50% from the M allele and 10% from the Z allele). The Z mutation results in the accumulation of α1-antitrypsin in the rough endoplasmic reticulum of the liver (fig 1A) and predisposes the homozygote to juvenile hepatitis, cirrhosis,6 and hepatocellular carcinoma.7 Z α1-antitrypsin inclusions are associated with abnormal liver function tests in over 90% of Z homozygotes in the first year of life but only 10–15% of these develop the prolonged cholestatic jaundice that can progress to cirrhosis and the requirement for hepatic transplantation.6 8



Figure 1 
(A) Electron micrograph of a hepatocyte from the liver of a child with Z α1-antitrypsin deficiency. The arrow shows the accumulation of α1-antitrypsin …
Long-Term Inheritance of the 28S rDNA-Specific Retrotransposon R2
Authors: Kenji K. Kojima, Haruhiko Fujiwara
Journal: Molecular Biology and Evolution (2005)

R2 is a non–long-terminal-repeat (LTR) retrotransposon that inserts specifically into 28S rDNA. R2 has been identified in many species of arthropods and three species of chordates. R2 may be even more widely distributed in animals, and its origin may be traceable to early animal evolution. In this study, we identified R2 elements in medaka fish, White Cloud Mountain minnow, Reeves' turtle, hagfish, sea lilies, and some arthropod species, using degenerate polymerase chain reaction methods. We also identified two R2 elements from the public genomic sequence database of the bloodfluke Schistosoma mansoni. One of the two bloodfluke R2 elements has two zinc-finger motifs at the N-terminus; this differs from other known R2 elements, which have one or three zinc-finger motifs. Phylogenetic analysis revealed that the whole phylogeny of R2 can be divided into 11 parts (subclades), in which the local R2 phylogeny and the corresponding host phylogeny are consistent. Divergence-versus-age analysis revealed that there is no reliable evidence for the horizontal transfer of R2 but supports the proposition that R2 has been vertically transferred since before the divergence of the deuterostomes and protostomes. The seeming inconsistency between the R2 phylogeny and the phylogeny of their hosts is due to the existence of paralogous lineages. The number of N-terminal zinc-finger motifs is consistent with the deep phylogeny of R2 and indicates that the common ancestor of R2 had three zinc-finger motifs at the N-terminus. This study revealed the long-term vertical inheritance and the ancient origin of sequence specificity of R2, both of which seem applicable to some other non-LTR retrotransposons.
Treatment challenges and investigational opportunities in autoimmune hepatitis
Authors: Albert J. Czaja, Francesco B. Bianchi, Herschel A. Carpenter, Edward L. Krawitt, Ansgar W. Lohse, Michael P. Manns, Ian G. McFarlane, Giorgina Mieli-Vergani, Gotaro Toda, Diego Vergani, John Vierling, Mikio Zeniya
Journal: Hepatology (2004)

New drugs and advances in molecular biology afford opportunities to upgrade the treatment of autoimmune hepatitis. The aims of this study were to define treatment problems, identify possible solutions, and stimulate investigations to improve patient care. A clinical subcommittee of the International Autoimmune Hepatitis Group reviewed current management difficulties and proposed corrective actions. The assessment of new front-line and salvage therapies for adults and children were given top priority. Cyclosporine and mycophenolate mofetil were endorsed as drugs worthy of rigorous study in severe disease, and budesonide was endorsed for study as front-line therapy in mild disease. Diagnostic criteria and treatment regimens for children required codification, and pharmacokinetic studies were encouraged to develop optimal dosing schedules based on therapeutic ranges. Collaborative efforts were proposed to help understand racial, geographical, and genetic factors affecting outcome and to establish definitions and therapies for variant syndromes and graft dysfunction after transplantation. The development of experimental animal models was deemed essential for the study of site-specific molecular interventions, and gene therapy was endorsed as a means of bolstering reparative processes . In conclusion, evolving pharmacological and technical advances promise to improve the treatment of autoimmune hepatitis, and investigations of these advances are timely, feasible, and necessary. (Hepatology 2005;41:207–215.)
1046 A NEW FIBROSIS STAGING METHOD PROVIDES VERY ACCURATE NON-INVASIVE DIAGNOSIS OF LIVER FIBROSIS WITHOUT LIVER BIOPSY
Authors: J. Boursier, V. de Ledinghen, V. Leroy, L. Castera, J.P. Zarski, F. Oberti, S. Michalak, Y. Gallois, I. Fouchard-Hubert, N. Dib, M.C. Rousselet, S. Bertrais, P. Calès
Journal: Journal of Hepatology (2010)
Thrombocytopenic purpura in a carrier of human T‐cell leukemia virus type I
Authors: Tomoko Matsuoka, Hiroshi Tamura, Masatoshi Fujishita, Ichiro Kubonishi, Hirokuni Taguchi, Isao Miyoshi
Journal: American Journal of Hematology (1988)

Thrombocytopenic purpura developed in a 64-year-old woman seropositive for human T-cell leukemia virus type I (HTLV-I). She had no underlying disorders and HTLV-I is suggested as a possible cause of her thrombocytopenia.
Antifibrotic Effect of MMP13-encoding Plasmid DNA Delivered Using Polyethylenimine Shielded With Hyaluronic Acid
Authors: Eun-Joong Kim, Hee-Jeong Cho, Daeui Park, Ji Yeon Kim, Young Bong Kim, Tae Gwan Park, Chang-Koo Shim, Yu-Kyoung Oh
Journal: Molecular Therapy (2010)

The imbalanced expression of matrix metalloproteinases (MMPs) is associated with liver fibrosis, one of the most common chronic liver diseases. Enhanced expression of MMPs by gene therapy is emerging as a promising antifibrotic strategy, but the effectiveness of this approach depends on reliable systems for delivering MMP genes. Here, we evaluated a newly designed hyaluronic acid (HA)-shielded delivery system for systemic administration of plasmid DNA encoding MMP13 (pMMP13), and tested whether the enhanced expression of MMP13 ameliorates liver fibrosis in mice. In the CCl4-induced liver fibrosis model, systemic administration of pMMP13 using HA and polyethylenimine (PEI) significantly increased the expression of MMP13 and reduced collagen deposition. Moreover, following delivery of pMMP13 in a HA-shielded PEI complex, the serum levels of aspartate transaminase were reduced to levels approaching those in untreated normal mice. These results indicate that the delivery of pMMP13 using HA-shielded PEI enhances the efficiency of MMP13 expression in the liver, and highlight the potential of pMMP13 gene therapy as an antifibrotic strategy. The imbalanced expression of matrix metalloproteinases (MMPs) is associated with liver fibrosis, one of the most common chronic liver diseases. Enhanced expression of MMPs by gene therapy is emerging as a promising antifibrotic strategy, but the effectiveness of this approach depends on reliable systems for delivering MMP genes. Here, we evaluated a newly designed hyaluronic acid (HA)-shielded delivery system for systemic administration of plasmid DNA encoding MMP13 (pMMP13), and tested whether the enhanced expression of MMP13 ameliorates liver fibrosis in mice. In the CCl4-induced liver fibrosis model, systemic administration of pMMP13 using HA and polyethylenimine (PEI) significantly increased the expression of MMP13 and reduced collagen deposition. Moreover, following delivery of pMMP13 in a HA-shielded PEI complex, the serum levels of aspartate transaminase were reduced to levels approaching those in untreated normal mice. These results indicate that the delivery of pMMP13 using HA-shielded PEI enhances the efficiency of MMP13 expression in the liver, and highlight the potential of pMMP13 gene therapy as an antifibrotic strategy.