tbuckley/cabot-search huggingface dataset:
An Outbreak of Shigellosis Associated with the Consumption of Raw Oysters
Authors: Gordon Reeve, Deborah L. Martin, Janeene Pappas, Richard E. Thompson, Katherine D. Greene
Journal: New England Journal of Medicine (1989)

We describe an outbreak of Shigella sonnei infection among 24 persons who had eaten raw oysters in restaurants in southeastern Texas within five days before the onset of symptoms. The oysters in all eight restaurants were supplied by the same dealer, but examination of a routine water sample collected six days before the probable time of contamination showed the waters where the oysters were harvested to be free of fecal contamination, making widespread sewage contamination unlikely. The suspect oysters were traced to a single boat. Stool swabs from that boat's oyster harvesters allowed the identification of one asymptomatic carrier who had a strain of S. sonnei (determined by colicin typing, plasmid analysis, and testing for susceptibility to antibiotics) that was similar to or the same as that infecting the patients. Although the source of this man's infection was unknown, he reported having eaten no oysters. Investigation revealed that 5-gallon (19-liter) pails were used as toilets aboard the oyster boats. Sewage collected in these pails was often dumped overboard into the harvesting area. We conclude that this outbreak of S. sonnei resulted from poor sanitary procedures that probably allowed stool from a carrier to contaminate oysters either just before or after they were taken aboard the boat.
Effect of Inhaled Formoterol and Budesonide on Exacerbations of Asthma
Authors: Romain A. Pauwels, Claes-Göran Löfdahl, Dirkje S. Postma, Anne E. Tattersfield, Paul O'Byrne, Peter J. Barnes, Anders Ullman
Journal: New England Journal of Medicine (1997)

The role of long-acting, inhaled β2-agonists in treating asthma is uncertain. In a double-blind study, we evaluated the effects of adding inhaled formoterol to both lower and higher doses of the inhaled glucocorticoid budesonide.
THU0388 Tocilizumab strongly suppresses the serum amyloid a level in refractory adult – onset still’s disease associated amyloidosis
Authors: H.M. Al Attia, M.A. Ibrahim
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background</h3> A amyloidosis, is a rare but serious complication of chronic inflammatory conditions including Adult-onset Still's disease (AOSD). Treatment can be frustrating too. <h3>Objectives</h3> We describe the case of refractory AOSD who developed secondary amyloidosis without proteinuria. As she failed to respond to several agents including anti-TNF alpha factory therapy, the treatment with Tocilizumab, an anti –human interleukin-6-receptor inhibitor was introduced. It brought the level of serum amyloid A (SAA) from several hundred times normal to almost normal value after 3 injections <h3>Methods</h3> A-27 year old female has carried the diagnosis of AOSD since 2008 after experiencing repeated attacks, fever, malaise, arthropathy, myalgia and pleura-pericarditis. She fulfilled the criteria of Yamaguchi (1) for the diagnosis. Her laboratory workup repeatedly showed a rise in the levels of inflammatory markers including C reactive protein (CRP), ESR, serum ferritin along with leucocytosis during relapses. She failed to respond adequately to several courses of agents including NSAIDs, corticosteroids, methotrexate, leflonamide, anti TNF alpha agents and anti-CD20 (Rituximab). Anti IL-1 was not available locally. Because of the refractory nature of the disease a monthly injection of Tocilizumab (8mg/kg) was commenced with reasonable response evidenced by spacing out relapses and declining of inflammatory markers. Despite the absence of proteinuria during the follow-up period a latent amyloidosis was suspected. <h3>Results</h3> The subcutaneous abdominal wall fat for Congo-Red staining was highly positive. Concomitantly, the SAA carried out by Bioscientia, Germany, revealed a level of 1140 mg/L (normal up to 6.4 mg/L). Within the subsequent three injections of tocilizumb the level went down further to 49 mg/L, and then lately to only 14 mg/L. <h3>Conclusions</h3> Undoubtedly the decline in the SAA is a reflection of a reduced amyloid activity, which is worth reporting. Tocilizumab, therefore, is a promising agent for treating secondary amyloidosis by suppressing the level of SAA. Such a successful outcome by this agent opens a new frontier for its indications. <h3>References</h3> Yamaguchi M, Ohta A, Tsunematsu T et al. Preliminary criteria for classification of adult Still's disease. J Rheumatol 1992;19:424–30 <h3>Disclosure of Interest</h3> None Declared
Abstract 2899: Doxorubicin-mitomycin co-loaded polymer lipid nanoparticle enhanced efficacy against breast tumor and decreased toxicity as compared to Doxil
Authors: Preethy Prasad, Adam Shuhendler, Ping Cai, Mei Sun, Peter Liu, Rob Bistrow, Andrew Rauth, Xiao Wu
Journal: Cancer Research (2012)

Abstract Background: Multidrug resistance acquired by cancer cells and the dose-limiting toxicity of anti-cancer drugs are contributing factors to the failure of cancer chemotherapy. Doxorubicin (Dox) -Mitomycin C (MMC) co-loaded stealth polymer lipid hybrid nanoparticles (DMsPLN) was developed to overcome these problems and demonstrated anti-cancer synergy in vitro. The purpose of the study is to evaluate in vivo efficacy and safety of DMsPLN in a breast cancer model. Method: The efficacy and systemic toxicity of DMsPLN were evaluated against clinically used Doxil in mice bearing murine or human mammary carcinomas. DMsPLN were administered intravenously at 50 mg/m2 doxorubicin single dose or once every 4 days for 4 cycles. Tumor size was measured as function of time to determine therapeutic efficacy of the treatment and systemic toxicity was monitored by repeated measurement of body weight. Results: Significant difference in the efficacy of DMsPLN relative to Doxil was observed in both sensitive and resistant tumor models. A clear enhancement of tumor growth delay (TLD) was evident with both single and 4 times doses of DMs PLN. In single dose and 4x dose DMsPLN groups, the TGD were significantly improved to 100% and 300% in the sensitive tumor model. In the resistant tumor model, the TGD ranged from 30%-130% for the single dose and the 4x dose DMsPLN, respectively. 10% of the mice showed complete tumor disappearance in DMs PLN and 25% complete tumor disappearance was observed in DMs PLN 4x group in the sensitive tumor model. 11% of the mice showed complete tumor disappearance in both DMs PLN and in DMs PLN 4x group in the resistant tumor model. In addition to enhanced efficacy, none of the toxicity associated with Doxil treatment were observed in single or 4x DMsPLN treatment. Conclusions: DMsPLN demonstrated enhanced efficacy and reduced toxicity over Doxil in aggressive mouse models of sensitive and resistant breast cancers. Therefore, DMsPLN may provide clinically relevant, more aggressive anti-cancer interventions. 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 2899. doi:1538-7445.AM2012-2899
Treatment of Lymphopenic Hypogammaglobulinemia and Bone-Marrow Aplasia by Transplantation of Allogeneic Marrow
Authors: H.J. Meuwissen, R. A. Gatti, P. I. Terasaki, R. Hong, R. A. Good
Journal: New England Journal of Medicine (1969)

A patient with lymphopenic hypogammaglobulinemia was treated with two bone-marrow transplantations, with establishment of immunologic competence after the first transplant. After this transplant, an immunologically induced pancytopenia occurred, attributed to a reaction of the grafted lymphoid cells against host constituents. The patient's bone marrow was then repopulated with a second marrow graft from the same donor. No further evidence of graft-versus-host disease was observed, and the recipient now possesses red blood cells and lymphocytes of donor type. The successful outcome of these transplantations depends to a large extent on the existence of histocompatibility between donor and host.
AB0857-PARE Beyond the clinic: qualitative analysis of stene award essays from poland
Authors: B. Moskalewicz
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Health care providers are well grounded on main aim of their activity. To treat a disease is the goal for specialists and medical institutions. A meaning of a chronic disease in lay – persons perspective ( a human, cultural approach) was not scientifically explored. Essays submitted for Edgar Stene Award brings an unique material on individuals' values and assessment of rheumatic disease presence in everyday life. Edgar Stene essays were prepared spontaneously. An expression of authors were not limited by research interest. A hierarchy of significant processes in authors' life should to be uncover as well as a role of chronic disease <h3>Objectives</h3> How authors answer the question of the sense and value of life with chronic disease in their essays. What is a meaning of disease given by writer experienced by arthritis? What is cultural/social influence on a process of giving this meaning? <h3>Methods</h3> A process of qualitative data analysis of 40 essays from Poland as primary documents, was supported by program ATLAS.ti. A program made easier data integration, organization and constant documentation of the process. <h3>Results</h3> Analyzed essays describe life challenges and experience of "crisis" in process of a disease. A model of meaning objects depends on a period of symptoms, an age of onset, gender, age and health status. The most important things for authors are: understanding and interpreting the disease and also incorporating chronic disease into mainstream of life. <h3>Conclusions</h3> Nonprofessional life writing is invaluable source of knowledge of individuals' sense of the worth of their existence with rheumatic disease. <h3>Disclosure of Interest</h3> None Declared
RHEUMATIC HEART DISEASE SCREENING IN SCHOOLS THROUGH PORTABLE ECHOCARDIOGRAPHY IN BRAZIL: DATA FROM THE PROVAR STUDY
Authors: Bruno Ramos Nascimento, Andrea Beaton, Maria do Carmo Nunes, Adriana Diamantino, Kaciane K. Oliveira, Cassio M. Oliveira, Vitoria M. Rezende, Eduardo L. Lopes, Amanda O. Lauar, Luise C. Barros, Michelle C. Galbas, Lindsay Perlman, Antonio Ribeiro, Craig Sable
Journal: Journal of the American College of Cardiology (2016)
Abstract 3086: Interactions of nucleolin and ribosomal protein RPL26 in the translational control of human p53 mRNA
Authors: Jing Chen, Kexiao Guo, Michael B. Kastan
Journal: Cancer Research (2011)

Abstract Our lab has previously shown that the ribosomal protein RPL26 enhances p53 translation and induction after DNA damage and that this regulation depends upon interactions between the 5′ and 3′ untranslated regions (UTR) of human p53 mRNA (Takagi et al Cell, 2005; Chen &amp; Kastan, Genes &amp; Dev, 2010). In contrast, nucleolin (NCL), a multifunctional nucleolar protein, suppresses the translation of human p53 mRNA and its induction after DNA damage. Interestingly, RPL26 and NCL also interact with each other. In order to understand how these two proteins cooperate with/antagonize each other to regulate p53 translation after stress, we first recapitulated the translational control of p53 by NCL in both an in vitro transcription/translation system and a cell-based, luciferase reporter system. In both systems, NCL repression required the presence of both the 5′UTR and 3′UTR of p53 mRNA. Further, NCL binds to the same 5′-3′ UTR interaction region that is critical for RPL26 recruitment after DNA damage. We also observed that NCL protein interacts with itself; the ability of NCL to dimerize/oligomerize and its reported ability to stabilize double strand nucleic acid structures suggests the possibility that NCL may stabilize the double-strand RNA structure involving the two p53 mRNA UTR's. Domain mapping demonstrated that the RNA binding domain of NCL participates in binding to p53 mRNA, is required for both NCL dimerization and NCL-mediated translational repression, and is the domain of NCL that interacts with RPL26. RPL26 was able to disrupt NCL dimerization in cell-based immunoprecipitation assays. We also identified the domain of RPL26 that is required to interact with nucleolin and found that point mutations in this region of RPL26 reduce RPL26-NCL interactions and attenuate both RPL26 binding to human p53 mRNA and p53 induction by RPL26. These observations taken together suggest a model for the interplay of NCL and RPL26 in the translational control of human p53 mRNA after DNA damage: NCL binds both p53 UTR's and NCL dimerization/oligomerization facilitates the double strand RNA structure by stabilizing the base pairing between the 5′ and 3′ UTR's. This “closed” structure of p53 mRNA might inhibit its translation by affecting the access of general translational machinery to the message. Upon stress stimulation, RPL26 binds to this double-stranded RNA structure containing the two UTR's and occupied by NCL, leading to a disruption of NCL dimerization and enhancement of p53 translation. 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 3086. doi:10.1158/1538-7445.AM2011-3086
CN-16 * INCIDENCE, PREVALENCE AND PREDICTORS OF CHEMOTHERAPY INDUCED PERIPHERAL NEUROPATHY: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: M. Seretny, G. Currie, E. Sena, S. Ramnarine, R. Grant, M. Macleod, L. Colvin, M. Fallon
Journal: Neuro-Oncology (2014)

BACKGROUND: Chemotherapy Induced Peripheral Neuropathy (CIPN) is a disabling side effect of chemotherapy. Severe CIPN may require chemotherapy dose reduction or cessation. There is no effective CIPN prevention strategy; treatment of established CIPN is limited, and the prevalence of CIPN is not known. Here we aim to calculate overall CIPN prevalence from published studies, and to identify risk factors for CIPN. METHODS: We used systematic review to identify studies reporting the prevalence of CIPN, and used random effects meta-regression to estimate the overall prevalence. We assessed study quality using the CONSORT and STROBE guidelines. We provide a qualitative summary of factors reported to alter the risk of CIPN. RESULTS: We included 31 studies with data from 4179 patients in our analysis. CIPN prevalence was 68.1% (57.7 to 78.4) when measured in the first month after chemotherapy, 60.0% (36.4 to 81.6) at three months and 30.0% (6.4 to 53.5) at six months or more. Different chemotherapy drugs were associated with differences in CIPN prevalence, and there was some evidence of publication bias. Genetic risk factors were reported in four studies. Clinical risk factors, identified in 4 of 31 studies, included neuropathy at baseline, smoking, abnormal creatinine clearance and specific sensory changes during chemotherapy. CONCLUSIONS: Although CIPN prevalence decreases with time, at six months 30% of patients continue to suffer from CIPN. Routine CIPN surveillance during post chemotherapy follow-up is needed. A number of genetic and clinical risk factors were identified that require further study.
PTU-163 Depression and carcinoid syndrome: is there any relationship? A cross-sectional study
Authors: J Garcia-Hernandez, M Mohmaduvesh, P Davies, C Toumpanakis, J R Goodhand, M Caplin, D Skuse
Journal: Gut (2012)

<h3>Introduction</h3> The relationship between brain serotonin and depression is well established. It is also widely accepted that serotonin hyperproduction in carcinoid syndrome does not cross the brain barrier. CNS serotonin is synthesised from tryptophan within serotonergic neurons and a deficiency of this precursor could be possible on carcinoid patients. In this cross-sectional study we evaluated, whether the feelings of depression are associated with neuroendocrine symptomatology. In addition, whether self-report of quality of life is associated with feelings of depression. <h3>Methods</h3> 47 patients with carcinoid syndrome completed a survey via clinic involving: QoL questionnaires and the Beck9s Depression Inventory-II (BDI-II). All questionnaires were counterbalanced. <h3>Results</h3> 45 out of 47 patients had low scores on the BDI-II and not likely to suffer from depression. Only two participants had moderate depression scores. These scores were negatively associated with self-report of QoL, r=−0.59, N=46, p&lt;0.001. Interestingly, endocrine symptoms that is, flushing and night sweats, were not associated with depressive symptoms: r=0.22, N=44, p=0.15, whereas, gastrointestinal symptoms that is, diarrhoea, abdominal discomfort, bloatedness and indigestion, were strongly associated with depression scores: r=56, N=43, p&lt;0.001. <h3>Conclusion</h3> Depressive scores in carcinoid patients are often attributed to the stress of diagnoses and adaptation to this chronic disease, however, although a causal relationship has not been established between carcinoid and depression, physicians should consider this possibility when psychological symptoms do not improve with conventional therapy. Further research is needed to understand why gastrointestinal, and not endocrine, symptoms were correlated with depressive symptoms. <h3>Competing interests</h3> None declared. <h3>References</h3> 1. <b>Lapeire LD</b>, Tansens A, Lemmens G, <i>et al.</i> Carcinoid encephalopathy: A single entity or a spectrum of different disorders. <i>Acta Oncologica</i> 2010;<b>49</b>:268–70. 2. <b>Major LF</b>, LaVonne Brown G, Wilson WP. Carcinoid and psychiatric symptoms. <i>South Med J</i> 1973;<b>66</b>:797–90. 3. <b>Rosenthal MA</b>. Carcinoid associated encephalitis successfully treated with tryptophan. <i>J Clin Neurosci</i> 2004;<b>11</b>:66–7. 4. <b>Williams MD</b>, Dolenic T. Selective serotonin reuptake inhibitors and patients with carcinoid tumor. <i>Psychosomatics</i> 2005;<b>46</b>:370–2.
New inspection regime in England sees Whipps Cross hospital downgraded
Authors: N. Hawkes
Journal: BMJ (2013)

England’s healthcare watchdog the Care Quality Commission has shown its teeth in a highly critical report on Whipps Cross University Hospital in east London.1 The hospital, part of Barts Health NHS Trust, has been issued with three formal warnings, covering cleanliness and infection control, equipment standards, and support to staff, and has been found to be in breach of 10 of the 16 national standards of quality and safety.

The strongly worded report is in contrast to the results of a routine inspection last November, in which the hospital met four out of five of the standards being inspected, failing only on “supporting workers,” where the commission said action was needed. Since then the CQC has a new chairman, David Prior, who has been outspoken in his criticism of the inspections carried out under his predecessors,2 and Mike Richards has been appointed chief inspector of hospitals.3

Either the hospital declined sharply in six …
Abstract 5384: Hrev107 enhances prostaglandin D2 synthase-mediated cancer cells suppression in the testis.
Authors: Fu-Ming Tsai, Chang-Chieh Wu, Rong-Yaun Shyu, Shun-Yuan Jiang
Journal: Cancer Research (2013)

Abstract Hrev107, also called HRASLS3 or PLA2G16, is a member of the HREV107 type II tumor suppressor gene family which includes HREV107, Retinoid-inducible gene 1 (RIG1), and HRASLS. The protein in this family contains an NC domain, with unknown function at the N-terminus, and a hydrophobic membrane-anchoring domain at the C-terminus. HREV107 has shown that expressed at high levels in differentiated tissues of post-meiotic testicular germ cells but not in human testicular germ cell tumors. Prostaglandin D2 (PGD2) has shown that can induce SOX-9 nuclear translocation and subsequent Sertoli cell differentiation. In addition, expression of the Prostaglandin D2 synthase (PTGDS) has been detected in the cellular lineage. This gives rise to the Sertoli cells, and the Sertoli cells appear to express the PTGDS only during the VI-VIII stages of the spermatogenic cycle after spermiation. These results suggested that PGD2 may play an important role in the testis differentiation. Our previous result showed that RIG1 (as RIG1 is expressed in the human species only) can interact with PTGDS. We further examined the effect of mouse Hrev107 on the growth of mouse testicular cells. When Hrev107 was expressed in TM3 or TM4 mouse testicular cancer cells, the cell migration and invasion were inhibited. Further, we found PTGDS was co-localized with Hrev107 in TM4 testis cells. In Hrev107-expressing NT2/D1 cells, elevated levels of PGD2, cAMP, and SRY-related high-mobility group box 9 (SOX9) were observed. This result indicated that Hrev107 can enhance PTGDS activity. Silencing of PTGDS expression significantly decreased h-REV107-mediated cAMP and PGD2 production. Furthermore, silencing of PTGDS or SOX9 alleviated Hrev107-mediated suppression of migration and invasion. These results suggest that Hrev107 will suppress cell migration/invasion through the PGD2 signaling pathway. In conclusion, Hrev107 can interact with PTGDS to enhance its function and to further suppress NT2/D1 cell migration and invasion. Citation Format: Fu-Ming Tsai, Chang-Chieh Wu, Rong-Yaun Shyu, Shun-Yuan Jiang. Hrev107 enhances prostaglandin D2 synthase-mediated cancer cells suppression in the testis. [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 5384. doi:10.1158/1538-7445.AM2013-5384
Intestinal Duplication: Imaging With Tc-99m Sodium Pertechnetate
Authors: CHARLES L. TORGERSON, DANIEL W. YOUNG, YOGINDER N. VAID, KEITH E. GEORGESON, DAVID R. KELLY
Journal: Clinical Nuclear Medicine (1996)

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Fertility Drugs May Raise Ovarian Cancer Risk
Authors: Tom Reynolds
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Fertility Drugs May Raise Ovarian Cancer Risk Get access Tom Reynolds Tom Reynolds Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 2, 20 January 1993, Pages 84–86, https://doi.org/10.1093/jnci/85.2.84 Published: 20 January 1993