tbuckley/cabot-search huggingface dataset:
Surveillance of antibiotics use in a community hospital
Authors: R. Latorraca
Journal: JAMA (1979)

An ongoing system of antibiotic surveillance was initiated in a community hospital. The system was based on the guideline audits of antimicrobial use published by the Veterans Administration Ad Hoc Interdisciplinary Advisory Committee on Antimicrobial Drug Usage. The surveillance is accepted well by the medical staff. It has proved to be cost-effective and educational. A changing pattern of antimicrobial drug use has been recognized that has resulted in decreased antimicrobial drug costs.
Abstract B46: Rac1 inhibition as a therapeutic strategy in breast cancer
Authors: Dana Senderoff, Georges Azzi, Erik Goka, Marc Lippman
Journal: Cancer Research (2016)

Abstract Over the past few decades, targeted therapies have accounted for most of the therapeutic advances in breast cancer. The purpose of this approach is to discover new, actionable therapeutic strategies for breast cancer. We previously used a forward genomic screening approach to identify novel genes capable of cooperating with HER2, and found that loss of HACE1 was prevalent in breast cancer, identifying it as a tumor suppressor gene. HACE1 had significantly lower expression in breast cancer patients compared to normals. HACE1 is an E3 ubiquitin ligase that ubiquitinates Rac1, marking it for degradation. Rac1, a Rho GTPase, is a central component of key signaling pathways in breast cancer. While we identified HACE1 in a HER2 cooperating screen, the observation that HACE1 levels were consistently low across different subtypes of breast cancer led us to suggest that Rac1 is commonly hyperactivated in breast cancer and therefore has potential as a therapeutic target. We tested a Rac1 inhibitor, EHT 1864, on 8 different breast cancer cell lines, starting with an initial soft agar assay screen for sensitivity versus resistance and found that 4 cells lines were sensitive to the Rac1 inhibitor in soft agar cloning assays (MCF7, T47D, BT549, and BT474), while 4 other cell lines were resistant (MDA231, MDA436, MDA468, HS578T). These results were confirmed in 2D proliferation assays. The majority of the cell lines that were resistant to Rac1 inhibition overexpressed EGFR, suggesting that overexpression of EGFR confers resistance to Rac1 inhibition via the MAP Kinase pathway. Isogenic cell lines (MCF7) that express multiple activating proteins of the MAPK signaling pathway including EGFR, HER2, and MEK were treated with EHT1864 to determine if MAPK signaling was capable of overcoming Rac1 inhibition. Interestingly, the expression of EGFR conferred resistance to the Rac1 inhibitor. We further showed that molecular knockdown of EGFR in HS578T cells (EGFR-overexpressing, Rac1 inhibitor-resistant cells) resensitizes this cell line to Rac1 inhibition. Pharmalogical inhibition of EGFR using Gefitinib, an EGFR tyrosine kinase inhibitor, demonstrated the same resensitization to the Rac1 inhibitor. Our results suggest that Rac1 inhibition may be a therapeutic strategy in the treatment of breast cancer, as a single agent alone or in the case of EGFR overexpressing (triple-negative) breast cancers, in combination with EGFR targeted therapies. Citation Format: Dana Senderoff, Georges Azzi, Erik Goka, Marc Lippman. Rac1 inhibition as a therapeutic strategy in breast cancer. [abstract]. In: Proceedings of the Fourth AACR International Conference on Frontiers in Basic Cancer Research; 2015 Oct 23-26; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2016;76(3 Suppl):Abstract nr B46.
Relationship of QBI-139, a human ribonuclease variant, and RNA in cancer cells.
Authors: L. E. Strong, J. A. Kink, B. Mei, M. N. Shahan, D. Pensinger, R. T. Raines
Journal: Journal of Clinical Oncology (2010)

e13650 Background: RNA has been recognized as a drug target for cancer therapy, as evidenced by the ongoing clinical trials of RNAi and antisense therapies. An alternative approach that circumvents the delivery and stability issues of RNAi and antisense is to harness the activity of naturally occurring enzymes that degrade RNA. The EVade Ribonucleases (RNases) are variants of the native RNases that have been modified to diminish their binding to their natural inhibitor, allowing the EVade RNases to kill cancer cells. The efficacy of one of the EVade RNases, called QBI-139, in in vivo models of human cancer has been examined relative to FDA approved cancer therapies. Methods: QBI-139 has been tested in nude mouse xenograft models using a variety of tumor types and multiple cell lines within the different tumor types. Each model compared the efficacy of QBI- 139 with control groups which included: vehicle and an effective commercial drug specific for each tumor type (e.g. 5-fluorouracil or cisplatin). The human cancer cells were grown in culture and then implanted subcutaneously into the flanks of nu/nu mice. The tumors were allowed to grow to a measureable size and then drugs were administered once weekly. Tumor volumes and animal body weights were recorded twice weekly. The percent tumor growth inhibition (TGI) was used as a measure of efficacy was determined by comparing final and starting tumor volumes of groups treated with drug relative to the vehicle. Results: QBI-139 demonstrated a efficacy in prostate cancer that was similar to docetaxel with both agents causing >80% TGI. In addition, the safety profile of QBI-139 was better than docetaxel, which led to the death of two animals in that arm of the study. Additional results will be presented in colorectal and non-small cell lung cancer models. Conclusions: QBI-139 is a broadly efficacious agent that provides a new way to attack cancer and may provide an innovative new tool for oncologists. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Quintessence Biosciences, Inc. Quintessence Biosciences, Inc.
F-18 FDG positron emission tomography to differentiate diabetic osteoarthropathy from septic arthritis.
Authors: NAHEEL ALNAFISI, MIJIN YUN, ABASS ALAVI
Journal: Clinical Nuclear Medicine (2001)

From the Division of Nuclear Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Received for publication September 25, 2000. Accepted October 24, 2000. Reprint requests: Dr. Abass Alavi, Division of Nuclear Medicine, Hospital of the University of Pennsylvania, Donner Building, Room
An Infiltrating Adenomatous Lesion of the Colon of Rats Ingesting Motor Lubricating Oil (S. G. F. No. 1 Oil)&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: Lushbaugh, Clarence C., Hackett, Adeline
Journal: JNCI Journal of the National Cancer Institute (1948)

Journal Article An Infiltrating Adenomatous Lesion of the Colon of Rats Ingesting Motor Lubricating Oil (S. G. F. No. 1 Oil) Get access Clarence C. Lushbaugh, Clarence C. Lushbaugh Search for other works by this author on: Oxford Academic PubMed Google Scholar Adeline Hackett Adeline Hackett Department of Pathology and Toxicity Laboratory, University of Chicago Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 9, Issue 3, December 1948, Pages 159–172, https://doi.org/10.1093/jnci/9.3.159 Published: 01 December 1948 Article history Received: 15 June 1948 Published: 01 December 1948
Interpersonal Attractiveness and Clinical Decisions in Alcoholism Treatment
Authors: Michael R. O’Leary, Dennis M. Donovan, Edmund F. Chaney, Diane E. O’Leary
Journal: American Journal of Psychiatry (1979)

The authors investigated the interactive contribution of patient characteristics and staff perceptions of the patient to decisions concerning the provision of continued alcoholism treatment following an initial 2-week evaluation period. Staff perceptions contributed significantly more to an individual’s acceptance or rejection than did patient characteristics. A high interpersonal attractiveness rating also led to a significantly more positive evaluation of the patients’ level of intelligence, knowledge of current events, morality, and adjustment. The present results and research findings with general psychiatric populations are compared.
Case 22-1964
Authors: Daniel S. Ellis, Benjamin Castleman
Journal: New England Journal of Medicine (1964)

Presentation of CaseA seventy-five-year-old man entered the hospital because of inability to void.He had been well until one year previously, when he became anorectic and depressed; his consumption of tobacco increased, and a chronic cough developed at that time. Six months before admission constipation occurred and progressed in severity. Three days before entry he was unable to void; a physician inserted a catheter, but only a few ounces of urine were drained. During the next two days the patient voided normally. On the day of admission he again was unable to void.The patient had lost 30 pounds . . .
Amish Study, II: Consensus diagnoses and reliability results
Authors: A M Hostetter, J A Egeland, J Endicott
Journal: American Journal of Psychiatry (1983)

Reliability of diagnosis is central to genetic research on mental illness. In the Amish Study of affective disorders, consensus diagnoses were derived by a psychiatric board using the Research Diagnostic Criteria (RDC). To verify the reliability of diagnoses, the authors 1) studied how well board members followed RDC procedures, 2) compared diagnoses based on abstracted medical records with those based on full medical records, 3) compared diagnoses based on the two data sources--abstracted medical records and the Schedule for Affective Disorders and Schizophrenia-Lifetime Version--and 4) studied diagnostic stability to determine validity of diagnosis. The results of these substudies demonstrate a high concordance of diagnosis.
Abstract IA27: The patient biosphere: Tumors live in people
Authors: Kenneth James Pienta, Sarah R. Amend
Journal: Cancer Research (2016)

Abstract Ecosystems are interactive systems involving communities of species and their abiotic environment. Tumors are ecosystems in which cancer cells act as invasive species interacting with native host cell species. As they grow, tumors fundamentally alter their microenvironment, disrupting the homeostasis of the host organ and eventually the patient as a whole. Lethality is the ultimate result of deregulated cell signaling and regulatory mechanisms as well as inappropriate host cell recruitment and activity that lead to the death of the patient. These processes have striking parallels to the framework of ecological biology: multiple interacting ecosystems (organ systems) within a larger biosphere (body), alterations in species stoichiometry (host cell types), resource cycling (cellular metabolism and cell-cell signaling), and ecosystem collapse (organ failure and death). In particular, as cancer cells generate their own ecosystem, displacing and co-opting normal cell function, resulting in systemic host (patient) effects that result in cytokine-mediated lethal syndromes that cause of majority of cancer patient deaths. Citation Format: Kenneth James Pienta, Sarah R. Amend. The patient biosphere: Tumors live in people. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Metastasis; 2015 Nov 30-Dec 3; Austin, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(7 Suppl):Abstract nr IA27.
Regulating Ethical Issues in Cell-Based Interventions: Lessons from Universal Declaration on Bioethics and Human Rights
Authors: Ana Rosa Tenório de Amorim
Journal: The American Journal of Bioethics (2009)

"Regulating Ethical Issues in Cell-Based Interventions: Lessons from Universal Declaration on Bioethics and Human Rights." The American Journal of Bioethics, 9(5), pp. 49–50
Relationship between changes in plasma amino acids and depression in alcoholic patients
Authors: L Branchey, M Branchey, S Shaw, C S Lieber
Journal: American Journal of Psychiatry (1984)

The authors studied the relationship between changes in amino acid precursors of biogenic amines and depression in 42 alcoholic patients with a secondary depression. Tryptophan and amino acids competing with it for brain entry were measured in the plasma of depressed alcoholics, nondepressed alcoholics, and control subjects. The ratio of tryptophan to its competitors was significantly lower in depressed patients than in nondepressed patients and controls. The decreased ratio was due primarily to decreased tryptophan and increased tyrosine and phenylalanine values. A decreased tryptophan ratio is known to result in decreased brain tryptophan and may contribute to depression through a deficiency of brain serotonin.
Brief Communication: Distribution of Anticancer Agents in Spontaneous Animal Tumors. II. Distribution of Gallium in Canine Lymphosarcoma2
Authors: James A. Straw, Philip Klubes, Michael M. Hart
Journal: JNCI Journal of the National Cancer Institute (1975)

The physiologic disposition of pharmacologic doses of gallium was studied in control dogs and dogs with spontaneous lymphosarcoma. Gallium 67 (67Ga) was administered iv with carrier gallium added at a dose of 8 mg/kg. About 50% of the injected dose was excreted in the urine by 48 hours (mostly in the first 12 hr), whereas negligible amounts were excreted in bile. The distribution of 67Ga in normal tissues was similar in control and tumor-bearing dogs. The tissue-to-plasma concentrations of gallium were considerably greater than 1 in the kidney cortex, bone marrow, bone, small intestine, and liver 6-72 hours after administration of the drug. At comparable time periods, tissue-to-plasma ratios of gallium were less than 1 in skeletal muscle and brain. In dogs with lymphosarcoma there was neither selective uptake nor selective retention of gallium in comparison to most normal tissues. In fact, several normal tissues, particularly kidney cortex and bone marrow, concentrated gallium greatly in excess of tumors. Qualitatively similar findings were obtained in a dog with malignant melanoma. These findings were contrary to what one would predict from reports showing that carrier-free 67Ga is selectively concentrated in various human and animal tumors. This indicates the need for more extensive studies of the physiologic disposition of pharmacologic (antitumor) doses of gallium in humans and appropriate animal models.
In patients ≥ 80 y with NSTEMI or unstable angina, an invasive strategy reduced CV outcomes
Authors: Aneesh V. Pakala, Sunil T. Mathew
Journal: Annals of Internal Medicine (2016)

Source Citation Tegn N, Abdelnoor M, Aaberge L, et al; After Eighty study investigators. Invasive versus conservative strategy in patients aged 80 years or older with non-ST-elevation myocardial infarction or unstable angina pectoris (After Eighty study): an open-label randomised controlled trial. Lancet. 2016 Jan 12. [Epub ahead of print]. 26794722
Abstract P1-07-03: Reproductive factors and subtype specific breast cancer risk
Authors: WF Anderson, RM Pfeiffer, J Wohlfahrt, B Ejlertsen, M-B Jensen, NT Kroman
Journal: Cancer Research (2016)

Abstract Introduction: Reproductive history and breast cancer risk reportedly differ by the estrogen receptor (ER±) and by the joint expression of ER and the human epidermal growth factor-2 receptor (ER±/HER2±). However, large sample sizes are needed to identify risk factor associations for the relatively less common ER- subtypes. Material and Methods: We, therefore, linked two large-scale and population-based Danish registries to assess the associations for parity, number of live births, and age at first live birth (AFLB) with receptor-specific breast cancer risk. Relative risks (RRs) and 95% confidence intervals (CIs) for associations were estimated with Poisson regression models. Results: With nearly 31 million women-years of follow-up, there were 45786 Danish women between the ages 20-84 years who developed an invasive breast cancer during the study period 1992-2011. Parity significantly reduced risk for ER+ and ER+/HER2- subtypes (RR for ER+/HER2- = 0.92; 0.87, 0.98) and suggestively increased risk for ER- and ER-/HER2- subtypes (RR for ER-/HER2- = 1.16; 0.99, 1.36). RRs increased with advancing AFLB for ER+ cancers, especially among premenopausal women; and were elevated for ER- cancers among age groups 12-19 years and 30-34 years compared to the reference age group 20-24 years. Conclusion: Associations of breast cancer risk and reproductive history varied among Danish women by ER± and by ER±/HER2±, consistent with receptor-specific etiological heterogeneity. Risk estimates for ER+ and ER+/HER2- cancers were similar to the well-established associations for breast cancer overall, whereas relative risks for ER- and ER/HER2- cancers tended to be null or the inverse of ER+ associations. Citation Format: Anderson WF, Pfeiffer RM, Wohlfahrt J, Ejlertsen B, Jensen M-B, Kroman NT. Reproductive factors and subtype specific breast cancer risk. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-07-03.
High Resource Utilizers From The Multicenter Compact Study Of Complications In Patients With Sickle Cell Disease and Utilization Of Iron Chelation Therapy
Authors: Lanetta B Jordan, Patricia Adams-Graves, Julie Kanter-Washko, Patricia A Oneal, Medha Sasane, Francis Vekeman, Christine Bieri, Andrea Marcellari, Matthew Magestro, Abigail Adams, Mei S. Duh
Journal: Blood (2013)
Abstract A12: Microenvironmental Interleukin-6 induced activation of STAT3 signaling in medulloblastoma: Implications for molecular pathology and therapy
Authors: Shuang Yan, Sampurna Chatterjee, Trupti Vardam, Shuji Kitahara, Tai Hato, Sylvie Roberge, Vasileios Askoxylakis, Mark Duquette, Dai Fukumura, Lei Xu, Rakesh Jain
Journal: Cancer Research (2016)

Abstract Aberrant activation of Janus kinase (JAK) / signal transducer and activator of transcription (STAT) 3 pathway has been implicated in tumor initiation, progression and metastasis which make it a potential therapeutic target in human malignancies. In vitro STAT3 inhibition exhibited anti-tumor effect in medulloblastoma (MB) cell lines; however, little has been reported about the mechanisms of STAT3 activation in medulloblastoma (MB). We found that STAT3 was constitutively activated in both medulloblastoma patient samples and 3 mice models that were clinically classified as SHH subgroup, Group 3 and Group 4 in pediatric MB patients. By using PCR arrays we investigated the early expression profile of local cytokines in host cerebellum during MB pathogenesis and found increased IL17B, IL6 and TNFα in the microenvironment of MB mice models. In vitro cytokine stimulation assay indicated that IL6 was the major activator of STAT3 in D283 MB cells. Confocal immunofluorescence staining of different cell components in the cerebellum in D283 xenografts showed that the endothelial cells and Purkinje cells were the two major sources of IL6 secretion. Our data provides molecular and cellular clue for the activation of STAT3 signaling during MB tumorigenesis and might help to develop more effective therapeutic targets for STAT3 blockade in MB. Citation Format: Shuang Yan, Sampurna Chatterjee, Trupti Vardam, Shuji Kitahara, Tai Hato, Sylvie Roberge, Vasileios Askoxylakis, Mark Duquette, Dai Fukumura, Lei Xu, Rakesh Jain. Microenvironmental Interleukin-6 induced activation of STAT3 signaling in medulloblastoma: Implications for molecular pathology and therapy. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; 2015 Nov 9-12; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(5 Suppl):Abstract nr A12.
Abstract P4-09-11: microRNA markers and risk of recurrence in women with ductal carcinoma in situ
Authors: Y Liu, C Baker, X Wang, G Colditz
Journal: Cancer Research (2016)

Abstract Background: Women with DCIS have increased risk for invasive breast cancer. Limited abilities to accurately identify aggressive DCIS have resulted in inappropriate treatment for many women with mammographically-detected DCIS. miRNAs play a critical role in tumorigenesis. It remains unknown if miRNAs are associated with recurrence and refine risk assessment for DCIS patients. Methods: The study included 16 DCIS cases that developed ipsilateral recurrence (cases) and 32 DCIS cases that did not develop any type of recurrence (controls). Cases and controls were treated with breast conserving surgery and matched on age, race, and year of diagnosis. Expression of 96 cancer-related miRNAs was quantified using RT-PCR. Results: Two miRNAs were differentially expressed between cases and controls (p&amp;lt;0.05). A combination of the two miRNA markers was significantly associated with recurrence risk (odd ratio=2.60 per 1-unit increase, 95% confidence interval=1.14-8.13), which was independent of family history of breast cancer, radiation and endocrine therapy. The miRNA-based score (c-statistic=0.73) performed better than individual miRNAs (c-statistic=0.64-0.69) in discriminating DCIS cases who did and did not develop recurrence. Conclusion: miRNA expression in DCIS was associated with recurrence risk, which warrants further investigations to identify new miRNA markers by including more DCIS cases and analyzing all breast cancer-related miRNAs. Citation Format: Liu Y, Baker C, Wang X, Colditz G. microRNA markers and risk of recurrence in women with ductal carcinoma in situ. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P4-09-11.
Differential Increases in Glutathione S-Transferase Activities in a Range of Multidrug-Resistant Human Tumor Cell Lines
Authors: Richard D. H. Whelan, Louise K. Hosking, Alan J. Townsend, Kenneth H. Cowan, Bridget T. Hill
Journal: Cancer Communications (1989)

Modified glutathione S-transferase (GST) activity was detected in MCF-7 cell lines selected in vitro for modest levels of resistance (2.6- to 13.7-fold) not only to Adriamycin but also to Novantrone, vincristine (VCR), and etoposide (VP-16). Western blot analysis revealed a qualitative increase in the expression of the pi class GST isozyme and some apparent down regulation of the mu class in these resistant lines relative to the parental line. Overexpression of GST pi protein was also observed after in vitro exposure of MCF-7 cells to fractionated x-irradiation, which resulted in a subline that exhibited 5-fold resistance to VCR and 3-fold resistance to VP-16. Northern blot analysis provided qualitative evidence that these changes in GST pi and mu appeared to be at the transcriptional level in these VCR- and VP-16-resistant MCF-7 sublines. In contrast, similarly selected VCR-resistant, VP-16-resistant, and x-ray-pretreated-resistant sublines, derived from the SuSa cell line established from a human testicular teratoma, did not exhibit significant alterations in GST isozyme profiles compared with their parental cell lines. All parental and resistant SuSa lines that were studied expressed the GST pi isozyme constitutively. Total glutathione content and glutathione peroxidase activities were not modified in parallel with the GST alterations in these human tumor drug resistant sublines. These data suggest that the increased cellular GST activity was associated with selection of resistance to many of the drugs associated with the multidrug resistant phenotype in MCF-7 sublines but that this was not the case for the other human tumor cell line (SuSa) tested.